The entire SARS story puzzles the heck out of me. Why did so many nurses die, even in locations that should have had strong infection control? Why did the disease seem so contagious in some places, and not at all contagious in others? Did the virus attenuate? Was the epidemiologic behavior due to an unidentified cofactor infection that was common in some places and not in others? (eg. a second virus was needed to develop full fledged SARS).
I can't believe that the infection control measures were so effective. The disease was loose in China for months. Why did it not spread in India at all?A year later I wondered if there were multiple strains circulating, all mutually immunogenic, some more toxic than others. (There may be multiple strains of SARS-CoV-2 as well.) I wondered if that suggested a pandemic management strategy - a kind of "backburning"...
Create a contagious synthetic pathogen that's relatively benign, but induces immunity to the major pathogen -- and spread it actively. I say not entirely novel, because this is how Polio was suppressed. The oral vaccine was an active contagious pathogen that was excreted in stool. It immunized a vast number of persons -- but some became sick, disabled, or dead. When Polio was less of a threat we switched to a non-pathogenic inoculation. The difference is the successful Polio strategy was probably unintentional (I suspect some people understood even in the 1950s), but in the future we'd be deliberately exposing an entire population to an immunogenic pathogen that would almost certainly harm many people.Now we are enjoying COVID-19, the bigger, uglier, brother. Again there's tremendous variability from place to place and time to time. Again India seems unbothered. Again young healthcare workers are vulnerable. Again I wonder if some of the sickest patients have multiple viral inflections or more aggressive strains. Perhaps as our seasonal flu finally fades so will the worst of COVID-19.
I hope this time we'll understand it better.