Interesting Stuff

Quantcast
NASTY RAP LYRICS AND VIOLENCE WE ARE LIVING IN AN AGE when many, especially the youth, have made an idol of thuggery. The word thug is, by definition, “one of a fraternity of robbers and assassins in India who practiced secret murder as an act of propitiation to the goddess Kali”. The word thug also means “a ruffian and an assassin”. The word ruffian means “a brutal, boisterous fellow; any base, low character, as a robber, etc.” Then the word assassin means “one who slays treacherously or by covert assault; one who kills, or attempts to kill, secretly as the agent of another or others, or for reward”. The word assassinate means “to kill”. So we see that in all of these definitions of the idol of our age, is nothing but the end goal of murder, robbery, brutality, low character and boisterous vileness. While the youth of today are led about by rap music in all of its variations and think that they have discovered something new, they are simply dupes for demonic powers which have nothing in mind but to kill, steal and destroy. The mesmerizing powers of the demon goddess Kali are well known worldwide, as the adherents to Kali’s demand for blood sacrifice are still in action today. Having been to India, I remember I was shocked when I first saw men, countless men with their fingernails painted bright red. When I inquired what the reason for this was, I was told that the followers of Kali must offer her blood, and human blood is her first preference. Of course it is claimed that no longer are her followers allowed to commit their murders in order to appease the demands of this wicked and cruel goddess. Now it is stated that her followers offer her goats. However, there is plenty of evidence that thuggery is as common now as it has ever been in that her known followers are still committing murder to appease her demands for blood. Now, since this type of murder stems back to Hinduism and this goddess, one would think, how in the world could such a thing have anything to do with the passion for murder and bloodshed that is prevailing in the western nations and even worldwide? The truth is that satan has one agenda and he repeats that agenda for all who will fall prey to his wicked devices. The fascination of the youth with death, the absorption in crime and murder is only too evident that the roots of rap are evil and those who adhere to the ultimate messages are adhering to the demands of goddess spirits every bit as cruel and blood thirsty as Kali, goddess queen of Hinduism. While youth proudly parade in their shirts and other clothing items which symbolize their faithfulness to their idols, do they ever stop and consider that the thugs they are worshiping are taking them into a lifestyle that can only end in imprisonment, harm to others as well as one’s self, and death? Does anyone stop and consider that the thugs who are enticing them to follow in the same lifestyle are often the victims of the very murder they are enticing others to commit? How deceptive are the ancient demons that have invaded through the music which is so base and thrilling in its message of destruction whereby the unsuspecting give themselves to demonic powers that are base, vile and completely boisterous in the message they give forth. It does not take much mentality to kill, to steal, to hurt and harm others, it simply takes a fool who will follow the commands of demons who are devising evil on every hand. Has anyone really stopped to consider that the idolatry of thuggery, which so many have given themselves unto, is nothing but the work of demons under the command of satan? And that while the youth and even some beyond youth are giving themselves over to murder, to robbery, to vileness and rottenness, that they are nothing but the fools who will perish in their sins? The Bible strictly forbids the very things which those involved in thuggery see as their goals in life. When they burn in Hell, will they boast of how many they have murdered, how many they have robbed and violated? Or will they be too absorbed in their own agonies, which will cause them torment, and the burning in the flames of Hell as their evil deeds are replayed over and over before their eyes and they will never escape the judgment they have received for the same? If you have been deceived by the idolatry of thuggery, you can confess your sins and repent before the Lord Jesus Christ today. He desires to free you from the burden of your sins, and if you repent He will set you free. It is stupid to go in a way of destruction when you could turn from idolatry and turn to the Lord. The Lord will hear you as you pray simply, “Jesus, I ask you to forgive me for my sins and the idolatry of thuggery which has caused those sins; please come into my heart and be my Savior and guide my life.” Amen. + The Greatest Racket in History THE POWER OF THE BLOOD OF JESUS by H.A. Maxwell Whyte JESUS was the only begotten of the Father (John 1:14) and His body was formed and fashioned wonderfully in the womb of Mary His mother; but the LIFE that was in Jesus Christ came alone from the Father by the Holy Spirit. Therefore, this life which flowed in the veins of the Lord Jesus Christ came from God. No wonder He said, “I am the LIFE.” God imparted His own life into the Bloodstream of Jesus. Adamic blood is corrupt and was carried by Mary, who declared that Jesus her Son was “God my Saviour” (Luke 1:47). Mary was the chosen carrier of the body of her Son, but all the Blood came from God. I do not know how many categories of human blood have been catalogued by medical science, but I do know that the “Blood type” of the Lord Jesus Christ was entirely different. The Blood that flowed in His veins was perfect, for it was not contaminated by Adam’s sin which brought sin and sickness into human blood. If Adam had not sinned, he would not have died. But by his sin, he introduced death into the human family. The human body, therefore, became subject to corruption and decay, and death ultimately comes to each one of us. It is at the time of death that the life that is in the blood takes its departure with the spirit and soul of man. Jesus Christ has no sin in His body, but He allowed Himself to die for the sins of a sinful humanity. He gave the perfect life that was in His perfect Blood to redeem poor mankind who carried death in their bodies -pure Blood for imperfect, contaminated blood. Life for life, for the life is in the blood. This is why Jesus is described as the last Adam. God sent Him to earth in the likeness of sinful Adam, but with pure uncontaminated Blood in his veins. God sent Him so that He might shed that pure Blood of His for the life of humanity. It is highly important for us to understand that the category of Jesus’ Blood was different. Peter rightly describes it as “precious blood” (1 Peter 1:19). It is not possible to evaluate the Blood of Jesus by human values. It is priceless. It is God’s price for the redemption of the whole human race. A great miracle takes place when a man trusts in Jesus and accepts Him as his personal Savior. Immediately, a great cleansing takes place, and the sin that is in the blood stream is purged. “For I will cleanse their blood that I have not cleansed: for the Lord dwells in Zion” (Joel 3:21). When we receive Jesus, the Bible declares that the heart is cleansed by the Blood of Jesus. This may be more literal than some would dare to believe. If the sin which is in our blood stream is purged and spiritual filth is washed out, then certainly the very heart which pumps the blood may be spoken of as being cleansed. By the miracle of salvation, we receive both eternal life and the divine health of the Son of God. The greatest disinfectant in the world is the Blood of Jesus Christ. It carries the eternal life of God in it. In this connection it is interesting to note that Satan’s nickname Beelzebub means “Lord of the Flies,” or “Prince of the flies.” Dead blood will quickly attract to itself flies, which will breed corruption in the coagulation blood; but the Blood of Jesus has exactly the opposite effect: it repulses Beelzebub and all his demons. When you put the Blood of Jesus on something, or place someone or something under the Blood by faith, Satan will flee because the Blood of Jesus is alive. The life is in the Blood. So, do not underestimate the power of the Blood of Jesus. In Leviticus 17, we read, “For the life of the flesh is in the blood: and I have given it to you upon the altar to make an atonement for your souls: for it is the BLOOD THAT MAKETH AN ATONEMENT FOR THE SOUL.” The Apostle, therefore, made no mistake when he wrote, “Without shedding of blood is no remission” (Hebrews 9:22). Some people say that it is enough to have just the name of Jesus. But this is not so. We need the Name and the Blood, for the life is in the Blood. There is power in the name of Jesus only because He shed His own Blood and offered it to His Father, who thereupon gave His power and His authority to His Son (Matthew 28:18). This same power and authority is given to all believers (Luke 10:19), but it only becomes operative as we honor His blood. When Jesus died upon the cross, His own Blood was shed and sprinkled by Himself as God’s High Priest on behalf of the people. He was crucified at the time of the feast of the Passover, the feast the Jews kept to remember the time when God said, “When I see the blood I will pass over you” (Exodus 12:23). At the very time when the jews were celebrating the first exodus, Jesus was making atonement for the second exodus. To all who will believe in this sacrifice and the efficacy of His precious Blood, there is an exodus from sin and the penalty of sin, which includes sickness. Jesus sprinkled His own Blood and fulfilled the following types: on the altar (the cross) (Exodus 24:6-8); round about the cross (Exodus 29:12-16); on the High Priest’s garments (Exodus 29:20-21). Jesus’ Blood was sprinkled seven times (or the number of perfection) (Leviticus 4:6-7); on the bottom of the cross (Leviticus 4:6-7); on the side of the cross (Leviticus 5:9); round about the cross, i.e. on the earth beneath (Leviticus 7:2); sprinkled before the tabernacle seven times (Numbers 19:4). This last was fulfilled in that the cross and the hill of Calvary were within sight of the temple in Jerusalem, for Calvary was outside the city wall. All these Old testament types were fulfilled in the crucifixion of Jesus, who made Himself our Passover, our vicar, our Savior, and our Blood sacrifice. His Blood alone covers our sins. If we honor the Blood of Jesus Christ, the Father will smile upon us with forgiveness and cleansing. But this must not be a dull theological honoring, but a continual, active and vital embracing of His Blood. We do not offer our own works; we offer only His Blood. When God sees the Blood of His Son, which we offer as our covering, pardon and plea, God does not see our sin at all; He can only see the covering -the Blood. Therefore we understand that “It is the BLOOD that maketh an atonement for the soul” (Leviticus 17:12). The Life of God is in the Blood of Jesus, thus, we can not be surprised at the strong reactions from demonic spirits. As soon as the Christian takes the precious Blood of Jesus on his tongue and sings it, talks it, or pleads it, the devil gets terribly disturbed. The devil understands the power of the Blood of Jesus, and he has done everything possible to blind Christians to this truth. Many of the people today who are Christians in name only, will have nothing to do with what they call “a slaughterhouse religion.” Theirs is a religion without the life of God in it, and the devil has no objection to our participating in this kind of religion. But as soon as we honor the Blood of Jesus IN AN ACTIVE SENSE, we stir up demons to a fever pitch. It is like fire in a hornet’s nest. It is surprising that so little has been taught about the Blood and so little is known about the activity of demon spirits, even within the Christian church. No wise Christian would dare try to cast out demons without faith in the Blood of Jesus. As Christians living in today’s exceedingly wicked world our only hope and salvation is by walking continually in the Blood of Jesus. The fact is that