@article{mbs:/content/journal/jgv/10.1099/vir.2008.006148-0, author = "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.", title = "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", journal= "Journal of General Virology", year = "2009", volume = "90", number = "4", pages = "915-926", doi = "https://doi.org/10.1099/vir.2008.006148-0", url = "https://www.microbiologyresearch.org/content/journal/jgv/10.1099/vir.2008.006148-0", publisher = "Microbiology Society", issn = "1465-2099", type = "Journal Article", 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.", }