Genetic studies suggest that polymorphisms observed in AAT, another component of the acute phase response, are linked to susceptibility to HIV-1 infection [32, 33] . AAT was initially reported to block the activity of HIV-1 protease [26, 34, 35] . Subsequently, an AAT-derived 26mer C-terminal peptide was shown to inhibit HIV-1 LTR gene expression in vitro [36, 37] . However, the strongest effect reported so far is exerted by VIRIP generated as a proteolytic product from AAT, which inhibits viral entry by binding to the gp41 fusion peptide and is active in the low micromolar range [10] . For both A-SAA and VIRIP, we were able to detect endogenous levels in plasma that are in the range capable of mediating viral inhibition, which raises the possibility that such factors play a role in combating viral replication, particularly in the earliest stages of infection.