Jesus’ Blood says something to God. The Blood cries out to God, “Our sin is covered! The penalty is paid!” We are redeemed. SALVATION? YES, JESUS CHRIST IS REAL!! Dear Jesus, I come to you with all the sins I’ve committed and I beg you to forgive me. I confess that I am a sinner and that I cannot save myself. Please cleanse my body, soul and spirit with your precious blood. I need your help and I ask you to come and live in my heart. I want to serve you, obey your commands and do what is right. I want to live for you everyday, please lead and guide me by your Spirit into righteousness. Thank you Jesus for hearing and answering my prayer. Amen! Read the BIBLE! JOIN US IN THE WAR TO SAVE SOULS! ARE YOU tired of a dead church existence? Are you sick of the once a week, song and dance routine? Are you being told the TRUTH by those who call themselves “Men of God”? Why not get bold, why not get radical, why not go ALL THE WAY FOR JESUS!! What are you waiting for, the “rapture”? Souls are slipping Christless into Hell all around you, what are you doing about it? We offer a wide range of newspapers, booklets, tracts and tapes to equip the Christian soldier in the war for souls. Write us today for more information about how you can join the SPIRIT REVOLUTION! You read the press reports in July about the DNA of Neanderthals, and you quickly grasped how the new findings suggest that this branch of humanoids is much more distantly related to modern Homo sapiens than you may have believed–they are not even direct human ancestors. Now you must apply these findings, and examine their implications for the world around you. Specifically, you must weigh their effect on certain theories in circulation, among them that Neanderthals still walk–or lumber–among us, and indeed that they have maintained their cohesion through the ages and still constitute a group apart. And, most importantly, that this group of living, lumbering Neanderthals is the Jews. You laugh? That may be a mistake. At least two theorists working separately have concluded precisely this: The Jews are surviving Neanderthals. Laughing at such ideas suggests you believe them to be absurd. But the validity of such theorizing is beside the point. What matters is the existence of such a premise, because it validates the question it seeks to answer: What explains the Jews? That Jews require a meta-explanation is the problematic premise, one that even philo-Semites have sometimes fallen for. Anyway, if you laugh at the idea that the Jews are Neanderthals, what will you do when you learn, as you shortly will, that the Jews are really aliens from outer space? A long and extraordinary history of speculation concerns the ultimate identity of the Jews. In its course, learned fellows have repeatedly announced they have stumbled on a Big Secret, a hidden truth that explains Jewish survival, character, behavior, and even the historical antipathy toward Jews by others. That Big Secret has often been that Jews are not what they seem to be: This line of thought provides for a certain macabre entertainment, but it is also a lesson in how the most inane ideas can have the most appalling consequences. Here is a whirlwind tour of the field, in approximately chronological order. The Jews are a Race of Lepers. An ancient argument in circulation in the first century. We know of it because Flavius Josephus, the traitorous Jewish general who joined the Romans, bothers to refute it in his surviving writings. Josephus attributes the argument to an Egyptian named Manetho who, in a counter-version to the Book of Exodus, asserted that the Hebrews weren’t led out of Egyptian bondage by Moses. Instead, they were an outcast group of lepers, forced to settle together, who were eventually chased out of the country by patriots. The existence of such a story is not necessarily evidence of general antipathy toward Jews; it is a likely reflection of the long struggle between Hellenism and the only Mediterranean culture of consequence that held out against it, Judaism. The idea that Jewish lineage is impure or malevolent reappears in Visigothic Spain in the early medieval period, and most notoriously in Nazi Germany. The Jews are a Race of Devils. References to the Jews as the children of the devil or as constituting a “Synagogue of Satan” appear in the New Testament, implying that they are in league with the devil. That they are themselves actually devils, complete with horns, is a folk belief that arises in the centuries following the Crusades, when European Jewry’s problems begin in earnest. The survival of such beliefs into the mid-20th century is illustrated by Carlo Levi, an anti-fascist Italian Jew sent into internal exile among dirt-poor southern peasants in the 1930s. His memoir of exile, Christ Stopped at Eboli, describes an encounter with a local woman who refuses to believe that Levi can be Jewish because he seems to be a person much like herself. Arguments that Jews are a race of nefarious devils are still being published in the Middle East, and have been exhibited at Cairo’s book fair. The Jews are a Separate Creation. “Polygenism,” the theory that God created different peoples in different acts of creation, blossomed during the Enlightenment. It was in part a “solution” to the “mystery” of Native Americans, whose startling existence seemed to require some explanation, and whose status as humans awaited papal resolution. It was also an attempt by early humanists to challenge clerical authority. They pointed to ambiguous passages in Genesis that might suggest more than one creation. Some prominent Jews of the period saw the hope of popular redemption by supporting such notions. However, Jew-haters also saw value in the idea, because it allowed them to regard the Jews as an entirely separate species. French scholar Leon Poliakov argues that the pseudoscientific foundations of racism were laid in this debate. The Jews are an Inferior Race. A still-familiar concept that arose in the wake of Jewish emancipation in 19th-century Europe, it argues that Jews constitute a separate racial group anthropologically inferior to European racial groups. The thesis attempted to provide a “scientific” rationale for hatred at a time when legal restrictions on Jews were disappearing. A great deal of detail was presented in support of the thesis, from relatively tiny cranial capacity to the idea of peculiar Jewish feet and a peculiar Jewish smell. The Jews are Khazars. An idea put into circulation by Arthur Koestler in his 1976 work, The Thirteenth Tribe, it is now widely disseminated among Jew-haters and anti-Zionists. The argument is that Europe’s eastern Jews have no connection to the Jews of the Bible, but are all descended from the Khazars, a once-powerful Turkic people who lived near the Caspian Sea and who are known to have converted to Judaism in the eighth century. Koestler argued from circumstance, asserting that it is unclear where all the eastern European Jews came from, that the fate of the Khazars is unknown, and that the solution to both problems is the same. Among the scant evidence he offered–in all seriousness–was a chart of noses. The appeal of the argument is apparent: It enables anti-Semites to embrace Scripture and hate Jews without inconsistency. The Jews are Africans. A thesis advanced by a number of authors, most notably, perhaps, by Yosef ben-Jochannan. His emotional book, We the Black Jews, is printed largely in uppercase. The central idea is that white Jews are all impostors, that the real Jews of the Bible exist, and that they are East Africans. Adherents of the idea draw on the Bible for support, including the often-cited “Black Jesus” passage in Revelations. The Jews are Space Aliens. First argued in 1974 by French thinker Marc Dem in his Les Juifs de L’espace, this thesis holds that Jews are ultimately space aliens, and that that explains their, um, difficult history. Dem’s book was part of the flood of Ancient Astronaut books inspired by the huge success of Erich von Daniken’s Chariots of the Gods?, and appeared here in 1977. Von Daniken, like many of his imitators, sought evidence for ancient visitations in the Bible, especially in such passages as the description of Ezekial’s flying chariot. Deducing that the whole of the Old Testament was the work of aliens is, therefore, perfectly logical. The Jews are Neanderthals. Advanced in this decade by heretic anthropologist Stan Gooch, who has also argued that the original, full-blooded Neanderthals were telepathic. The thesis was taken up last year by Canadian Michael Bradley in his incoherent book Chosen People From the Caucasus. Bradley is known for a book-length rant titled The Iceman Inheritance, which identifies the origins of white racial evil in prehistoric psychosexual tensions of some sort. Chosen People is an extension of his ideas: Biblical evidence that Jews are Neanderthals includes the Esau incident (Esau is hairy, remember?). The reason Jews have an injunction against portraying God is that Neanderthals cannot draw. However, Bradley adduces evidence that they were quite good with numbers and were overly sentimental about their mothers. Interestingly, Bradley also believes that modern European Jews are Khazars, which means he must argue not only that biblical Hebrews were Neanderthals, but that so were Khazars. He actually does so. News that Neanderthals have little in common with modern humankind should be welcome to admirers of Bradley’s work. Among his blurbists, by the way, is Dr. Leonard Jeffries, of New York’s City College. “It is not my intention to give anti-Semitism any support whatever,” wrote Marc Dem, as he argued that Jews were from outer space. Certainly not. Arthur Koestler wrote the same thing in his Thirteenth Tribe, stating that if most of the world’s Jews come from the Volga region, then “anti-Semitism will become void of meaning.” Sure. We’re all out here just looking for the Truth. And no matter where we look for it, over our shoulders among the hominids of prehistory, or out on the interplanetary horizon, we can find whatever Truths we’re looking for: Those that set us free, and those that prove us mad, too. =================================================== +++++++++++++++++++++++++++++++++++++++++++++++++++ =================================================== PATENTED to KILL in US PATENT OFFICE! Genetic Engineering is a nightmare technology that has caused many disease epidemics, documented but unpublicized. This is the 2nd in a series revealing the epidemics. It features the horrors of GE MEDICINE. Read and take heed — it may save your health or life. GMO DISEASE EPIDEMICS: (2) Hepatitis B Vaccine I. The Face of Frankenstein’s Monster Genetic Engineering Biotechnology (GE, GM, GMOs) evades Evolution’s safeguards by injecting genes of one species into a totally unrelated species, something impossible in Nature. GM evades Evolution’s safeguards, and may therefore give rise to PATHOGENS that can — and HAVE, many times — caused crippling and deadly DISEASE EPIDEMICS — documented but unpublicized. Genetic Engineering is also ideal for developing horrific biological and other military weapons — sufficient cause to OUTLAW GM. The Greatest Racket in History (Listen to this !): — GM contamination is virulent, spread by wind, bird, insect, animals and travelling human beings. Co-Existence with GM is completely impossible, only fools or liars would say differently. GM has contaminated crops in areas of North America which dwarf the UK and even Western Europe. Planetary contamination is inevitable, if We don’t stop it. The Biotechnology corporations know oh-so-well how contamination spreads and spreads and spreads. Now get this: Through their political influence, these Corporations have been able to acquire the obscene, sacrilegious, and indeed revolutionary PATENTS on LIFE-FORMS. Before these revolutionary Patents on Life, a farmer could have sued — successfully without any doubt — the Biotechnology corporation for having contaminated, poisoned his crops. However, given these Patents on Life (here, on the seeds), the Corporation can — and DOES, successfully — sue the victimised farmer for (Hold your nose) “infringement of patent”. [Our tainted, corrupted political systems