Simian immunodeficiency virus-induced CD4+ T cell deficits in cytokine secretion profile are dependent on monkey origin.

Facets of the immune response early after human immunodeficiency virus (HIV) infection influence the course of disease. In the simian immunodeficiency virus (SIV)-rhesus monkey system, a global dysfunction of CD4(+) T cell cytokine secretion was reported to develop early after infection [McKay PF, Barouch DH, Schmitz JE, Veazey RS, Gorgone DA, Lifton MA, Williams KC, and Letvin NL: J Virol 2003;77:4695-4702]. Because differences have been found in SIV pathogenesis depending on the origin of the monkeys, we investigated the correlation between animal background, defined by country of origin (India or China), and circulating T cell cytokine secretion as well as cycling ability within the first 3 mo of SIV infection. An early loss of CD4(+) T cells that produce interferon (IFN)-gamma and interleukin (IL)-2, those that produce IFN-gamma but not tumor necrosis factor (TNF)-alpha, as well as those that do not express IFN-gamma but can express IL-2 or TNF-alpha, was observed in animals of Indian, but not of Chinese, origin after SIV infection. After infection CD4(+) T cells in Chinese macaques developed an increased proliferating pool of T cells compared with Indian animals. These data reveal host diversity in the global effects of SIV infection on functional subsets of immune cells, which can add to a better understanding of differences observed in populations from diverse ethnic origins.