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CD32-RNA Co-localizes with HIV-RNA in CD3+ Cells Found within Gut Tissues from Viremic and ART-Suppressed Individuals.
Vásquez, Joshua J; Aguilar-Rodriguez, Brandon L; Rodriguez, Leonardo; Hogan, Louise E; Somsouk, Ma; McCune, Joseph M; Deeks, Steven G; Laszik, Zoltan G; Hunt, Peter W; Henrich, Timothy J.
Affiliation
  • Vásquez JJ; Department of Medicine, Division of Experimental Medicine, University of California, San Francisco.
  • Aguilar-Rodriguez BL; Department of Medicine, Division of Pulmonary, Critical Care, Allergy, and Sleep Medicine, University of California, San Francisco.
  • Rodriguez L; Department of Medicine, Department of Medicine, Division of HIV, Infectious Diseases, and Global Medicine, University of California, San Francisco.
  • Hogan LE; Department of Medicine, Division of Experimental Medicine, University of California, San Francisco.
  • Somsouk M; Department of Medicine, Division of Experimental Medicine, University of California, San Francisco.
  • McCune JM; Department of Medicine, Division of Experimental Medicine, University of California, San Francisco.
  • Deeks SG; Department of Medicine, Division of Experimental Medicine, University of California, San Francisco.
  • Laszik ZG; Department of Medicine, Division of Gastroenterology, University of California, San Francisco.
  • Hunt PW; Department of Medicine, Division of Experimental Medicine, University of California, San Francisco.
  • Henrich TJ; Department of Medicine, Department of Medicine, Division of HIV, Infectious Diseases, and Global Medicine, University of California, San Francisco.
Pathog Immun ; 4(1): 147-160, 2019.
Article in En | MEDLINE | ID: mdl-31139759
ABSTRACT

BACKGROUND:

Identifying biomarkers for cells harboring replication-competent HIV is a major research priority. Recently, there have been mixed reports addressing the possibility that CD32-expressing T cells are enriched for HIV. There is growing evidence that CD32 expression increases with cellular activation that may be related to, but not necessarily specific for, infection with HIV. However, the relationship of CD32 expression to HIV-infection in subtypes of tissue-resident leukocytes is unclear.

METHODS:

First, we used duplex chromogenic in situ hybridization to identify cells actively transcribing RNA for both CD32 and HIV on human gut tissues. Then we performed multiplexed immunofluorescence and in situ hybridization (mIFISH) on sections from the same tissues to determine the phenotype of individual cells co-expressing HIV-RNA and CD32-RNA.

RESULTS:

HIV-RNA+ cells were more abundant in tissues from viremic individuals than in those receiving suppressive anti-retroviral therapy (ART). However, staining by both methods indicated that a higher proportion of HIV-RNA+ cells co-expressed CD32-RNA in ART-suppressed individuals than in those with viremia. The majority of HIV-RNA+ cells were CD3+.

CONCLUSIONS:

Our data suggest that the transcription of CD32-RNA is correlated with HIV transcriptional activity in CD3+ cells found within human gut tissue. Whether or not up-regulation of CD32-RNA is a direct result of HIV transcription or more global T-cell activation remains unclear.
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