allow this monstrosity.] Thus the formula the reader might keep in mind: GM Contamination + Patents on Life-Forms equals Corporate Ownership Rights in the crops of victimised farmers. This formula spells the serfdom and ruin of all small family farmers on this planet. (They are the majority of the population in Asia, Africa, and Latin America). The Chemical-Drug-Biotechnology syndicate and its Enforcers (corrupted governments in the West and Third World, corporation-dominated organisations like the WTO, World Bank, IMF) have started a WORLDWIDE AGRICULTURAL REVOLUTION. They want to destroy small family farming, and have only gigantic Corporate GM Plantations with farmers working as serfs. [This process is underway, especially in South America where the U.S. Military has begun to intervene on behalf of GM Plantations to crush farmer opposition.] Already, according to the Research Foundation for Science, Technology and Ecology (RFSTE) in New Delhi, 40,000 farmers in India have committed suicide primarily as a result of the Corporate Enforcers’ so-called “free trade” policies — dumping heavily-subsidised Western farm produce onto glutted Indian markets, pushing GM crops, insisting that Patents on Life-Forms be accepted so farmers must sign contracts with GM Corporations and can no longer save seeds, etc. The Greatest Racket in History — GM Contamination + Patents on Life-Forms equals Corporate Proprietary Rights in the crops of victimised farmers, and spells the serdom and ruin of small family farmers everywhere on this planet. We MUST OUTLAW GM and PATENTS on LIFE-FORMS — or else !! (e.g. No more organic, healthy food — you and your children will only be able to eat unsafe GM) See the Action Plan in Part III designed to OUTLAW GM and PATENTS on LIFE-FORMS. But beforehand, read about the first in our series of “GM Disease Epidemics”. – – – – – – – – – II. The Horror of Genetically-Engineered Medicine and the GM Hepatitis B Vaccine Epidemic (a) Genetically engineered medicine and vaccines are extremely dangerous and should be outlawed. GM medicine/vaccines are entirely unnecessary as well, and insult the Hippocratic Oath. [Comment: The Drug Corporations would drop genetically-engineered drugs like a hot potato were it not for the abusive Patent laws (awarding monopolies), especially Patents on Life-Forms, and the corruption of Government which insulates the corporations from serious liability.] – – – – – – – – – – (b) Item: London, March 2006 — Six healthy male volunteers were given an experimental drug manufactured by a German biotechnology company, TeGenero. The drug, supposedly intended as an “immune stimulant”, wasgenetically engineered. It came as little surprise to this observer when it was announced that all 6 men suffered multiple organ failure and nearly died, and that one of them may remain in a coma for a year or more. One of the 6 victims said he felt like his brain was “on fire”. “I thought my eyeballs were going to pop out.” Either this victim or another has been nicknamed “the Elephant Man’, because his head swelled out to three times its normal size !! It was also unsurprising that the BBC, International Herald Tribune (New York Times), etc.,apparently suppressed the fact that the drug was genetically engineered. (Could they conceivably be accused of ignorance? Surely not possible.) [“Calamitous GM Drug Trial Raises Questions About Modern Science”, GM Watch, Weekly Watch 170, 6 April 2006; “A drug trial catastrophe”, Prof. Joe Cummins, Ban-GEF online newsletter, 19 March 06; “Victims’ agony as ‘Elephant Man’ drugs firm goes bust”, Neil Sears, Daily Mail, 4 July 2006] – – – – – – – – – – – (c) The Hepatitus B vaccine was genetically engineered. On account of this vaccine, during the 1990s there were, in the USA alone, more than 17,000 cases of hospitalisations, injuries and deaths, including the deaths of 72 children, reported to the Vaccine Adverse Event Reporting System (VAERS) of the U.S. government. [ [Dr. Philip Incao’s testimony to the Health Committee of the Ohio House of Representatives, 1 March 1999] Note: a former FDA (U.S. government Food and Drug Administration) Commissioner wrote in 1993 in the prestigious medical journal, JAMA, that a study showed “only about 1 percent of serious events attributable to drug reactions are reported to the FDA”. USA Question: Are serious events attributable to vaccines better reported to VAERS? UK Question: Is the MMR vaccine genetically engineered? If it is, one can readily understand why AUTISM might conceivably be linked to it. – – – – – – – – – – – (d)Labelling, Identification and GM Causation of Diseases GM drugs are generally (entirely?)unlabelled. This alone is outrageous. If you want to have a little fun, ask your doctor if the drug he/she is prescribing happens to be genetically engineered. Doctors do not like being asked important questions for which they have not the foggiest notion of an answer. In the last two decades, any drug that has been associated with particularly nasty adverse reactions, should have been analysed (and its patent searched) for possible GMO content and GM causation of those adverse reactions. This of course has not been done. (never? probably Never. Ordinary scientists, who are pretty uniformly on ‘Their side’ — they wouldn’t dare. And ‘Our side’ is not bright enough to have thought of it. ) Recommendation: Start doing it now. – – – – – – – – (e) Extremely Important Fact: “The third largest cause of death and illness in the [western] world is medical intervention [essentially, prescribed drugs].” — Paul Flynn MP, House of Commons Health Select Committee report on “The Influence of the Pharmaceutical Industry”, April 2005, vol. 2, p. 153 Only cancer and heart disease are bigger killers than prescribed drugs. As for heart disease, mark that the arthritis pain reliever, Vioxx, caused an estimated 140,000 heart attacks and up to 55,000 deaths in the USA alone. [ Dr. David J. Graham, former associate safety director of the FDA; and see “Intimidation, Politics and Drug Industry Cripple U.S. Medicine”, Ritt Goldstein, Inter Press Service, 31 December 2004 ] Question:Is Vioxx genetically engineered? Will anyone ever do an analysis or search the patent for that information?? Indeed, in the United States (can Europe be any different?)prescribed drugs are surely the leading cause of death and illness, at least equal to cancer and heart disease combined, and quite possibly a multiple of this. [see “Modern Health Care System is the Leading Cause of Death”, Gary Null PhD, Carolyn Dean MD ND, Martin Feldman MD, et al, http://www.mercola.com] – – – – – – – – – – (f) How many drugs are now genetically engineered? 8% of total global pharmaceutical market sales are accounted for by genetically engineered drugs. [Memorandum by the BioIndustry Association (PI 147), “The Influence of the Pharmaceutical Industry”] Worse, one-third of all drugs in development are biologics ! [It is unclear whether the Memorandum refers to the UK only, or the Western drug corporations in general. I think the latter.] This ought to frighten anyone who thinks he or she may ever again see a doctor or hospital. – – – – – – – – – – – III. Conclusion and What To Do Human beings and Nature, as we have known them, cannot survive in a GMO-Frankenstein world. The nightmare technology of Genetic Engineering Biotechnology, and its incestuous Patents on Life-Forms, must be OUTLAWED. How To Do It? There is only one way to overcome this extremely powerful, ruthless Corporation-Government-corporate Mass Media axis. It is to conduct grassroots Public Education Campaigns to educate and politically activate the General Public, university / college students in particular. The General Public !! Stop forever talking to the Converted. To get around the corporate media’s suppression and distortion of truth, one must talk to people and go door-to-door with leaflets and vocal messages. And major efforts must be made to inform and activate university students. Important Hints: (1) Concentrate on university students. And senior citizens. I speak to you now, elder citizens like myself. Put moral purpose into your lives and help rescue this planet and your grandchildren. (2) AVOID NGOs and all established organisations, especially large ones. They are not what they seem. Their hierarchies and decision-making are corporation-influenced if not outright purchased. Never ever join them. Never ever give them Money. [see George Monbiot’s very important article in The Guardian, 4 September 2001, “Sleeping with the Enemy: Consumer and Environmental Groups are Getting into Bed with Big Corporations] [Note: In developing countries there are some exceptions, but very, very, very few in the West. If by a miracle one of them ever conducts a genuine and sensible public education campaign, then you can help out. But NEVER join or give money to them.] The environmental field especially is riddled with wealthy, prestigious, deceptive organisations adept at dilutng and derailing environmental causes, GM in particular. [I am thinking at this moment of one such organisation I have observed over a long period of time, in my view a very slick and dangerous FOE of environmentalism, originally created by polluting Corporations to deal with the growing environmental movement. Don’t go anywhere near this one.] When they talk about being ‘practical’ and seeking ‘Coexistence’ with GM, let a red flag go up. Nothing short of OUTLAWING GENETIC ENGINEERING and PATENTS ON LIFE-FORMS will save us and our planet. Do your educational work as individuals or in small groups of people you know. In a little of your SPARETIME (perhaps 3 or 4 hours a week, but regularly, as part of an ethical life-style): Educate and activate the Public by writing and telephoning and just talking to your family members, friends and acquaintances; Write letters and make telephone calls to local, regional and national media; Write, call and especially visit your legislative representatives and other government personnel, and Take appropriate Direct Action. Good Luck to You. P.S. For a detailed Action Plan on conducting education/activation campaigns (e.g. composing A4 leaflets for distribution, lobbying your legislative representative) see “Creating a Grassroots Democracy While Outlawing Genetic Engineering” on the Indymedia Biotech website. Or email me and request it. For extensive information on the casualties and unprecedented dangers of Genetic Engineering, see “Genetic Engineering Fact-Sheet” on the website of the Concerned Citizens Information Network, http://www.ccin.info homepage: homepage: http://www.ccin.info =================================================== ++++++++++++++++++++++++++++++++++++++++++++++++++==================================================== US Patent 5733540 – Protection from viral infection via colonization of mucosal membranes with genetically modified bacteria BACKGROUND OF THE INVENTION 1. Field of the Invention This invention relates to the manipulation of the bacterial flora normally residing harmlessly on mucosal surfaces to interfere with infectious processes. Specifically, this invention provides for modification of non-pathogenic floral bacteria to confer upon them the capacity to bind to (and functionally inactivate) specific viruses. Although this disclosure describes a method of preventing infection by viruses which infect through mucosal surfaces, the skilled practitioner will recognize that the invention may potentially be applied to any pathogen which infects at a mucosal surface, including bacteria, fungi, and parasites. 