Last updated August 1, 2018 at 10:12 am
Study suggests they integrated into the Myotis genome 18 million years ago.
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You don’t read a lot of good things about Ebola, but it appears the Myotis or mouse-eared bat may have the deadly virus to thank for reducing its susceptibility to viral infection.
Researchers from Georgia State University in the US believe that genes encoding viral proteins 35 (VP35s) produced by the Ebola and Marburg viruses integrated into the genomes of Myotis bats around 18 million years ago.
In a paper published in Cell Reports they shed light on the potential functional role of these non-retroviral integrated RNA viral sequences (NIRVs). Despite their structural similarity, Myotis VP35s are less potent immune suppressors than filoviral VP35s, and that difference could help the bats resist infection.
“We are the first to study in detail a family of NIRVs from a combined evolutionary, structural, and functional perspective,” said senior author Christopher Basler. “The study also 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, but in the past Ebola virus essentially donated one of its genes to the benefit of Myotis bats.”
NIRVs are rare mutations thought to result from the integration of viral genes from RNA (ribonucleic acid) viruses into a host species genome through the co-option of a host reverse transcriptase – an enzyme that catalyses the formation of DNA from an RNA template.
NIRVs found in mammals
NIRVs are common in eukaryotic genomes and are present in fungi, plants, insects and mammals. For example, VP35 sequences have been identified in seven genera of mammals, including the tammar wallaby, the Philippine tarsier, rodents and all members of the Myotis genus.
“NIRVs serve as a viral fossil record, providing evidence of historical viral interactions with a host and allowing for the study of the timescale and evolution of the virus-host interaction,” said first author Megan Edwards. “But relatively little is known about the biological significance of these genetic elements.”
To address this question, Basler, Edwards and colleagues from Washington University School of Medicine and the University at Buffalo characterised VP35s from 16 species of Myotis bats and from the Ebola and Marburg viruses.
The structure of bat VP35 remains nearly identical to its viral counterparts, even after millions of years, but compared with filoviral VP35s the Myotis VP35s were less potent suppressors of the production of an antiviral immune protein called interferon beta (IFNβ) in human and Myotis cells.
“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,” Edwards said. “The VP35-like gene in Myotis bats could also have other roles that we are not yet aware of.”
