Adaptive responses are known to play an important role in containment of the acute burst of viral replication in AHI [3] , but events in the earliest stages of infection are also likely to be heavily influenced by components of the innate immune system [3] . These include cellular determinants of the efficiency of viral entry into and replication within host cells such as the CCR5-delta32 allele, CCR2, CCL5 (RANTES), CX(3)CR1, CXCL12, or TRIM5, all of which can influence host resistance or susceptibility to HIV infection [3] . Interaction of virions with dendritic cells (DCs) early after virus transmission can have outcomes including virion destruction (following binding to langerin on resting Langerhans cells), efficient viral transmission to CD4+ T cells (following binding to DC-SIGN on sub-epithelial DCs), or the triggering of DCs (via interaction with TLRs) to produce cytokines/chemokines that may mediate antiviral activity, but may also drive immunopathological immune activation including cellular apoptosis [4, 5] . Genetic studies have helped to cast light on the in vivo importance of certain components of the innate immune system in acute/early HIV infection. These include associations between expression of certain KIRs and their cognate HLA alleles and resistance to, and/or control of HIV replication, implicating NK cells in control of HIV replication [6, 7, 8] . Furthermore, b-defensins, secreted from oral and mucosal epithelial cells appear to inhibit HIV-1 infection [9] . More recently, a peptide fragment derived from alpha-1 antitrypsin (AAT), a serine protease inhibitor and acute phase protein present in blood plasma, was shown to inhibit HIV host cell infection by blocking gp41 mediated cell entry [10] . Other natural factors exist that modulate HIV infection, such as a proteolytic product of the prostate phosphatase that is present in semen, which has the ability to dramatically enhance HIV infection [11] .