Endogenous retrovirus

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Endogenous retroviruses are retroviruses thought to be derived from ancient infections of germ cells in humans, mammals and other vertebrates; as such their proviruses are passed on to the next generation and as such now remain in the genome. Retroviruses are viruses that reverse-transcribe their RNA into DNA for integration into the host's genome. Most retroviruses (such as HIV-1) infect somatic cells, but some can also infect germline cells and once they have done so and have been transmitted to the next generation, they are termed endogenous. Endogenous retroviruses can persist in the genome of their host for long periods. However, they are generally only infectious for a short time after integration as they acquire 'knockout' mutations during host DNA replication. They can also be partially excised from the genome by a process known as recombinational deletion.

Human endogenous retroviruses (HERVs) are suspected of involvement in some autoimmune diseases, in particular with multiple sclerosis. Investigations also suggest possible HERV involvement in the HELLP syndrome and pre-eclampsia. There are many thousands of endogenous retroviruses within human DNA (HERVs comprise .03% of the human genome, with 98,000 elements and fragments^[1]). All appear to be defective, containing nonsense mutations or major deletions, and cannot produce infectious virus particles. This is because most are just ancient fossils, having first integrated many of millions of years ago. However, there is one family of viruses that have been active since the divergence of humans and chimpanzees. This family, termed HERV-K(HML2), makes up less than 1% of HERV elements but is one of the most studied. There are indications it has even been active in the past few hundred thousand years, as some human individuals carry more copies of the virus family than others. But the absence of known infectious members of the HERV-K(HML2) family, and the lack of elements with a full coding potential within the published human genome sequence, suggests that the family is less likely to be active at present.^[2]

Research also eyes a link between HERVs and schizophrenia, according to a Robert Yolken abstract, a publication of Stanley Division of Developmental Neurovirology, Johns Hopkins Medicine. See publication titled "VIRUSES AND SCHIZOPHRENIA; A FOCUS ON HERPES SIMPLEX VIRUS" (2005). http://www.stanleylab.org/publications/VIRUSES.asp

In 2006, researchers led by Thierry Heidmann at the Institut Gustave Roussy in Villejuif, France were able to recreate a HERV, which they dubbed Phoenix.^[3]