Based on our finding that a common epitope exists between HIV-1 gp41 and hu
man type I interferons (IFN-alpha and IFN-beta), and increased levels of an
tibodies against human IFN-alpha and IFN-beta were observed in HIV-1-infect
ed individuals, we tried to explain the mechanism of increased levels of an
tibodies. Mouse antisera recognizing HIV-1 recombinant soluble (rs) gp41 (a
a 539-684) interacted with two synthetic peptides sequence-corresponding to
the IFN-alpha/beta receptor binding site on human IFN-alpha and IFN-beta,
white normal mouse serum (pooled normal sera) did nor. The anti-rspg41 anti
sera after adsorption by IFN-beta sepharose column lost the activity of int
eraction with both synthetic peptides. In another experiment, rsgp4? could
bind to sepharose column conjugated with anti-IFN-beta polyclonal antibodie
s (IgG). These results indicate that the common epitope on gp41 and type 1
interferons could induce antibodies recognizing the receptor binding site o
n IFN-alpha and IFN-beta, suggesting that increased levels of antibodies ag
ainst IFN-alpha and IFN-beta in HIV-1-infected individuals could be induced
by gp41. Copyright (C) 2000 S. Karger AG, Basel.