2. Information Disclosure Cytoplasmic expression of heterologous proteins by bacteria has been widely practiced for well over two decades. However, expression of heterologous proteins specifically onto the external surfaces of bacteria has been achieved only in the past few years. Surface expression systems for both gram-positive and gram-negative bacteria are known, e.g., U.S. Pat. No. 5,348,867, and WO 93/18163. SUMMARY OF THE INVENTION This invention provides for a method of protecting an animal from a viral infection comprising contacting a mucosal surface of the host with an amount of transformed bacteria sufficient to colonize the mucosal surface and to protect the animal from viral infection, said bacteria having been transformed with genetic material so as to confer upon the bacteria the capacity to bind the virus. More specifically, this invention provides for transformed bacteria that bind virus or other pathogens using naturally occurring receptors, domains of receptors or antiviral antibodies that are the products of the genetic material. Preferred hosts are humans. Where the naturally occurring receptors are known, genes encoding those receptors may be used to transform the bacteria. When the specific viral/host receptors are not known, genes encoding antiviral antibodies or fragments thereof may be used to transform the bacteria. For example, for retroviruses that are covered with human leukocyte antigens ?HLA DR!, antibodies against these antigens are useful. Accordingly, this invention can be used against rotavirus, papillomavirus, adenovirus, respiratory syncytia virus, corona virus, cytomegalovirus, coxsackievirus, echovirus, hepatitis A virus, rhinovirus, human immunodeficiency virus, poliovirus, Epstein-Barr virus, parainfluenza virus and herpes simplex virus using bacteria able to bind to conserved determinants on their respective capsids. The bacteria may also be modified to express a specific carbohydrate moiety which serves as the receptor for the virus onto its normal surface proteins. For example the bacteria may be transformed with genetic material which causes the addition of sialic acid which permits the bacteria to bind to an influenza virus. The bacteria may also be modified to cause fusion between the bacterial membrane and the viral envelope, if present. An example is the transformation of bacteria so that it can fuse with bound viral particles through a fusogenic domain engineered into the virus-binding polypeptide. Colonization of mucosal membranes is an essential element of this invention and it is preferred that the transformed bacteria is conferred with sufficient selective advantage to permit it to compete effectively with resident bacteria to allow said transformed bacteria to successfully colonize and survive indefinitely on a selected mucosal surface. One selection advantage is an enhanced ability to adhere to a host mucosal surface through a domain in the heterologous protein which binds to a determinant on a selected mucosal surface. Selective advantage might also be conferred by the use of antibiotic resistant transformed bacteria where antibiotics are co-administered with the transformed bacteria. Other advantages include the use of products that degrade the biofilm of the mucosal membrane. Such products would include DNAses, peptidases, and hyaluronidases. Preferred mucosal surfaces are in the following organs: nasopharynx, oropharynx, esophagus, small intestines, large intestines, rectum, vagina, and penis. Transformed bacteria are applied to a mucosal surface through the use of a liquid solution, foam, suppository, sponge, or capsule. Where the target mucosal layer is in the vagina, the bacteria can be transformed to target sexually transmitted pathogens such as but not limited to HIV, HPV, HSV, gonorrhea, syphilis and chlamydia. Nonbacteriocidal spermicides might be co-administered with the bacteria. The invention also embraces a means to prevent the spread of a viral pathogen from an infected individual to others with transformed bacteria by administering an amount of transformed bacteria sufficient to colonize the mucosal surfaces of the infected individual wherein said bacteria bind and inactivate infectious viral particles exiting the infected host. The modifications and targets being as stated above. The transformation of the bacteria can be either in vitro or in vivo whereby the resident musocal bacterial flora of a host is transformed with a desired foreign genetic material by directly introducing into resident microfloral bacteria a genetic vector said vector conferring the ability of the bacteria to bind and inactivate viral pathogens of the host and thereby affording protection of the host from infection by the viral pathogen. Examples of vectors include replication defective bacteriophage. The invention further includes inactivating infectious viral particles in suspect water supplies by the addition of engineered bacteria capable of binding and irreversibly inactivating specific viruses. In addition to methods, this invention also embraces compositions of matter comprising a bacteria selected for its ability to colonize the mucosal membrane of a host and transformed to express a host receptor or an antibody specific for a target virus on its cell surface in an amount sufficient to bind and inactivate the target virus. The preferred compositions are as described above for the various methods. BRIEF DESCRIPTION OF THE DRAWINGS FIG. 1 illustrates the ViroShield™ concept. Viruses normally gain entry into a host by binding to specific receptors expressed on the host cell surface. Expression of the same receptors on the surface of bacteria on mucosal surfaces will cause the majority of the viruses to bind to the bacteria instead, where they are functionally inactivated, thus preventing infection of the underlying host cells. DETAILED DESCRIPTION A. Introduction. Most viruses infect via mucosal surfaces. A review of this process can be found in Murray, P. R., et al., Medical Microbiology, 2nd Edition, (hereinafter Murray, et al., 1994). The creation of a virus blocking bacterial flora in the mucosal surfaces by allowing colonization of bacteria transformed to bind and inactivate virus is particularly advantageous. Colonization of mucosal layers is a routine undertaking. Most mucosal layers are typically teeming with bacteria, and changes in flora attendant to pathogenic bacterial infection and administration of antibiotics is a common event. The routine nature of the floral changes on mucosal surfaces is a key advantage of the invention. The following discussion will also provide means to enhance the ability of transformed bacteria to colonize mucosal layers. B. General methods The techniques of amplification of genetic sequences with the polymerase chain reaction (PCR), cutting and splicing DNA into plasmids, transformation of bacteria with plasmids, and assays for antibody binding are all well known biotechnology methods and detailed descriptions of these methods can be found in a number of texts including Protocols in Molecular Biology, Molecular Biology of the Cell, and Sam brook, et al., Molecular Cloning-A Laboratory Manual, Cold Spring Harbor Laboratory, Cold Spring Harbor, N.Y. 1989. C. Viral targets. The following is a list of viral targets. They are categorized by their respective organs of entry. 1. Upper respiratory tract (URT). A large number of viruses infect the naso- and oropharynx, either via air droplets or direct contact. These include human rhinoviruses (HRV), adenovirus, coxsackievirus, influenza, parainfluenza, respiratory syncytia virus (RSV), Epstein-Barr Virus (EBV), and cytomegalovirus (CMV). 2. Gastrointestinal (GI) tract. These viruses include rotavirus, Norwalk agent, hepatitis A (HAV), poliovirus and other picornaviruses. 3. Vaginal: human immunodeficiency virus (HIV), human papilloma virus (HPV), herpes simplex virus (HSV) 2, CMV, hepatitis B virus (HBV), hepatitis C virus (HCV). D. Viral receptors. A virus must enter a host cell to replicate. To enter a cell, viruses require surface receptors on the host cell (Murray, et al., 1994). More specifically, the virus must first bind to a molecule on the surface of the target cell. The receptors for a number of viruses have been determined in recent years. The following is a representative list and is not meant to be a limitation of the invention. 1. HRV, major group?ICAM-1, domains 1 and 2 (Lineberger, D. W., et al., Virus Research, 24(2):173-86, 1992.) 2. Influenza virus?sialic acid 3. HIV?CD4, domains 1 and 2 4. Poliovirus?PVR (poliovirus receptor, an immunoglobulin superfamily protein) 5. EBV?CD21 (complement receptor 2, the receptor for C3d) 6. HSV?heparin sulfate 7. HBV?IgA receptor 8. Adenovirus?Vitronectin receptor E. Mucosal Surfaces are Normally Colonized by Bacterial Flora (Murray, et al., 1994) The upper respiratory tract (URT) consists of the nasopharynx, oropharynx (oral cavity and larynx), paranasal sinuses, and the middle ear. The paranasal sinuses and the middle ear are normally sterile. However, the stratified squamous epithelium of the naso- and oropharynx are teeming with a varied microbial flora. The microflora of the nose consists mainly of coagulase-negative staphylococci, with some diphtheroids (aerobic and anaerobic), and nonhemolytic streptococci. The most prominent members of the flora of the mouth and pharynx are the alpha streptococci. Some gram-negative anaerobes (esp. Bacteriodes) and other cocci are also found. The colon contains the largest total population of bacteria of any mucosal surface in the human body. It is estimated that >1011 bacteria/g of colonic content exists in healthy individuals, representing over 400 species. Anerobic bacteria outnumber aerobic ones by a factor of 100-1,000. Bacteroides is the predominant genus. Bifidobacterium, Enterobacteriaceae, Streptococci, and Lactobacilli are also prominent. The small intestine is populated by a similar profile of organisms as the colon, but at much lower numbers. The stomach and proximal small intestine are nearly sterile, while the distal small intestine contains approximately 1/10 of the bacterial content of the colon. The vaginal mucosa is also colonized by a large number of bacteria. Lactobacilli are the predominant species in the normal menarchal vaginal microflora, being present in nearly 100% of normal women. Lactobacilli are facultative anaerobes, and produce large amounts of lactic acid as the end products of sugar fermentation. This creates an acidic environment which is not suitable for many bacterial strains. F. ViroShield™: Prevention of pathogen binding to host cells will prevent infection Since viruses require binding to a receptor on the target cell surface for infection, strategies directed at inhibiting the interaction of a virus with its host receptor should be effective at preventing infection. The use of a bacterial shield against viral pathogens on mucosal surfaces is termed a ViroShield™. The concept of the ViroShield™ type bacteria can be illustrated by the viral agents causing the common cold. The viral agents for the common cold are mainly consisting of the rhinovirus major group which bind to the ICAM-1 receptor in humans. Soluble ICAM-1 molecules expressed through recombinant DNA technology have been found to be effective in inhibiting HRV binding to susceptible cells and preventing infection (Martin, S., et al., Antimicrob Agents Chemother, 37(6):1278-84, 1993, hereinafter Martin, et al., 1993). Approximately 60 ICAM-1 molecules can bind to a single HRV virion (Hoover-Litty, H. and Greve, J. M., J Virol, 67(1):390-7, 1993). This correlates with the fact that the HRV capsid is an icosahedral complex composed of 60 copies of each of the viral coat proteins (Smith, T. J., et al., J Virol, 67(3):1148-58, 1993). The actual receptor binding site on the HRV capsid was found to be a surface depression or “canyon” by X-ray crystallography (Oliveira, M. A., et al., Structure, 1 (1):51-68, 1993). This canyon is sufficiently small in size such that antibody molecules cannot fit, and this is one reason why humans are susceptible to repeated infections by HRV since the virus is resistant to antibody binding at this key neutralization site. After binding to ICAM-1, a conformational change is induced in the capsid which causes the release of the viral RNA into the host cell (Martin, et al., 1993). Soluble ICAM-1 molecules are relatively ineffective at inducing capsid conformational change and thus functional inactivation of virions (Martin, et al., 1993, and Crump, C. E., et al., Antimicrob Agents Chemother, 38(6):1425-7, 1994 hereinafter Crump, et al., 1994); however, chimeric molecules combining the HRV-binding domains (1 and 2) of ICAM-1 and constant regions of immunoglobulin (Ig) molecules (IgA, IgG, or IgM) showed some effect. This effect is thought to be due to the ability of chimeric molecules to