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J Virol. 2003 Apr;77(8):4695-702.

Global dysfunction of CD4 T-lymphocyte cytokine expression in simian-human immunodeficiency virus/SIV-infected monkeys is prevented by vaccination.

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  • 1Division of Viral Pathogenesis, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215, USA.

Abstract

Human immunodeficiency virus type 1 infection results in a dysfunction of CD4(+) T lymphocytes. The intracellular events contributing to that CD4(+) T-lymphocyte dysfunction remain incompletely elucidated, and it is unclear whether aspects of that dysfunction can be prevented. The present studies were pursued in a rhesus monkey model of AIDS to explore these issues. Loss of the capacity of peripheral blood CD4(+) T lymphocytes to express cytokines was first detected in simian immunodeficiency virus-infected monkeys during the peak of viral replication during primary infection and persisted thereafter. Moreover, infected monkeys with progressive disease had peripheral blood CD4(+) T lymphocytes that expressed significantly less cytokine than infected monkeys that had undetectable viral loads and intact CD4(+) T-lymphocyte counts. Importantly, CD4(+) T lymphocytes from vaccinated monkeys that effectively controlled the replication of a highly pathogenic immunodeficiency virus isolate following a challenge had a preserved functional capacity. These observations suggest that an intact cytokine expression capacity of CD4(+) T lymphocytes is associated with stable clinical status and that effective vaccines can mitigate against CD4(+) T-lymphocyte dysfunction following an AIDS virus infection.

PMID:
12663776
PMCID:
PMC152134
[PubMed - indexed for MEDLINE]
Free PMC Article
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