performed immunoblot assays with specific antibodies (Fig. 3B ). In 4 out of 10 plasma donor panels tested by immunoblotting (9011, 9013, 9016 and 9018), we confirmed the initial increase in A-SAA levels prior to viral ramp-up. In addition to this first wave of A-SAA induction that occurred prior to detection of viremia, immunoblotting also confirmed a second, more intense phase of elevation, observed in six of the ten donors tested (9011, 9012, 9016, 9018, 64012, 64122) that coincided with the increase in viral load. Other individuals either had very low or consistently high levels of A-SAA over the time-frame analyzed. By contrast to A-SAA, a major acute phase reactant that is inducible during the infection process, C-SAA, which was observed in an unmodified and glycosylated form, was detected with only minor inductions in all panels examined. To further explore whether elevation of A-SAA was specifically attributable to HIV-1 infection, we examined 6 plasma panels from donors who became positive either for hepatitis C virus (HCV) or hepatitis B virus (HBV) during the period of sample collection [14] . We detected increased levels of A-SAA over the time course of infection in 1/3 panels from subjects with acute HBV infection and 3/3 panels from subjects with acute HCV infection ( Fig. 3C and Fig. S2 B and C), indicating that A-SAA induction may represent a common host response to microbial infection.