Date Published:
2019 Feb

Publication Type:
Journal Article

Authors:

B. Quitadamo
P.J. Peters
M. Koch
K. Luzuriaga
C. Cheng-Mayer
P.R. Clapham
M.Paz Gonzalez-Perez

Secondary:
Arch Virol

Volume:
164

Pagination:
473-482

Issue:
2

PMID:
30415390

URL:
https://pubmed.ncbi.nlm.nih.gov/30415390

DOI:
10.1007/s00705-018-4094-1

Keywords:
Brain;CD4 Antigens;HIV Envelope Protein gp120;HIV Infections;HIV-1;Humans;Macrophages;Nervous System Diseases;Phylogeny;Receptors, CCR5;Receptors, Virus

Abstract:
<p>Macrophage (mac)-tropic human immnunodeficiency virus type 1 (HIV-1) and simian immnunodeficiency virus (SIV) in brain are associated with neurological disease. Mac-tropic HIV-1 evolves enhanced CD4 interactions that enable macrophage infection via CD4, which is in low abundance. In contrast, mac-tropic SIV is associated with CD4-independent infection via direct CCR5 binding. Recently, mac-tropic simian-human immunodeficiency virus (SHIV) from macaque brain was also reported to infect cells via CCR5 without CD4. Since SHIV envelope proteins (Envs) are derived from HIV-1, we tested more than 100 HIV-1 clade B Envs for infection of CD4-negative, CCR5 Cf2Th/CCR5 cells. However, no infection was detected. Our data suggest that there are differences in the evolution of mac-tropism in SIV and SHIV compared to HIV-1 clade B due to enhanced interactions with CCR5 and CD4, respectively.</p>