Global Dysfunction of CD4 T-Lymphocyte Cytokine Expression in Simian-Human Immunodeficiency Virus/SIV-Infected Monkeys Is Prevented by Vaccination

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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.

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