dimerize (IgA and IgG) or multimerize (IgM) via the association of the Ig domains. Multimeric receptors more closely resemble the natural state on cell surfaces, where several immobilized receptors binding to a virion may induce conformational distortion to the capsid to cause vital RNA release. Expression of ICAM-1 on the external surface of mucosal bacteria is an extension of the multimeric-molecule strategy, with key additional benefits. Since bacteria are considerably larger than viral particles, bound HRV should be readily immobilized onto the bacterial surface. A key advantage of this invention is that only a few ICAM-1 receptors must be bound in order to effectively immobilize and neutralize a virion, whereas strategies involving soluble ICAM-1 molecules potentially must cover all 60 binding sites in order to ensure complete neutralization of a single virion. Furthermore, ICAM-1 molecules on bacterial surface are efficient in inducing capsid conformational change because simultaneous binding of several ICAM-1 molecules immobilized on a bacterial surface to several faces of a vital capsid will distort the geometry of the viral capsid and lead to conformational change and premature viral RNA release. Viral RNA released into the bacteria are readily degraded by the abundant nucleases within bacterial cytoplasm. This leads to irreversible inactivation of viral particles, which is a key advantage of this invention because binding itself is a reversible process, and binding of soluble ICAM-1 molecules, chimeric molecules, or other drugs to HRV without functional inactivation would still leave a significant fraction of viral particles free to bind host cells at any given time. With ViroShield™ type mucosal bacteria, each bacteria is capable of irreversibly inactivating a large number of viral particles, ensuring that the majority of any vital inoculum would be eliminated before they can infect underlying host cells. Accordingly, soluble CD4 molecules have also been shown to be effective in binding and preventing infection of HIV to target cells in vitro (Orloff, S. L., et al., J Virol, 67(3):1461-71, 1993). However, results of clinical trials with intravenously administered soluble CD4 molecules have been disappointing (Moore, J. P., et al., Aids Res Hum Retroviruses, 9(6):529-39, 1993). The reason is not due to lower binding affinity of primary vs. laboratory isolates of HIV to soluble CD4, but rather that primary isolates are less prone to inactivation after binding to soluble CD4 (Ashkenzai, A., et al., Proc Natl Acad Sci, 88:7056-7060, 1991 and Turner, S., et al., Proc Natl Acad Sci USA, 89(4):1335-9, 1992). The expression of CD4 on bacterial surfaces should facilitate irreversible inactivation of all strains of HIV. In particular, CD4 expression on the surface of Lactobacilli on the vaginal mucosa would be effective at preventing HIV infection through vaginal intercourse. E. coli similarly transformed would be effective against HIV transmission via rectal intercourse. An important point to keep in mind is the distinction between infection and clinical disease. For any pathogen, there is a minimum inoculating dose necessary to cause clinical symptoms from an infection. Exposure to an inoculum below this dose normally does not lead to clinical disease. Therefore, to successfully prevent disease, a strategy does not necessarily need to inactivate every particle of an inoculating dose of a virus, but rather to reduce the number of viable viral particles below the minimum infectious dose. Since the ViroShield™ approach aims to prevent entry of a viral pathogen into a host, it not only prevents clinical disease, but should prevent infection altogether. Standard vaccines do not prevent entry of viral pathogens into a host. This may be important as certain viruses are known to trigger autoimmune processes in some hosts, regardless of whether they cause clinical infection. Potential applications: ______________________________________ Virus Receptor Portal of Entry Suitable Bacterial Host ______________________________________ HRV ICAM-1 URT URT flora- Strept gordonii or Influenza sialic acid URT/LRT Staph xylosus Adenovirus Vitronectin URT Strept or Staph HIV CD4 vaginal mucosa Lactobacillus HSV 2 heparin sulfate vaginal Lactobacillus ______________________________________ G. Neutralization of pathogens upstream of their infection site The only mucosal surfaces in the body relatively free of bacterial colonization are that of the stomach, upper small intestines, and lower respiratory tract. A few important viruses infect at the upper small intestines, the most significant of which are rotavirus and poliovirus (Murray, et al., 1994). Since bacterial counts in this area are low, even if all of these bacteria express receptors for the virus, it may not be possible to completely inactivate an inoculating dose of that virus. However, to reach the small intestines, viral particles must first enter the oral cavity and travel through the esophagus both are heavily colonized by bacteria. Therefore, it may be possible that bacteria on oropharyngeal/esophageal mucosal surfaces expressing viral receptors can absorb/inactivate enough viral particles to significantly decrease the infectious inoculum delivered to the small intestines. Viruses that infect the lower respiratory tract include influenza, parainfluenza, and RSV (Murray, et al., 1994). Vital particles inhaled into respiratory tract via droplets will settle out along various portions of the respiratory mucosa depending on the physical properties of the virion, droplet, and flow. Engineered bacteria along these viruses’ path through the URT may absorb/inactivate sufficient numbers of vital particles to reduce the inoculating dose reaching the lower respiratory tract below the minimum required for clinical disease. H. Prevention of exit of pathogens to infect other uninfected hosts. This invention also provides for a method of preventing the exit of the virus from an infected host. Preventing a pathogen from exiting an infected host would mean preventing spread of the pathogen to a number of uninfected individuals, which would be extremely important from a public health viewpoint. Rapid spread of a pathogen may wipe out entire villages in third world countries. ViroShield# should be useful even in already infected hosts by absorbing/inactivating viral particles as they exit the host. Even if ViroShield™ is unable to prevent infection of rotavirus or poliovirus for reasons discussed above (section G), engineered bacteria in the colon may still absorb/inactivate viral particles before they exit the host. I. Use of engineered bacteria in potentially-contaminated water to inactivated virions In third-world countries, viruses may be transmitted rapidly through inadequately treated water supplies. Fecal-orally transmitted viruses, such as rotavirus, may exist in low titers in the drinking water of a village after contamination by a single infected individual, and go on to infect a number of uninfected individuals. Non-pathogenic bacteria expressing rotavirus receptors may be added to suspect water supplies to absorb/inactivate viral particles in these settings, as long as the ingestion of the engineered bacteria is not harmful to a host. This approach should be an effective and economical means of quickly controlling orally-transmitted viruses in third-world countries. J. Sources of genes which confer virus-binding capacity The capacity to bind a virus may be conferred onto a bacteria in at least three ways. The first is by making the bacteria express on its surface the normal host receptor for the virus, such as ICAM-1 for HRV (major group) and CD4 for HIV. These are normal human proteins and the complete sequences of many of these genes have been determined and are stored in the database GeneBank. An advantage to this approach is that it is not readily avoided by viral mutation. If the virus mutates such that it no longer binds to the receptor expressed on bacteria, it would also lose its ability to bind to its target cell and thus no longer be infectious. The second method is by expressing an antibody fragment (or any peptide with the capacity to bind a specific target on the surface of the virus) on the bacterial surface against a conserved determinant on the viral surface, such as VP4 on poliovirus, or gp120 on HIV. Antibody fragments (and peptides) against essentially any antigen can now be selected from a phage-display library (Marks, J. D., et al., J Biol Chem, 267(23):16007-10, (1992)). Once appropriate clones are found, the gene coding for the antibody fragments can then be isolated and used. In addition, it was recently found that enveloped viruses, in the process of budding out of a host cell, carry along on their envelope certain host surface proteins, such as HLA DR on HIV (Arthur, et al, Science, 258(5090):1935-1938, (1992)). Thus, the human HLA DR molecule is a normal constituent of the HIV envelope. Antibody fragments directed against a conserved epitope of the HLA DR molecule may be capable of binding all isolates of HIV, and would be particularly effective in preventing male-to-female HIV spread when expressed on the surface of bacteria on the vaginal mucosa, or HIV transmission via anal intercourse when the engineered bacteria is applied to the rectum. The third means of binding a virus by a bacteria is through the expression of certain carbohydrate moieties on the bacterial surface. A number of viruses use carbohydrate moieties as the receptor for entry into a host cell. One prominent example is the influenza virus which binds to sialic acid. Bacteria may be made to produce the enzyme sialic acid transferase in its cytoplasm which would lead to addition of sialic acid residues on normal surface proteins, thus causing influenza viruses to bind to said bacteria. The complete gene sequences of many bacterial carbohydrate transferases are known and appear in the literature. K. Expression Systems for surface expression in bacteria The expression of heterologous proteins on the surface of bacteria generally takes advantage of the normal surface proteins of the bacteria. It is becoming known that certain sequences within proteins direct them for export out of the bacterial cytoplasm, while others help to anchor a protein to the cell membrane. Hybrid proteins are created in which a heterologous protein sequence replaces the exposed portion of a normal surface protein, leaving the localization signal sequences intact. Several outer membrane proteins have been exploited as targeting vehicles for the localization of heterologous proteins, including the E. coli outer membrane protein maltoporin (LamB), E. coli pilin proteins K88ac and K88ad, E. coli outer membrane porins PhoE, OmpA, and OmpC, and the S. typhimurium Flagellin and TraT lipoprotein (U.S. Pat. No. 5,348,867). A more detailed discussion of surface expression of proteins on the surface of gram-negative bacteria may be found in U.S. Pat. No. 5,348,867, and for gram-positive bacteria in PCT WO 93/18163. 1. Construction of Vectors Plasmids are circularized DNA molecules commonly found in bacteria. They replicate independently from the bacterial host genome via an origin of replication (ori) site. Genes inserted into a plasmid are readily transcribed if placed downstream of appropriate promoter sequences. Certain promoter sequences exist which are regulated by external factors such as the molecule IPTG. A number of plasmids have been optimized for individual bacterial host strains, most notably E. coli. Plasmids have been constructed for surface expression of heterologous proteins in E. coli (e.g. pTX101 as described in U.S. Pat. No. 5,348,867), Streptococcus gordonii (e.g. pVMB20-GP232 transformation system, as described in PCT/US93/02355), and others. Both systems contain a signal sequence which directs a polypeptide to the cell surface, with an insert site for the desired heterologous gene, and an antibiotic resistance gene to help in selection of transformed bacteria. Other suitable streptococci include the lactic streptococci which have been widely transformed (De Vos, FEMS Microbiology Reviews, 46:281-295 (1987)). Starting from the appropriate vector plasmid for each selected bacterial host, the plasmid will be digested with appropriate restriction enzymes to expose the cloning site. Then the desired heterologous gene will be ligated into the plasmid. 