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A virus is a form of life with very simple requirements. The basic needs of a virus are a nucleic acid to be transmitted from generation to generation (the genome) and a messenger RNA to direct the synthesis of viral proteins. The critical viral proteins that the messenger RNA must encode are those that coat the genome and those that help replicate the genome. One of the great surprises of modern virology has been the discovery of the variety of genetic systems that viruses have evolved to satisfy their needs. Among the animal viruses, at least 6 totally different solutions to the basic requirements of a virus have been found.
Autoimmune diseases, which are the third leading cause of morbidity in the industrialised world, afflict tens of millions in the United States. The idea that viruses can trigger autoimmunity in those with genetic predisposition through molecular mimicry has been simmering for a while. Viruses have been shown to have the potential to play a role in provoking and modifying the clinical manifestations of several auto-immune diseases, such as coxsackie virus in type 1 diabetes, coronaviruses in rheumatoid arthritis, and Epstein–Barr Virus in systemic autoimmune diseases. However, obtaining conclusive evidence of a connection between viral infection and subsequent autoimmune diseases is challenging, not only because it is frequently impossible to extract the virus from diseased tissues, but also because the collection of sufficient amounts of epidemiological evidence is constrained by lengthy process and geographic distances.
Viruses play a significant role in the environmental factors that affect human immune system. Cytomegalovirus 28 and Epstein–Barr virus 6 are examples of viruses that have been linked to numerous autoimmune diseases, and now SARS-CoV-2 has the potential to be added to the list. The definite mechanisms underlying such phenomena are unknown. According to recent research, viruses can trigger autoimmunity through a number of different mechanisms, including molecular mimicry, epitope spreading, and bystander activation.
Contrarily, there is also mounting evidence that viruses could play a protective role against autoimmunity, whereby viral infections trigger regulatory immune responses, which in turn prevent the onset of autoimmune reactions. It is reasonable that the dual impact of viral infections on autoimmunity is coordinated by different host, viral and environmental factors.
Over the course of human history, scientists have identified only two instances of true virus superdodgers. That is, where a specific mutation in their genes makes people completely resistant to a virus. So that it slides off their cells, "like water sliding off a glasswindow," as Casanova puts it. In 2003, a team in London showed how some people never get a stomach bug, called norovirus, which causes vomiting and diarrhea. The researchers found that one mutation in their genes prevents them from making a molecule the virus needs to infect the cell. (In 1995, researchers in France figured out why some people appeared to never be infected with a species of malaria known as Plasmodium vivax. However, over the past decade, further studies have clarified that these superdodgers actually do become infected with the parasite; they simply don't show symptoms.)
When my colleagues and I discovered the first human retrovirus that causes a form of leukemia, a fatal neurological disease, the Journal of Virology rejected the paper. They more or less told me, "Bob, everybody knows it's not real — and go away." I said, "Wow." But then it got published in the Proceedings of the U.S. National Academy of Sciences.
We learned that a virus freshly isolated from man or animal did not necessarily behave like the virus strain that we maintained in the laboratory, so-called tame virus, which might have been passaged through animals or tissue culture for generations. Virologists had to recognize that by transmission of a virus from animal to animal or from culture to culture over a period of time, what we ended up with through a process of natural selection or genetic selection was a virus adapted to growth in a new environment. A population of viruses is no more homogeneous than the human population; by passage, one culls out all of the inhomogeneous particles and leaves behind those which survive and grow so well,
In 1910 I described a malignant chicken sarcoma which could be propagated by transplanting its cells, these multiplying in their new hosts and forming new tumors of the same sort. In other ways the growth showed itself to be a neoplasm of a classical sort, yet, as reported in 1911, its cells yielded a causative virus. Numerous workers had already tried by then to get extraneous causes from transplanted mouse and rat tumors but the transferred cells had held their secret close. Hence the findings with the sarcoma were met with down-right disbelief, though soon several other, morphologically different, “spontaneous” chicken tumors were propagated by transplantation and from each a virus was got causing growths of its kind. Not until after some 15 years of disputation amongst oncologists were the findings with chickens deemed valid, and then they were relegated to a category distinct from that of mammals because from them no viruses could be obtained. Only in 1925, through the efforts of a British worker, W.E. Gye, was much attention given them by scientists.
Why has it been so difficult to identify infectious agents as cancer-inducing factors in humans? Because there is no human pathogenic infectious agent causing cancer as the acute consequence of infection ... Infections linked to human cancers are common in human populations, most of them were present during the whole human evolution,and only a small proportion of infected individuals develops the respective cancer type ... Except for rare germline mutations, (XLLP), cancers linked to infection commonly occur decades after primary infection ...