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 Koopman, Gerrit and Mortier, Daniella and Hofman, Sam and Koutsoukos, Marguerite and Bogers, Willy M. J. M. and Wahren, Britta and Voss, Gerald and Heeney, Jonathan L.,, 90, 915-926 (2009), doi = https://doi.org/10.1099/vir.2008.006148-0, publicationName = Microbiology Society, issn = 0022-1317, abstract= 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 (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 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., language=, type=