When a mosquito bites, it vomits up a little numbing agent on your skin first — so you don’t feel the sting of its tiny proboscis stabbing you. Other organisms may use similar principle, and perhaps even viruses. And there is in fact evidence that SARS-CoV-2, the virus that causes COVID-19, suppresses a pain pathway (see Moutal et al; see also Cantuti-Castelvetri et al and Daly et al).
This was a study of infection of cells in petri dishes, not disease in humans, so the error bars here are like skyscrapers, but it’s a fascinating line of inquiry, and it does make broad biological sense that infectious pathogens might benefit from muting host pain. Exactly why a disease-causing virus might do this is a much more exotic equation than anaesthetic mosquito bites, but the authors speculate that “a ‘silencing’ of pain via subversion of VEGF-A/NRP-1 signaling may underlie increased disease transmission in asymptomatic individuals.”
COVID-19 is indeed notoriously and disastrously stealthy — at least one third of SARS-CoV-2 infections are asymptomatic — and maybe some of those virus-spreading victims are not merely symptom-free but actually “feeling no pain,” their symptoms actually suppressed by the infection, at least at first. I can hardly think of a better way for a virus to spread than to hit the snooze button on our alarm system, buying itself time to spread.
But there’s a lot left to learn here. Virologist Dr. Vincent Racaniello: “I am not buying it yet, because the experiments were done in irrelevant cells and culture, and the effects are not huge. I would like to know if neuropillin works in an infected animal, and we don’t know that yet” (This Week In Virology, episode 675 @ 1:49). Their whole discussion of this research is worthwhile.