The persistence of HIV reservoirs, including latently infected, resting
CD4+ T cells, is the major obstacle to cure HIV infection. CD32a
expression was recently reported to m ark CD4+ T cells harboring a
replication-competent HIV reservoir during antiretroviral therapy (ART)
suppression. We aimed to determine whether CD32 expression marks HIV latently or
transcriptionally active infected CD4+ T cells. Using peripheral
blood and lymphoid tissue of ART-treated HIV+ or SIV+
subjects, we found that most of the circulating memory CD32+
CD4+ T cells expressed markers of activation, including CD69,
HLA-DR, CD25, CD38, and Ki67, and bore a TH2 phenotype as defined by
CXCR3, CCR4, and CCR6. CD32 expression did not selectively enrich for HIV- or
SIV-infected CD4+ T cells in peripheral blood or lymphoid tissue;
isolated CD32+ resting CD4+ T cells accounted for less
than 3% of the total H IV DNA in CD4+ T cells. Cell-associated HIV
DNA and RNA loads in CD4+ T cells positively correlated with the
frequency of CD32+ CD69+ CD4+ T cells but not
with CD32 expression on resting CD4+ T cells. Using RNA fluorescence
in situ hybridization, CD32 coexpression with HIV RNA or p24 was detected after
in vitro HIV infection (peripheral blood mononuclear cell and tissue) and in
vivo within lymph node tissue from HIV-infected individuals. Together, these
results indicate that CD32 is not a marker of resting CD4+ T cells or
of enriched HIV DNA-positive cells after ART; rather, CD32 is predominately
expressed on a subset of activated CD4+ T cells enriched for
transcriptionally active HIV after long-term ART.
Our results indicate that cross-group binding and neutralizing antibody responses primarily targeting the stalk region can be elicited after natural influenza virus infection. These data support our understanding of the breadth of the postinfection immune response that could inform the design of future, broadly protective influenza virus vaccines.
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