Focus on mad cow disease likely inappropriate, since it is important to understand the various CJD classifications:
Variant CJD is the one associated with contamination from food, eg the mad cow disease stuff. It has tended to be noticed because of the much younger age profile of sufferers than typically seen with other CJD cases.
Familial CJD involves some inhered genetics which predispose the person to developing the condition.
Acquired CJD involves the mutated proteins being introduced to the persons by other means, typically via contamination via an affected persons tissue being used in surgery or a bunch of other medical procedures. All the forms of CJD protein misfolding lead to infectious protein material that can be transmitted in this way, not just the mad cow disease variant.
Spontaneous CJD, where the protein misfolding is said to have started spontaneously in the person. This form is what the majority of CJD cases end up being classified as.
The research you mention is pointing towards spontaneous CJD (sCJD), although the patient also had a particular genetic makeup that could well be a risk factor. The term spontaneous is really a cover for the fact that there are no obvious, well understood triggers, infection pathways etc for this form of CJD. As research improves, specific triggers for this form will likely emerge, and when those triggers are better understood the concept of this really being spontaneous will fade away. For example the full version of that research paper says:
Triggering factors for PrPc misfolding in sCJD are still unclear, and may include stress, mutation, age and overexpression of the protein itself [12]. However, it has been shown that an influenza A strain can directly induce PrPc misfolding into PrPSc, forming infectious prions. This current line of evidence highlights a possible causative link between viral infections and induction of prion diseases [13], as already suggested for other sporadic neurodegenerative diseases such as Alzheimer disease and Parkinson disease [14,15]. We hypothesize that a COVID-19-related neuroinflammatory state acted on a predisposing genetic background to induce the misfolding and subsequent aggregation of PrP.
So we can see that even before this pandemic, some research implied that particular viral infections can be a trigger for this form of CJD. So its not surprising that COVID might end up being implicated and be added to that tentative list.
The eventual implications of this will come down to the number of people that end up affected, and whether it makes a notable difference to the age profile of disease onset. Existing knowledge is underdeveloped, but based on what we already know it is quite plausible that more cases will be seen. That doesnt mean that we should expect the number of cases to be huge with any degree of certainty, but the very high number of covid infections is certainly going to test what the implications are, what proportion of the public are susceptible to CJD and how many will have it triggered, and what age this happens at, than would otherwise have been the case in the pre-COVID world.
Frankly I expect that the same sort of thing could be said for a bunch of other conditions where we already have some clues about viral triggering of those diseases. The paragraph I quoted also mentions a few of those. This stuff will gradually emerge as a 'nasty surprise' to those unfamiliar with the detail of the role of viruses as triggers of other serious conditions, but for those already familiar with such things this sort of thing will already have been on the radar. Some detectable changes to public health along these sorts of lines are to be expected as a result of the pandemic and the number of infections involved. We'll just have to wait and see whether other properties of the COVID virus also cause other problems that are even less easy to anticipate or get a sense of scale about.
At the worst end of the scale of possibilities, if the implications end up being huge in the decades ahead, then these sorts of outcomes are certainly one of the main things that could cause 'the public' to reevaluate attitudes towards trying to prevent mass infections (zero covid etc) during the acute stage of the pandemic, and to look back with much regret and anger towards authorities. But I dont consider this to be anything remotely close to inevitable, because I dont have a means to guess the scale and age of onset for many cases. Nor am I able to judge what affect if any the vaccines and evolution of the virus will have made after a certain point. And in terms of the future generations to come, we might also expect that the overall very long term public health picture will gradually change as a result of 'everyone' first being exposed to COVID at a very young age, which will unlock a slightly different set of implications in some areas.
pubmed.ncbi.nlm.nih.gov
