Using our in vitro model of normal B cell infection that functions wit
h low doses of HIV but requires virus opsonization by seropositive pat
ient serum, and complement, me analyzed what receptors allowed virus e
ntry. Here, we show that HIV infection of B cells occurs through 2 maj
or receptors: the CD4 antigen and the CR1/CR2 complex, These 2 pathmay
s work independently since a complete inhibition of virus entry requir
es both CD4 and CD21/CD35 blockade on CD4(dim) tonsillar B cells where
as only the latter is critical on CD4-negative B cells.