21–30 of 105 posts
Maybe I have bad information, but cold plus high humidity caused it to persist on fomites longer (9+ days). Wouldn't heat plus low humidity be better than heat plus high humidity? What is/are the breakdown mechanism(s)?
Here's a likely related paper from 2007: https://jvi.asm.org/content/82/4/1899 In this study, a human immunodeficiency virus (HIV)-based pseudovirus system was employed to address these issues. Our results indicated that the SL-CoV S protein is unable to use ACE2 proteins of different species for cell entry and that SARS-CoV S protein also failed to bind the ACE2 molecule of the horseshoe bat, Rhinolophus pearsonii.…
Maybe that's why Singapore hasn't been badly impacted?
Singapore is included in how they determined this result, therefore you shouldn't use this result to explain why singapore is doing better.
Even assuming this result is meaningful, it still leaves an R way above 1.
Earlier quoted context omitted.
IF this is the case, we should be way more prepared including possibly having a vaccine available.
Still no vaccine for SARS 18 years later, what makes you think we'll have a vaccine for this?
To be pedantic, COVID-19 is the disease, SARS-CoV-2 is the virus. It's like HIV vs AIDS.
It is foolhardy to think spring and summer weather will save us.
Here's a likely related paper from 2007: https://jvi.asm.org/content/82/4/1899 In this study, a human immunodeficiency virus (HIV)-based pseudovirus system was employed to address these issues. Our results indicated that the SL-CoV S protein is unable to use ACE2 proteins of different species for cell entry and that SARS-CoV S protein also failed to bind the ACE2 molecule of the horseshoe bat, Rhinolophus pearsonii.…
Can someone with a better understanding of molecular biology and virology explain what this means? I don't want to jump to conclusions.