Scientists at Fred Hutchison Cancer Research Centre, using the combination of evolutionary biology and virology, have been able to trace the birth of the ability of some HIV virus that can defeat a recently discovered defence mechanism at the cellular level in some primates. The research was led by Michael Emerman, Ph.D. besides being a member of the Hutchinson Centre’s Human Biology and Basic Sciences Division and Hermit Malik, Ph.D. also, a member of the Centre’s Basic Sciences Division. The findings along with the study were published online before the Feb 16th print issue of the magazine Cell Host and Microbe.
The study focuses on SAMHD1, the recently discovered cellular defence protein. The work also involved the researchers from Hutchinson Centre’s Computational Biology Program. SAMHD1 is the protein that is supposed to protect the key cells of the immune system against the attacks from the HIV virus. The HIV virus needs nucleotides in order to replicate itself inside the host body. The SAMHD1 protein protects the cells by inhibiting or reducing the available no. of nucleotides for the virus thus making it difficult for the virus to replicate itself.
However, some virus related to HIV-1, as the HIV-2 and a few simian immunodeficiency viruses that infect other primates produce a counter protein called Vpx. This protein binds itself to the SMAHD1 protein and completely destroys it. HIV-1 though does not secrete Vpx, it on the other hand it encodes another protein called Vpr. The team of researchers tried to find whether the HIV-1 virus lost the ability to degrade SAMHD1 or it never had the ability to do so. Both the Vpx and the Vpr protein were tested by the researchers from a sample that represented all known lentiviruses, which have the ability to bind themselves to SAMHD1. This was done by the team in order to distinguish between the two possibilities mentioned before regarding the ability of the HIV-1 virus.
Hermit Malik, who is an evolutionary geneticist said, “We have not only recreated the birth of SAMHD1-degrading activity in these viruses but also have captured the immediate evolutionary consequence on the host genes they antagonize. While such arms races between viruses and host genomes have been documented previously, this is the first instance where the beginning of the Darwinian arms race has been captured in both viral and primate genomes.” A virologist, Emerman said, “It is possible that HIV-1 is so pathogenic because it needs to grow rapidly in order to compensate for the lack of the ability to deal with SAMHD1.”