2. Transformation of bacterial cells Appropriate bacterial host strains are selected for individual pathogens, heterologous protein or molecule, mucosal surface, and expression plasmid combination. The bacterial host will be rendered competent for transformation using standard techniques, such as the rubidium chloride method. Once transformed with the recombinant plasmid containing the desired heterologous gene, the bacteria will be grown in the appropriate media (e.g. LB media with 0.2% glucose). Transformed bacteria will be selected by adding the antibiotic to which the plasmid contains a resistance gene such that only transformed bacteria would survive. 3. Demonstration of expression of desired heterologous molecule on bacterial surface Expression of the heterologous gene can be constitutive or induced by stimulating the promoter to which it is attached, such as with IPTG. Surface expression of the heterologous molecule will be demonstrated by staining the bacteria with fluorescent-labeled antibodies against the desired molecule, looking for a surface fluorescence pattern. Furthermore, binding of the target pathogen by the transformed bacteria can be demonstrated by fixing the transformed bacteria onto a slide, incubating with the target pathogen, then staining with fluorescent antibodies against the target pathogen in one color (e.g. red), and against the transformed bacteria in another color (e.g. green), showing that the target pathogens (red) are closely associated with the transformed bacteria (green). L. Irreversible inactivation of bound viruses To ensure inactivation of the virus after binding to the transformed bacteria, the process of binding must trigger concomitant release of viral genetic material. In this way, bacterial nucleases can degrade the viral genetic material, thus irreversibly inactivating the virus. Many viruses, such as HRV, release their genetic material after binding to immobilized receptors on the target cell surface through a conformational shift of the viral capsid (Martin, et al., 1993). This situation should be successfully mimicked by expression of the receptor on the surface of bacteria. Some viruses, such as HIV and influenza, contain fusogenic domains in their coat proteins which facilitate release of genetic material after binding (Murray, et al., 1994). Different mechanisms are engineered into bacteria to ensure release of genetic material and thus irreversible inactivation of specific viruses. M. Successful Colonization of Engineered Bacteria Colonization of mucosal membranes with non-recombinant bacteria is well-known. It was optimally achieved by co-administering antibiotics along with bacteria resistant to that antibiotic (Freter, R., et al., Infection and Immunity, 39(2):686-703, 1983). Under normal conditions colonization disappears within 1-2 weeks after antibiotics are discontinued, as the resident microflora recovers and reestablishes itself (Bennet, et al., 1992). To enhance colonization the following three methods are suggested. The first method is to repetitively select for rapid colonizing bacteria on animal or human mucosal layers. For example, one would apply a wildtype bacterial strain to a mucosal surface and repetitively isolate and in vitro culture bacteria, returning at each step to the mucosal surface. Ultimately, an enhanced colonizing bacterium is obtained. The second method is to have the recombinant bacteria express fusion proteins on their surface, which consist of a virus-binding domain and a host-binding domain. The host-binding domain will allow the bacteria to bind to certain determinants (protein or carbohydrate) on a selected host mucosal surface with high affinity, thus conferring the bacteria a slight survival advantage over the resident microflora. This has the added advantage of ensuring continued co-expression of the virus-binding domain, which would otherwise serve the bacteria no intrinsic survival benefit and therefore its expression may otherwise dwindle with time. The third method is to induce the already resident microflora themselves to express the virus-binding protein by introducing the gene via bacteriophage. Bacteriophage has been used successfully to introduce genetic material into bacteria for some time. A number of bacteriophage vectors have been developed for different bacteria. Lactobacillus is likely the most suitable strain for vaginal mucosa and bacteriophage vectors optimized for lactobacillus are available for this invention. A bacteriophage vector has recently been developed for Lactobacillus gasseri based on the temperate bacteriophage fadh (Raya, R. R., et al., J Bacteriology, 174(17):5584-5592, 1992 and Fremaux, C., et al., Gene, 125:61-66, 1993). This vector undergoes site-specific integration into the host chromosome at defined phage (attP) and bacterial (attB) attachment sites. Optionally, the fusion gene may be placed under control of a strong promoter optimized for lactobacillus into the vector, along with a `suicide` gene under control of an inducible promoter. Certain agents may also be added to a unit dose of the bacteria to aid in colonization. Many bacteria on mucosal surfaces secrete capsular materials which coalesce to form a biofilm which covers the entire mucosal surface. It may be beneficial to add an enzyme which digests this biofilm material to promote penetration of the engineered bacteria into the biofilm for more successful colonization. The enzymes include DNAses, peptidases, collagenases, hyaluronidases, and other carbohydrate degrading enzymes. Antibiotics (to which the engineered bacteria itself is not susceptible) may also be added to decrease the number of resident bacteria on the mucosal surface in order to make room for the engineered bacteria. N. Persistent Expression of Heterologous Protein As mentioned above, theoretically, expression of a foreign gene which serves a bacteria no purpose would likely dwindle over time, and the foreign gene would eventually be lost (Cardenas, L. and Clements, J. D., Vaccine, 11(2):126-135, 1993). To enhance persistent expression of the heterologous protein construct, an incentive may be created for the bacteria to express the gene. One way is the approach outlined above: create a fusion protein with virus-binding and host-binding domains so that the host-binding capability would confer a selective advantage to the bacteria to ensure the fusion proteins persistent expression. Another approach may be to create an internal requirement for the heterologous protein such that transformed bacteria that stop expressing the protein would die. 0. Vehicles for delivery/dosing regimen Delivery of engineered bacteria to a desired mucosal surface depends on the accessibility of the area and the local conditions. Engineered bacteria may be placed in a saline solution for delivery to the naso- and oropharynx, or in a foam for delivery onto the vaginal or rectal mucosa. Mucosal surfaces less readily exposed–e.g. esophagus and trachea–may require a more viscous vehicle such as glycerin or sugar which facilitates the coating of the lining as it travels down the tract. Access to the small intestines and colon will require survival through the acid conditions of the stomach, hydrolytic enzymes secreted by the pancreas, and the antimicrobial effects of bile. Protective capsules have been suggested for protecting bacteria through the upper GI transit (Henriksson, A., et al., Appl Environ Microbiol, 57(2):499-502, 1991, hereinafter Henriksson, et al., 1991). It has been found that some strains in the colonic flora are inherently capable of surviving these conditions and therefore would be suitable for use in the GI tract. Bacteria are self-replicating, so theoretically if an engineered bacteria successfully colonizes a mucosal surface, it should persist indefinitely. However, numerous factors may limit the indefinite survival of an engineered bacterial population on a given mucosal surface, the most significant factor being the fierce competition for space by a number of different bacteria on any mucosal surface. Therefore, it is envisioned that applications of engineered bacteria to a mucosal surface will need to be repeated on a regular basis; optimal dosing intervals are routine to determine, but will vary with different mucosal environments and bacterial strain. The dosing intervals can vary from once daily to once every 2-4 weeks. Oral administration of 108 -1011 viable bacteria has produced transient colonization of colonic mucosa (Henriksson, et al., 1991 ). It is expected that colonization of the URT and vaginal mucosa will require less, as low as 106 viable bacteria, since these surfaces are more directly accessible and do not pose the acid and other harsh conditions of the upper GI tract. To deliver genes directly into bacteria already resident on a mucosal surface, bacteriophage which specifically infect a selected bacteria will be used as the vector. Bacteriophage are viruses which infect bacteria. Examples include bacteriophage lambda, M13, and T7 which all infect Escherichia coli, and fadh which infects Lactobacillus gasseri. The nucleic acid of the selected bacteriophage may be manipulated such that the heterologous gene(s) replaces the genes coding for bacteriophage coat proteins, rendering the bacteriophage replication-defective. Adding these recombinant DNA molecules into cell lysates containing functional bacteriophage proteins will lead to assembly of functional bacteriophage particles carrying the heterologous gene(s). These replication-defective bacteriophage particles can then be introduced onto a desired mucosal surface to infect selected floral bacteria. The typical dosage would be 108 to 1012 PFU/ml applied to the mucosal surface. The proportion of solution to the treated surface should approximate 0. 1 to 1.0 ml per square centimeter of mucosal surface. The vehicle would be similar to the vehicle described above for the bacteria. P. Situations particularly suited for this invention 1. To prevent infection from viruses for which no effective vaccine is presently available: HIV, HPV, HSV, Hepatitis A Virus, Varicella Zoster Virus (chickenpox), Rotavirus, etc. 2. Any individual who wants to minimize his/her risk of contracting viral URIs/influenza, especially those who travel frequently, work at public places (healthcare providers, school teachers, etc.), have young children, and those with important upcoming events who cannot risk being ill. 3. Immunosuppressed individuals-since ViroShield™ represents a completely additional layer of protection on the mucosal surfaces, it does not rely on normal function of the immune system, and in fact should work in conjunction with the immune system. 4. Third world countries where administration of vaccines may be difficult and unreliable; ViroShield™ against rotavirus would be particularly useful in these situations. 5. Individuals with allergic reactions to certain components in a vaccine preparation, such as eggwhite proteins in the preparation of the flu vaccine. 6. Individuals traveling to third-world countries where certain viruses are endemic, such as Hepatitis A and Poliovirus. 7. Individuals with significant risk factors for sexually-transmitted diseases. 