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This Article Full Text (Papers in Press[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 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 SHIV89.6p infected macaques.

¹ Biomedical Primate Research Centre;
² GlaxoSmithKline Biologicals;
³ Karolinska Institutet;
⁴ Biomedical Primate Research Centre/University of Cambridge

⁵ E-mail: koopman{at}bprc.nl

HIV infection in humans as well as SIV infection in macaques is accompanied by a combined early loss of CCR5 (CD195) expressing CD4 memory T-cells, loss of T-helper function and T-cell hyper-activation, which all have been associated with development of high virus load and disease progression. Here a cohort of vaccinated SHIV89.6p 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 hyper-activation as an independent factor in 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 as well as 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 inversely correlated with acute phase, but not chronic phase, HIV/SIV specific IFN responses. The data highlight a central role for acute but transient, CD4 decrease as well as CD4 T-cell activation as independent factors for prediction of set point levels of virus replication.

Received 1 August 2008; accepted 4 December 2008.