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Antagonism of BST-2/Tetherin is a conserved function of the Env glycoprotein of primary HIV-2 isolates
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Orientador(es)
Resumo(s)
Although HIV-2 does not encode a vpu gene, the ability to antagonize bone marrow stromal antigen 2 (BST-2) is conserved in some HIV-2 isolates, where it is controlled by the Env glycoprotein. We previously reported that a single-amino-acid difference between the laboratory-adapted ROD10 and ROD14 Envs controlled the enhancement of virus release (referred to here as Vpu-like) activity. Here, we investigated how conserved the Vpu-like activity is in primary HIV-2 isolates. We found that half of the 34 tested primary HIV-2 Env isolates obtained from 7 different patients enhanced virus release. Interestingly, most HIV-2 patients harbored a mixed population of viruses containing or lacking Vpu-like activity. Vpu-like activity and Envelope functionality varied significantly among Env isolates; however, there was no direct correlation between these two functions, suggesting they evolved independently. In comparing the Env sequences from one HIV-2 patient, we found that similar to the ROD10/ROD14 Envs, a single-amino-acid change (T568I) in the ectodomain of the TM subunit was sufficient to confer Vpu-like activity to an inactive Env variant. Surprisingly, however, absence of Vpu-like activity was not correlated with absence of BST-2 interaction. Taken together, our data suggest that maintaining the ability to antagonize BST-2 is of functional relevance not only to HIV-1 but also to HIV-2 as well. Our data show that as with Vpu, binding of HIV-2 Env to BST-2 is important but not sufficient for antagonism. Finally, as observed previously, the Vpu-like activity in HIV-2 Env can be controlled by single-residue changes in the TM subunit.
Descrição
Palavras-chave
BST-2/Tetherin Env Glycoprotein Primary HIV-2 Isolates
Contexto Educativo
Citação
Chen C-Y, Shingai M, Welbourn S, Martin MA, Borrego P, Taveira N, Strebel K. 2016. Antagonism of BST-2/tetherin is a conserved function of the Env glycoprotein of primary HIV-2 isolates. J Virol 90:11062–11074. doi:10.1128/JVI.01451-16
Editora
American Society for Microbiology