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Critical Discovery Explains How HIV Replicates
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Why does the human immunodeficiency virus (HIV) envelope protein feature an abnormally long tail when compared to other similar viruses? The reason may finally have been uncovered.
Why does the human immunodeficiency virus (HIV) envelope protein feature an abnormally long tail when compared to other similar viruses? The reason may finally have been uncovered.
A collaborative team of virologists from Emory University School of Medicine, Yerkes National Primate Research Center, and Children’s Healthcare of Atlanta discovered a small part of the tail that they believe is responsible for assembling the infectious covering of HIV. This critical detail may be the key to explaining multiple aspects of the virus’ function.
“The new paper shows that the protein we found is the key factor in determining envelope incorporation in T cells and macrophages,” lead author Paul Spearman, MD, said in a news release.
Previous work by the researchers revealed that Rab11-FIP1C, a protein from host cells, is essential in order for the envelope protein to join the infected particles that HIV is attracted to. Building off of this finding, the team observed the lentivirus’ envelope glycoproteins (Env) with long cytoplasmic tails (CTs) and documented the conclusions in the Proceedings of the National Academy of Sciences.
“Here, we used viruses bearing targeted substitutions within CT to map the FIp1C-dependent incorporation of Env,” the authors explained. “We identified YW795 as a critical motif mediating cell-type—dependent Env incorporation.”
The research suggested that YW795 helps with the assembly and replication of HIV. Furthermore, not only did this give insight as to why HIV has an unusually long tail, it also provided further evidence supporting the thought that the tail assists the virus with avoiding the immune system.
“Now we know the part of the envelope protein required, which is probably the part that binds to Rab11-FIP1C, and have more evidence that this pathway is really important for the virus,” Spearman said.
Now that the researchers identified this significant element, they can work more efficiently to interfere with the disease and find better vaccines.