8. Protection of livestock animals from pathogenic viral infection. Q. Definitions Bacteria: Minute, unicellular prokaryotic organisms that are classified as lower protists. They may occur as symbionts, parasites, or pathogens of humans and other animals, plants, and other organisms. Most of the mucosal surfaces of humans and animals are heavily colonized by a wide variety of bacteria, which serve a number of useful functions to the host. Biofilm: A complex network of different bacteria and extracellular matrix materials secreted by the bacteria which become confluent as a film on many mucosal surfaces. Colonize: As applied to the bacterial flora, a state in which a bacteria resides harmlessly on a host mucosal surface. The residency time may be from 2 days to permanent, but more typically 1 week to 1 month. Conserved determinant: The portion of a protein which is common amongst many variants of the protein. This is important in viruses because there are often numerous strains of a single virus, each with slightly different variations in the viral proteins. A conserved determinant on a viral protein refers to an epitope which is common in all strains of the virus. Disease: As applied to a viral infection, this is a state in which a host suffers harmful effects from a viral infection, either immediate (e.g. fever, chills, bodyaches, etc.) or long-term (e.g., chronic hepatitis and hepatocellular carcinoma from chronic hepatitis virus types B and C infections, and cervical cancer from chronic HPV infection). Fusion: As used in this document, refers to the act of merging of two membranes such that the contents of the two entities combine into a single unit. Genetic material: Generally DNA which contains at least one gene and the regulatory elements which affect the expression of that gene. Host receptor: A molecule on the surface of the host (target) cell to which a virus attaches in order to gain entry into the host cell. Hosts: The hosts include both animals and humans. The invention is useful for protecting livestock animals including mammals and birds. Inactivation: The process of rendering an infectious agent no longer capable of infecting a host. Mucosal surface: The epithelial membranes which line the inner interface of the body with the environment, including the respiratory tract, gastrointestinal tract, and genitourinary tract. Receptors: As applied to viral receptors include the native protein and the functional domains that provide the specific binding characteristics that define these proteins as receptors of virus binding. Selected for its ability to colonize the mucosal layer: As applied to bacteria refers to bacteria which have been chosen by either selective pressure or by deliberate genetic transformation to enhance ability to colonize mucosal surfaces. The ability whether in terms of absolute numbers or in residency time is defined as at least double the wildtype’s ability to colonize. Selective advantage: Certain features which when conferred upon a bacteria cause the bacteria to be better adapted to survive in a specific environment such that it will have a greater chance than other bacteria in the same environment to survive and flourish in that environment. Transform: As applied to bacteria, the introduction of foreign genetic material into a bacteria for the purpose of causing said bacteria to express the foreign gene(s). Viral infection: The introduction of a virus into a host or a host cell. This does not necessarily suggest harmful effects suffered by the host and needs to be distinguished from clinical disease. This is an important concept since ViroShield™ represents a way to prevent infection altogether, while standard vaccines do not actually prevent infection but may prevent disease. Virus: An infectious agent that consists of proteins and genetic material, either DNA or RNA, both of which are arranged in an ordered array and are sometimes surrounded by an envelope. A virus is generally smaller than a bacterium and is an obligate intracellular parasite at the genetic level; it uses the cell machinery to produce viral products specified by the viral nucleic acid. They are classified into 5 classes based on the type of nucleic acid (ssDNA, dsDNA, dsRNA, +strand RNA, -strand RNA), and a sixth class which is capable of reverse-transcribing +RNA into DNA (retroviruses, e.g. HIV). All publications and patent applications cited in this specification are herein incorporated by reference as if each individual publication or patent application were specifically and individually indicated to be incorporated by reference. EXAMPLES The following examples are provided by way of illustration only and not by way of limitation. Those of skill will readily recognize a variety of noncritical parameters which could be changed or modified to yield essentially similar results. A. The following examples teach the expression of the receptor for HRV, major group, ICAM-1, on the surface of Esherichia coli. 1. Expressing ICAM-1 domain on the surface of E. coli using plasmid pTX101 ICAM-1 domains 1 and 2 (the minimal receptor for HRV, major group) are expressed on the surface of E. coli through the creation of a fusion protein with aa 1-9 of normal surface protein Lpp and aa 46-159 of OmpA using a system described in U.S. Pat. No. 5,348,867. The DNA segment coding for domains 1 and 2 of ICAM-1 will be amplified using polymerase chain reaction (PCR) with primers designed to introduce in-frame EcoRI restriction sites flanking aa 1-168 of ICAM-1. Plasmid TX101, as described in U.S. Pat. No. 5,348,867, contains the ß-lactamase gene spliced into an EcoRI site, which is removed by EcoRI digestion followed by separation of the linearized plasmid and the ß-lactamase gene with agarose electrophoresis. The PCR amplified ICAM-1 gene segment is ligated to the purified plasmid. E. coli strain JM109 is rendered competent by the rubidium chloride method and transformed with the pTX101-ICAM construct using electroporation. The Lpp-OmpA-ICAM construct is under the control of the strong Ipp promoter, which is inducible by IPTG (isopropyl thiogalactoside). Thus, IPTG stimulation will lead to high-level expression of the fusion protein. Transformed bacteria will be grown at 24° C. as this expression system works best (highest surface expression) at that temperature. 2. Ascertaining surface expression of ICAM-1 and demonstrating HRV binding. Immunofiuorescence is used to confirm proper ICAM-1 expression on the bacterial surface. Transformed bacteria are applied to a glass slide and fixed with methanol. Slides will be treated with murine mAbs against ICAM-1, washed extensively, then reacted with goat-anti-mouse IgG conjugated with rhodamine. Fluorescence is observed under a Confocal Fluorescence Imaging System MRC-500 Bio-Rad microscope. To demonstrate HRV binding to the transformed bacteria, slides with fixed bacteria are incubated with HRV, washed extensively, then reacted with murine mAbs against HRV coat protein. After washing, the slides will be treated with goat-anti-mouse IgG conjugated with rhodamine and visualized as described above. 3. Neutralization of HRV infection of HeLa cells by transformed bacteria in in vitro assay. Early infection of HeLa cells in vitro by HRV will be monitored by detecting HRV mRNA inside infected HeLa cells by Northern blot analysis. A semipermeable membrane with pores of sufficient size to allow passage of HRV but not bacteria or HeLa cells is placed on top of a monolayer of HeLa cells in a tissue culture flask. Transformed or unmodified bacteria are layered onto the semipermeable membrane, then HRV is added on top of the bacteria and allowed to infect the underlying HeLa cells. After an appropriate amount of time for infection, (2-6 hrs), the bacteria and semipermeable membrane are removed, and the HeLa cells washed extensively. The cells are then lysed, and their total RNA isolated for Northern analysis which is a standard method useful for detecting HRV mRNA which is an indication of infection. 4. Methods of formulating transformed bacteria in an appropriate vehicle (foam, DNAse, etc.) for use in animal and human hosts: Transformed bacteria are formulated in a number of vehicles for animal application, For use in the nasopharynx, transformed bacteria may be mixed in saline and applied as a nasal spray. The bacteria are added to the saline at concentration of 106 to 108 cells/ml and applied twice daily in a directed spray of 0.1 ml solution/cm2 area of nasal mucosa. B. The expression of a viral receptor on the surface of Streptococcus gordonii. The following examples teach the expression of ICAM-1 on the surface of a gram-positive bacteria, since gram-positive bacteria are prominent members of the nasopharyngeal flora. The expression system is based on the one described in patent PCT/US93/02355. The examples provided herein use Streptococcus gordonii, but are readily adaptable to other gram-positive bacteria due to a common motif, LPXTGX, which allows the anchoring of proteins on the surface of essentially all gram-positive bacteria. 1. Expression of ICAM-1 on the surface of Streptococcus gordonii. S. gordonii, strain GP232 described by Fischetti et al. in WO 93/18163 is used. In this strain, the gene which encodes for the M6 surface protein of S. pyogenes (contains the LPXTGX motif), emm-6.1, and an ermC gene (erythromycin resistance) disrupted by a cat (chloramphenicol acetyltransferase) gene have been inserted into the chromosome of GP232 downstream of a strong chromosomal promoter. GP232 expresses M6 on its surface, and is susceptible to erythromycin. Integration vector pVMB20 constructed by Fischetti et al. allows for the insertion of heterologous DNA sequences into emm-6.1. pVMB20 contains a functional (undisrupted) ermC gene, and is a 6.3-kb E. coli plasmid which does not replicate in S. gordonii. pVMB20 is digested with KpnI and HindIII to release a 538-bp KpnI/HindIII segment within emm-6.1, but leaving the LPXTGX motif intact. The ICAM-1 gene is PCR amplified using amplification primers specially designed to obtain an in frame KpnI/HindIII insert containing domains 1 and 2 of ICAM-1. The insert is then ligated into the digested vector. Nucleotide sequence analysis of the pVMB20:ICAM-1 construct confirms the proper (in frame) insertion. The plasmid will be linearized and used to transform GP232 by standard methods. Homologous recombination between the 5′ end of the emm-6.1 gene and the 3′ end of the ermC gene, present on both the GP232 chromosome and the plasmid, allows for the integration of the ICAM-1 gene and the functional ermC gene into the GP232 chromosome. Transformants are selected by screening for erythromycin-resistance, in media containing 5 µg/ml erythromycin. 2. Ascertaining surface expression of ICAM-1 and demonstrating HRV binding. As in example A2, surface expression of ICAM-1 is verified by immunofluorescence using antibodies specific for ICAM-1. HRV binding will also be demonstrated as in example A2. 3. Neutralization of HRV infection of HeLa cells by transformed bacteria in in vitro assay. Neutralization of HRV infection of HeLa by transformed GP232 will be demonstrated as in example A3. C. Antibody expression on a E. coli. The following examples teach the expression of an antibody fragment against a conserved determinant on the HLA DR molecule on the surface of E. coli. Since the HIV envelope is found to contain approximately 375 copies of the HLA DR molecules from its host (Arthur, L. O., et al., Science, 258(5090):1935-8, 1992.) an antibody fragment against a conserved determinant on HLA DR will bind to all isolates of HIV. A phage display system exists which allows for the rapid selection of antibody fragments against essentially any target (Marks, J. D., et al., J Biol Chem, 267(23):16007-10, 1992.) is utilized to select for an antibody fragment with high affinity against a conserved determinant on HLA DR. 1. Selection for an antibody fragment with high affinity against a conserved determinant on HLA DR. A phage library consisting of approximately 1014 bacteriophage each displaying a unique antibody fragment (scFv) on its surface is used (E.g., G. Winters, MRC, Cambridge, UK). Phage binding to HLA DR is selected by taking advantage of the fact that activated T cells express HLA DR, while resting T cells do not. All phage that bind activated T cells will be selected, then of this population, phage that bind resting T cells are removed. This process effectively isolates the subpopulation of phage that bind to HLA DR, and a few T cell activation markers. B cells express HLA DR constitutively. Subjecting this subpopulation of phage to B cells allows for selection of anti-HLA DR phage only, because B cells do not express T cell activation markers. Of the phage that bind HLA DR, the ones that bind to conserved determinants are selected by screening the subpopulation against B cells of a variety of HLA DR specificities, and selecting only the clones that bind to every B cell specificity. If more than one clone is identified, the one with the highest binding affinity is used. Binding affinities in excess of 10-8 to 10-12 are preferred. 