More than 90% of people with AIDS develop circulating immune complexes
(CICs) and lymphocytotoxic antibodies (LCTAs). Animals infected with
HIV, however, never display CICs or LCTAs, and remain healthy. Similar
ly, HIV-infected people who do not develop CICs or LCTAs also do not p
rogress to AIDS. The appearance of CICs and LCTAs is, however, highly
prognostic for AIDS and death. Since HIV infection does not, per se, l
ead to the development of CICs and LCTAs, other causes are likely. One
such cause, for which both epidemiologic and experimental evidence ex
ists, is semen. Semen components include sperm, seminal fluid, lymphoc
ytes, and sometimes infectious agents, including HIV, mycoplasmas, and
herpes and hepatitis viruses, all of which independently cause immune
suppression. Extensive evidence demonstrates sperm (and various virus
es) contains many proteins mimicking the CD4 protein of T-helper cells
, while HIV, mycoplasmas, and seminal fluid mimic class II MHC protein
s of other lymphocytes. We identify a large number of protein sequence
s that display such mimicry using computer homology searching, and dem
onstrate experimentally that sperm antibodies specifically precipitate
antibodies against class II MHC mimics such as mycoplasmas, which in
turn precipitate antibodies to lymphocyte antigens. These data prove t
hat immunologic exposure to sperm and lymphocytes (as may occur in rec
eptive anal intercourse, needle sharing, or blood transfusions) is the
oretically capable of initiating lymphocytotoxic autoimmunity. Such au
toimmunity may play a significant role in the pathogenesis of AIDS, an
d will need to be addressed clinically in high risk individuals regard
less of HIV status and regardless of the success of anti-HIV prophylax
is and treatment.