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This Article Full Text Full Text (PDF) All Versions of this Article: vir.2008.006148-0v1 90/4/915    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Koopman, G. Articles by Heeney, J. L. Search for Related Content PubMed PubMed Citation Articles by Koopman, G. Articles by Heeney, J. L. Agricola Articles by Koopman, G. Articles by Heeney, J. L.

Acute-phase CD4⁺ T-cell proliferation and CD152 upregulation predict set-point virus replication in vaccinated simian–human immunodeficiency virus strain 89.6p-infected macaques

¹ Department of Virology, Biomedical Primate Research Centre, Rijswijk, The Netherlands
² GlaxoSmithKline Biologicals, Rixensart, Belgium
³ Swedish Institute for Infectious Disease Control, Karolinska Institutet, Stockholm, Sweden
⁴ Department of Veterinary Medicine, University of Cambridge, UK

Correspondence
Gerrit Koopman
koopman{at}bprc.nl

Human immunodeficiency virus (HIV) infection in humans and simian immunodeficiency virus (SIV) infection in macaques are accompanied by a combined early loss of CCR5 (CD195)-expressing CD4⁺ memory T cells, loss of T-helper function and T-cell hyperactivation, which have all been associated with development of high virus load and disease progression. Here, a cohort of vaccinated simian–human immunodeficiency virus strain 89.6p (SHIV_89.6p)-infected rhesus macaques, where preferential depletion of these memory T-cell subsets does not take place and CD4⁺ T cells are relatively well maintained, was used to study the role of hyperactivation as an independent factor in the establishment of set-point virus load. In the acute phase of the infection, a transient loss of CD4⁺ T cells, as well as strong increases in expression of proliferation and activation markers on CD4⁺ and CD8⁺ T cells, together with CD152 expression on CD4⁺ T cells, were observed. Peak expression levels of these markers on CD4⁺ T cells, but not on CD8⁺ T cells, were correlated with high virus replication in the chronic phase of the infection. In addition, the peak expression level of these markers was correlated inversely with acute-phase, but not chronic-phase, HIV/SIV-specific gamma interferon responses. These data highlight a central role for an acute but transient CD4 decrease, as well as CD4⁺ T-cell activation, as independent factors for prediction of set-point levels of virus replication.