The susceptibility of primate lentiviruses to nucleosides and Vpx during infection of dendritic cells is regulated by CA.

Abstract

The block toward human immunodeficiency virus type 1 (HIV-1) infection of dendritic cells (DCs) can be relieved by Vpx (viral protein X), which degrades sterile alpha motif-hydroxylase domain 1 (SAMHD1) or by exogenously added deoxynucleosides (dNs), lending support to the hypothesis that SAMHD1 acts by limiting deoxynucleoside triphosphates (dNTPs). This notion has, however, been questioned. We show that while dNs and Vpx increase the infectivity of HIV-1, only the latter restores the infectivity of a simian immunodeficiency virus of macaques variant, SIVMACΔVpx virus. This distinct behavior seems to map to CA, suggesting that species-specific CA interactors modulate infection of DCs.

• Authors: Véronique Barateau, Xuan-Nhi Nguyen, Fanny Bourguillault, Grégory Berger, Stéphanie Cordeil, Andrea Cimarelli
• Journal: Journal of virology (J Virol) Vol. 89 Issue 7 Pg. 4030-4 (Apr 2015) ISSN: 1098-5514 [Electronic] United States
• PMID: 25609804 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2015, American Society for Microbiology. All Rights Reserved.

Chemical References

• Capsid Proteins
• Nucleosides
• VPX protein, Simian immunodeficiency virus
• Viral Regulatory and Accessory Proteins

Topics

• Animals
• Capsid Proteins (metabolism)
• Cells, Cultured
• Dendritic Cells (virology)
• HIV-1 (growth & development, physiology)
• Host-Pathogen Interactions
• Humans
• Macaca
• Nucleosides (metabolism)
• Simian Immunodeficiency Virus (growth & development, physiology)
• Viral Regulatory and Accessory Proteins (metabolism)