Nonpathogenesis of Simian Immunodeficiency Virus Infection Is Associated with Reduced Inflammation and Recruitment of

Divergent Toll-like receptor 7 (TLR7) and TLR9 signaling has been proposed to distinguish pathogenic from nonpathogenic simian immunodeficiency virus infection in primate models. We demonstrate here that in-creased expression of type I interferon in pathogenic rhesus macaques compared to nonpathogenic African green monkeys was associated with the recruitment of plasmacytoid dendritic cells in the lymph nodes and the presence of an inflammatory environment early after infection, instead of a difference in the TLR7/9 response. Type I interferons (IFNs) are synthesized in response to a variety of pathogens, including bacteria, protozoa, and viruses. DNA and RNA viruses induce type I IFN expression by plas-macytoid dendritic cells (pDCs) through stimulation of Toll-like receptor 7 (TLR7) and TLR9 (46). The IFN response is an early event in simian immunodeficiency virus (SIV)-infected monkeys (1, 21, 28, 41). SIV infection of nonhuman primates remains an invaluable animal model for studies of AIDS pathogenesis, therapeutics, and vaccines. In particular, under