Based on the 10-15-fold induction of plasmablasts and expression of intracellular Ki67 during ongoing immune responses (Brokstad et al., 1995; Bernasconi et al., 2002; Sasaki et al., 2007; Smith et al., 2009; Wrammert et al., 2008) , we can assume that most plasmablasts result from the ongoing infection sorted cells (defined as CD19 + , CD20 lo/ , CD3  , CD38 high , CD27 high cells; Fig. 1 E; Wrammert et al., 2008; Smith et al., 2009) . These genes were cloned and expressed as mAbs in 293 cells, and the antibodies were screened for reactivity by ELISA. Thresholds for scoring antibodies as specific to the influenza antigens were empirically determined based on being two standard deviations greater than the background level of binding evident from 48 naive B cell antibodies (Fig. S1 A) . Of 86 antibodies generated in this fashion, 46 (53%) bound pandemic H1N1 (Fig. 1 F) and one third (15 antibodies) were reactive to HA ( Fig. 1 G and Fig. S2 A) , most of them at sub-nanomolar avidities (based on surface plasmon resonance analyses; Fig. S2 B) . On a per donor basis, 55% of the mAbs bound to purified pandemic H1N1 virions (range: 33 to 77%). Of the virus-specific antibodies, 31% bound to recombinant HA (range: 14 to 55%). We conclude that virus-specific plasmablasts are readily detected after pandemic H1N1 influenza virus infection and that virus-specific human mAbs can be efficiently generated from these cells.