Yes, if you pay me what the establishment has been apid to investigate
the matter thoroughly.  It was known within the first few years of the
"epidemic," yet it was not investigated properly, because they made
their minds up before actually doing the science.  What appears to be
happening is that the "immune system" is being rerouted, in a sense.
Read Kremer's book, if you can read German, for a technical discussion
of the mechanisms involved.   My sense is that first comes the
immunosuppression, then the pathogens become problematic, and that
damages the body in a way that Kremer describes, leading to the
"markers" used to tell people that they "have AIDS."

Here's the first study that mentioned PGE2 in this context.  They had
the mechanism from nearly the beginning, but instead wanted to act like
they were great scientific geniuses, making "great discoveries."  PGE2
in semen was not something that would play well with the media, and no
profits could be made by just telling people to avoid it.

Proc Natl Acad Sci U S A. 1986 May;83(10):3487-90.    Related Articles,
Links

Prostaglandin E2, a seminal constituent, facilitates the replication of
acquired immune deficiency syndrome virus in vitro.

Kuno S, Ueno R, Hayaishi O, Nakashima H, Harada S, Yamamoto N.

Acquired immune deficiency syndrome (AIDS)-associated virus is thought
to be transmitted effectively through semen during sexual activities
from male to male or from male to female. Prostaglandin (PG) E2 is one
of the immunosuppressive compounds present in high concentrations in
human semen. We, therefore, investigated direct effects of PGE2 and
other PGs on AIDS-associated virus infection and replication in vitro.
First, type III human T-lymphotropic virus (HTLV-III) was used to
infect a T-cell line (MT-4) in culture. PGE2 (10 nM to 10 microM) added
to the culture medium enhanced the production of infectious virus in a
dose-dependent fashion. In the presence of 5 microM PGE2, 2.5-fold more
virus were released from the infected MT-4 cells as compared to
untreated control cells on day 3 after infection. Second, when we used
an HTLV-III continuous-producer cell line (Molt-4/HTLV-III), PGE2 and
PGD2 added to the culture medium increased the number of viruses
released from Molt-4/HTLV-III cells. Other PGs such as PGF2 alpha and
13,14-dihydro-15-keto PGE2 did not affect the replication of HTLV-III
in this system. These results indicate that some PGs including seminal
PGs enhance the AIDS-associated virus replication in vitro. We propose
that PGE2 in human semen might directly facilitate the infection of
AIDS-associated virus and cause the efficient transmission of the virus
during sexual activities.