2. Method of expressing an antibody fragment against a conserved determinant on HLA DR on surface of E. coli using plasmid pTX101. The VH and VL domains of the selected scFv are cloned using suitable primers designed to introduce in-frame EcoRI restriction sites at the N-terminus of the VH and the C-terminus of the VL. The PCR amplified gene segment is ligated into the EcoRI site of pTX101. JM109 bacteria are transformed with the plasmid, and surface expression of the fusion protein will be induced with IPTG at 20° C. as described in example 1. 3. Method of ascertaining surface expression of antibody fragment and demonstrating HIV binding. Immunofluorescence is performed to confirm proper anti-DR scFv expression on the bacterial surface. Transformed bacteria are applied to a glass slide and fixed with methanol. Slides are treated with soluble human HLA DR molecules, washed, murine mAbs against HLA DR, washed, then reacted with goat-anti-mouse IgG conjugated with rhodamine. Fluorescence will be observed under a Confocal Fluorescence Imaging System MRC-500 Bio-Rad microscope. To demonstrate HIV binding to the transformed bacteria, slides with fixed bacteria are incubated with HIV, washed extensively, then reacted with murine mAbs against the HIV coat protein gp120. After washing, the slides are treated with goat-anti-mouse IgG conjugated with rhodamine and visualized as described above. 4. Neutralization of HIV infection of T cells by transformed bacteria in in vitro assay Early infection of CEM cells (a laboratory T cell line) in vitro by HIV is monitored by detecting reverse transcriptase activity within infected cells. A semipermeable membrane with pores of sufficient size to allow passage of HIV but not bacteria or CEM cells is placed on top of CEM cells in a tissue culture flask. Transformed or unmodified bacteria are layered onto the semipermeable membrane, then infective HIV is added on top of the bacteria and allowed to infect the underlying CEM cells. After an appropriate of time for infection, (i.e. 2-6 hrs), the bacteria and semipermeable membrane are be removed, and the CEM cells washed extensively. These cells are lysed, and their cytosolic contents assayed for reverse transcriptase activity as an indication of early HIV infection. 5. Methods of formulating transforming bacteria in appropriate vehicle (foam, DNAse, etc.) for use in animal or human hosts. For the GI tract, transformed E. coli bacteria are cultured and added to a mixture of various fatty acids conventionally used for rectal administrations such as: hydrogenated cocoa nut oil, glycerin, hydrogenated palm kernel oil, or other suitable material for rectal administration. The bacteria is added to the excipients at a concentration of 106 to 108 cells per mg of excipient. Each suppository is between 3-8 grams. Although the foregoing invention has been described in some detail by way of illustration and example for purposes of clarity of understanding, it will be readily apparent to those of ordinary skill in the art in light of the teachings of this invention that certain changes and modifications may be made thereto without departing from the spirit or scope of the appended claims. * * * * * Other References * Marshall, Science, 269: 1050-1055, 1995 * Int.J.Tiss REACXIII(2) 115-122 (1991), “Lactobacilli in Relation to Human Ecology and Antimicrobial Therapy,” 1991 Bioscience Ediprint, Inc * Gastroenterology 1992;102:875-878, “Fecal Recovery in Humans of Viable Bifidobacterium sp Ingested in Fermented Milk,” 1992 by the American Gastroenterological Association * Am J Clin Nutr 1992;55:78-80, “Survival bifidobacteria ingested via fermented milk during their passage through the human small intestine: an in vivo study using intestinal perfusion 1-4,” 1992 American Society for Clinical Nutrition * Human Health: The Contribution of Microorganisms Formulation, Production and Marketing of Probiotic Products, “Commercial Aspects of Formulation, Production and Marketing of Probiotic Products,” Chapter 10, S. Laulan Inventor * Lee, Peter Poon-Hang Application No. 401070 filed on 03/08/1995 US Classes: 424/93.1, WHOLE LIVE MICRO-ORGANISM, CELL, OR VIRUS CONTAINING424/93.2, Genetically modified micro-organism, cell, or virus (e.g., transformed, fused, hybrid, etc.)424/93.4, Bacteria or actinomycetales424/93.45Lactobacillus or Pediococcus or Leuconostoc Field of Search 435/173.1, TREATMENT OF MICRO-ORGANISMS OR ENZYMES WITH ELECTRICAL OR WAVE ENERGY (E.G., MAGNETISM, SONIC WAVES, ETC.)435/173.8, Metabolism of micro-organism enhanced (e.g., growth enhancement or increased production of microbial product)435/252.3, Transformants (e.g., recombinant DNA or vector or foreign or exogenous gene containing, fused bacteria, etc.)435/244, Chemical stimulation of growth or activity by addition of chemical compound which is not an essential growth factor; stimulation of growth by removal of a chemical compound435/252.1, Bacteria or actinomycetales; media therefor424/93.1, WHOLE LIVE MICRO-ORGANISM, CELL, OR VIRUS CONTAINING424/93.2, Genetically modified micro-organism, cell, or virus (e.g., transformed, fused, hybrid, etc.)424/93.4, Bacteria or actinomycetales424/93.45Lactobacillus or Pediococcus or Leuconostoc Examiners Primary: Ziska, Suzanne E. Attorney, Agent or Firm * Townsend and Townsend and Crew LLP US Patent References 5348867, Expression of proteins on bacterial surface Issued on: 09/20/1994 Inventor: Georgiou, et al.5531988Bacteria and immunoglobulin-containing composition for human gastrointestinal health Issued on: 07/02/1996 Inventor: Paul Foreign Patent References * WO 93/18161 WO. 09/19/1993 International Class A01N 063/00 US Patent Application 20060283080 – Method of creating and preserving the identity of non-genetically modified seeds and grains 192.168.1.100 http://www.patentstorm.us/applications/20060283080/fulltext.html 1. A method of ensuring the exclusion of genetically modified material from food products comprising: selecting seeds from certified sources that are known to contain only non-genetically modified and non-genetically-engineered varieties (non-GMO); planting the selected seeds to produce a non-GMO crop; inspecting a grower operation and machinery to verify that the operation is free of contaminates and conforms to processing and cleanliness criteria prior to harvest; harvesting the non-GMO crop; inspecting processing facility to verify that the operation is free of contaminants and conforms to processing and cleanliness criteria prior to processing; tracking containers holding the non-GMO crop each time the crop is moved into and out of a storage container, wherein the tracking includes monitoring the field in which the non-GMO crop was grown, monitoring each of the storage containers used to hold the non-GMO crop, and recording the date of all crop transfers; and processing the non-GMO crops into a food product, wherein said food product is placed in containers for shipment, wherein the containers possess lot-based tracking information which permits the food product to be tracked back to the field and to containers used to produce or ship the food product; and shipping the food product for use by a food processor. 2. The method of claim 1, further comprising obtaining genetic test results indicative that the crop substantially excludes genetically modified crop material. 3. The method of claim 2, further comprising certifying that the crop excludes genetically modified crop material. 4. The method of claim 3, wherein certifying that the crop excludes genetically modified crop material comprises testing for application susceptibility. 5. The method of claim 3, wherein the certifying is sufficient to indicate that the crop contains 0.01% or less genetically modified material. 6. The method of claim 3, wherein the act of certifying comprises making a non-visual verification that the crop substantially excludes genetically modified crop material. 7. The method of claim 1, further comprising obtaining genetic test results indicative that the food product substantially excludes genetically modified crop material. 8. The method of claim 7, further comprising certifying that the food product substantially excludes genetically modified crop material. 9. The method of claim 8, wherein the certifying is sufficient to indicate that the food product contains 0.01% or less genetically modified material. 10. The method of claim 7, wherein the lot-based tracking information comprises a lot identification number established when the crop is harvested. 11. The method of claim 1, wherein the lot-based tracking information comprises a lot identification number established when the crop is harvested. 12. A method of ensuring the exclusion of genetically modified material from food products comprising: planting seeds selected from sources known to contain only non-genetically modified and non-genetically-engineered varieties to produce a non-GMO crop; harvesting the non-GMO crop; and processing the non-GMO crop into shipping containers identified with non-varietal lot-based tracking information. 13. The method of claim 12, further comprising obtaining genetic test results indicative that the crop substantially excludes genetically modified crop material. 14. The method of claim 13, further comprising certifying that the processed crop excludes genetically modified crop material. 15. The method of claim 14, wherein the certifying is sufficient to indicate that the processed crop contains 0.01% or less genetically modified material. 16. The method of claim 14, wherein the act of certifying comprises making a non-visual verification that the crop substantially excludes genetically modified crop material. 17. The method of claim 12, further comprising obtaining genetic test results indicative that the unprocessed crop substantially excludes genetically modified crop material. 18. The method of claim 17, further comprising certifying that the food product substantially excludes genetically modified crop material. 19. The method of claim 17, wherein the non-varietal lot-based tracking information comprises a lot identification number established when the crop is harvested. 20. The method of claim 12, wherein the non-varietal lot-based tracking information comprises a lot identification number established when the crop is harvested. 21. A method of ensuring the exclusion of genetically modified material from food products comprising: obtaining crop products grown under controlled conditions to exclude genetically modified material; tracking the crop products using lot-based tracking information; genetically testing the crop products to determine whether genetically modified material is present; and excluding the crop products if the genetic testing indicates that genetically modified material is present at an excess level. 22. The method of claim 21, further comprising associating information obtained at multiple stages of the development of the crop products with the lot-based tracking information in a single document. 23. The method of claim 21, wherein the genetic testing is variety-independent. Description CROSS-REFERENCE TO RELATED APPLICATIONS Posted by boxcarro at 7:46 AM 0 comments Subscribe to: Posts (Atom) Genetic Murder Patent * ? 2009 (1) o ? May (1) + PATENTED to KILL in US PATENT OFFICE!

About homelessholocaust

Tijuana Hobo , Hebrew Hobo Railroad Rabbi, The Truth Teller Tell True Truth Truthfully. If the Truth is Repugnant to you, You are a Reagan Cultist. Ronald Reagan was Taught by L. Ron Hubbard, Reagan & Hubbard FOUNDED THE SCIENCE FICTION MIND FUCKING GAME- SCIENTOLOGY- then REAGAN USED NERO LINGUIST PROGRAMMING as PRESIDENT to MURDER THE MINDS of AMERICANS!
This entry was posted in Uncategorized. Bookmark the permalink.

Leave a Reply

Fill in your details below or click an icon to log in:

WordPress.com Logo

You are commenting using your WordPress.com account. Log Out / Change )

Twitter picture

You are commenting using your Twitter account. Log Out / Change )

Facebook photo

You are commenting using your Facebook account. Log Out / Change )

Google+ photo

You are commenting using your Google+ account. Log Out / Change )

Connecting to %s