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<\/div>Human endogenous retroviruses are remnants of viral genes in the human genome<\/p>\n
NICOLLE R. FULLER\/SCIENCE PHOTO LIBRARY<\/p>\n<\/div>\n<\/figcaption><\/figure>\n<\/p>\n
Ancient viruses embedded in human DNA millions of years ago may play a role in raising people\u2019s risks of depression, schizophrenia and bipolar disorder. The viral genes have unusual activity levels in people who have a higher genetic risk of experiencing these mental health<\/a> conditions, a study has found.<\/p>\n Retroviruses are a large group of viruses whose life cycle involves inserting their genetic information into the DNA of their host. Remnants of such viral genes can be seen in the DNA of many animal species, and these sequences are called human endogenous retroviruses (HERVs)<\/a> when found in the human genome.<\/p>\n Until recently, most HERVs were thought to remain dormant and were called \u201cfossil viruses\u201d. But previous studies have suggested that some of the viral genes may in fact be active \u2013 although not producing infectious viruses<\/a> \u2013 and may even play a role in neurological conditions, such as multiple sclerosis.<\/a><\/p>\n In a new study, Timothy Powell<\/a> at King\u2019s College London and his colleagues investigated the possible role of these viral remnants in mental health conditions by looking at viral proteins in nearly 800 brains that had been donated for medical research.<\/p>\n <\/p>\n While the team didn\u2019t record if any of the donors had been diagnosed with mental health<\/a> conditions while alive, they found that some genetic variants that are known to raise the risks of depression, schizophrenia and bipolar disorder were associated with altered activity of genes from five different HERVs.<\/p>\n It wasn\u2019t possible to estimate how much of a raised risk was linked with the unusual viral gene activity, but it is probably in the range of a few per cent, as most human gene variants affect psychiatric risk by such small amounts, says Powell.<\/p>\n The findings also don\u2019t necessarily mean that the altered HERV activity is causing the conditions \u2013 it could be a consequence, he says.<\/p>\n \u201cThe methods used look pretty robust,\u201d says Rachael Tarlinton<\/a> at the University of Nottingham in the UK. \u201cThe results are likely real that these things are markers of these diseases, but [the researchers] are rightly cautious in saying they don\u2019t know what that means.\u201d<\/p>\n Topics:<\/p>\n<\/section><\/div>\n