The human immunodeficiency virus (HIV) is responsible for the acquired immunodeficiency syndrome (AIDS). The first cases of AIDS were reported in 1981 and it is one of the world's most serious health problems. The risk of adults becoming infected through the oral route appears to be relatively low and it is generally assumed that HIV transmission does not occur through casual oral contact, even among patients with high viral load. People with advanced HIV infection are vulnerable to life-threatening malignancies and opportunistic infections such as candidiasis. Oropharyngeal candidiasis affects up to 50% of untreated HIV-1 subjects and 90% of AIDS patients. Interestingly, HIV-1 directly interacts with Candida spp and this interaction abrogates the production of HIV-1 by infected macrophages. Our preliminary data provide new insights into the mechanisms by which Candida albicans acts against HIV-1. The putative pathways by which C. albicans affects HIV-1 infection involve the upregulation of cc-chemokines. Therefore, the hypothesis of the proposed study is that C. albicans are involved in the inhibition of HIV pathogenesis. To explore our hypothesis, we propose to: 1) Elucidate the specific host cell-signaling pathways induced by C. albicans PAMPs relevant to production of anti-HIV cc-chemokines and 2) Determine how C. albicans PAMPs driven responses impact the host antiviral restrictions factors.