Platelet activation and platelet-monocyte aggregate formation contribute to decreased platelet count during acute simian immunodeficiency virus infection in pig-tailed macaques

Kelly A. Metcalf Pate, Claire E. Lyons, Jamie L. Dorsey, Erin N. Shirk, Suzanne E. Queen, Robert J. Adams, Lucio Gama, Craig N. Morrell, Joseph L. Mankowski

Research output: Contribution to journalArticle

Abstract

Platelets are key participants in innate immune responses to pathogens. As a decrease in circulating platelet count is one of the initial hematologic indicators of human immunodeficiency virus (HIV) infection, we sought to determine whether decline in platelet number during acute infection results from decreased production, increased antibody-mediated destruction, or increased platelet activation in a simian immunodeficiency virus (SIV)/macaque model. During acute SIV infection, circulating platelets were activated with increased surface expression of P-selectin, CD40L and major histocompatibility complex class I. Platelet production was maintained and platelet autoantibodies were not detected during acute infection. Concurrent with a decrease in platelet numbers and an increase in circulating monocytes, platelets were found sequestered in platelet-monocyte aggregates, thereby contributing to the decline in platelet counts. Because the majority of circulating CD16+ monocytes formed complexes with platelets during acute SIV infection, a decreased platelet count may represent platelet participation in the innate immune response to HIV.

Original languageEnglish (US)
Pages (from-to)874-883
Number of pages10
JournalJournal of Infectious Diseases
Volume208
Issue number6
DOIs
StatePublished - Sep 15 2013

Keywords

  • CD16 monocyte
  • HIV
  • SIV
  • macaque
  • platelet activation
  • platelet-monocyte aggregate
  • thrombocytopenia

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases

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