Perhaps this was not clear, but the hypothesis isn't claiming that outbreaks tend to happen at the point of vaccination. Contaminated vaccine lots would introduce smoldering, subclinical retroviral infections into the population. As shown by HIV and HTLV, most people don't show acute symptoms upon initial infection, and when they do the symptoms are rather general (fever, etc).
So no, I wouldn't expect many patients to descend into ME/CFS soon after vaccination (though that's not to say some don't, in particular as is reported with Hep B vaccine, since it can trigger acute immune activation).
However, once a retroviral contaminant (that resides in immune cells and proliferates via clonal expansion) had been introduced into the population, an "outbreak" of ME/CFS could emerge from an outbreak of any acute infection that triggers retroviral proliferation through immune activation (e.g. enterovirus, EBV, CMV, etc). Hence, while most of the population recovers from said acute infection, those with a smoldering retroviral infection have their immune systems sent into tailspin.
The ordering of events is important as well. Having an existing "co-infection" at the point of vaccine contamination wouldn't necessarily be problematic. Having latent retroviral infection at the point of acute immune activation via co-infection would.
The problem with looking primarily at enteroviruses/EBV/etc is that there is a gaping hole these hypotheses: why do the vast majority of people recover yet a small percentage descend into ME/CFS? At best, enteroviruses/EBV/etc are necessary but not sufficient. And they don't even appear to be necessary, given gradual onset cases and apparent variability in type of triggering infection. This hypothesis would fill that hole.
