The current game plan seems to require insisting there are no exogenous retroviruses causing a wide range of diseases for which such a cause has been proposed. I happen to disagree, but this is a matter of debate. I think there is enough evidence of clustering to indicate person-to-person transmission, requiring an exogenous virus of some kind. I also think there is good reason to suspect involvement by retroviruses.
We are now told one rather disturbing virus existing in laboratories is an artifact, which cannot be present in the population at large. We are variously told this is a mouse virus or a purely endogenous virus. This precludes the person-to-person transmission behind clusters.
What gets lost in the debate is one alternative, transmission of a laboratory contaminant via vaccines. The usual arguments about screening preventing this typically concentrate on the idea of an exogenous virus being present in samples of vaccines. There is an important exception -- retrotransposons.
These are defective sequences from retroviruses which are not competent to produce infectious virions, and thus cannot be transmitted easily from host to host, even of the same species. Their effects are all over known genomes, particularly mouse genomes. The idea that retrotransposons from one host might be picked up inside another virion, and transmitted inadvertently through vaccination, is not completely ridiculous, especially for unusually small viral genomes. It is also very hard to rule out.
Part of the problem is that the existence of these movable genetic elements, though discovered in the late 1940s, was not acknowledged until the 1970s. Barbara McClintock, who did the pioneering work, was so disheartened by the sheer incomprehension of her peers that she stopped publishing her work on this subject in 1953, and did not resume until 1973. Many vaccines were developed prior to this acceptance.
Next, we have to ask how one would have gone about testing for contamination by retrotransposons prior to the introduction of PCR in 1983. Finally, once that technique became available, we have to ask what sequences were being sought in testing, since the technique is highly specific.
You can't test animals like mice to show they are free from many sequences because endogenous sequences are present in thousands of copies -- in every nucleated cell. You have to test the vaccine itself not only for sequences incorporated during vaccine development, but also for host sequences incorporated during production runs. Anyone care to bet on the rate of testing failures, if no distinctive virions are produced and retrotransposon sequence replication is slow?
Myself, I think that exogenous viruses present a better explanation, with limited damage to public health systems, and reasonable prospects for stopping the spread and for treatment of those already infected, provided we act while those numbers are manageable. I insist the subjective correlation apparent to those being vaccinated is due to latent provirus infecting immune cells and waiting for any immune challenge by a range of pathogens to trigger the clonal expansion of those cells. If people do not get the vaccination, the challenge will come, sooner or later, from the wild-type virus for which immunization was designed. This will defeat large-scale statistical analysis done without knowing who is already infected with this unknown co-factor.
I don't have to tell anyone on this forum why confidence in public health institutions is shaky. With steadily growing incidence of several diseases, and no exogenous cause, the idea of transmission via a universal practice central to public health is certain to gain ground. Some will avoid vaccination. Vanished epidemics will return.
Do we really want to go there?