Filoviruses like Marburg and Ebola produce terrifying and often fatal haemorrhagic fevers. New research, however, shows that for bats these diseases might just be part of their DNA.
About 18 million years ago protein-encoding genes from a virus became part of the genetic makeup of mouse-eared bats (genus Myotis). Most viral genes that become part of other organisms originate in retroviruses, which manufacture and insert their own DNA into the host’s genome. These are called ‘proviruses’.
Rather more rarely, other viruses do something similar by co-opting the host’s cellular machinery and it leads to the integration of viral sequences into the germline cells (sex cells, like sperm and ova). These are known as ‘non-retroviral integrated RNA viral sequences’ (NIRVs) and are thought to be a crucial part of the fossil record of viruses.
A team of international researchers led by senior author Christopher Basler, the Director of the Center for Microbial Pathogenesis in the Institute for Biomedical Sciences at Georgia State University in the US, has now conducted the most detailed study on the way evolution has affected the structure and function of NIRVs.
Basler and the team focused on Myotis bats, and NIRVs in their genome called VP35s. VP35s derive from filoviruses, so the team set out to compare these 18-million-year-old living fossil genes with the genetic makeup of contemporary Ebola and Marburg viruses.
Strangely, they discovered that while the structure of the genes is almost identical to their viral counterparts, their function had changed. VP35s work to suppress the immune system of Ebola victims. In Myotis these genes show a much-reduced function and display evidence of having been subject to positive selection pressure. While the researchers aren’t clear on what the VP35s actually do in Myotis, it is clear that evolution has favoured them, indicating that they positively contribute to the bats’ survival.
“Our study provides the most detailed characterisation available of the effect of multi-million-year evolution on the structure and function of a NIRV, identifying striking structural conservation and related but altered function to the viral VP35 gene,” says lead author Megan Edwards also from Georgia State University. “The Myotis VP35 could have a regulatory role in the Myotis immune response, where you would expect the host to keep its immune system intact. The VP35-like gene in Myotis bats could also have other roles that we are not yet aware of.”
The team have plans for further work to uncover the function of VP35 NIRVs, but Basler says their research, published in the journal Cell Reports, “provides a unique and interesting perspective on how Ebola virus and related viruses can interact with the host”.
“We think of Ebola virus as a deadly virus,” she adds, “but in the past, Ebola virus essentially donated one of its genes to the benefit of Myotis bats.”
Stephen Fleischfresser is a lecturer at the University of Melbourne's Trinity College and holds a PhD in the History and Philosophy of Science.
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