What studies are these? All the info I have seen talks about transmission requiring close contact with an infected person or directly breathing in droplets from their cough or sneeze.
> you can catch it more than once since for some reason the body doesn't fully make immunity
Where are you getting this from?
Abstract: "32 HCoV-19 (SARS-2) has caused >88,000 reported illnesses with a current case-fatality ratio of ~2%. Here, we investigate the stability of viable HCoV-19 on surfaces and in aerosols in comparison with SARS-CoV-1. Overall, stability is very similar between HCoV-19 and SARS-CoV-1. We found that viable virus could be detected in aerosols up to 3 hours post aerosolization, up to 4 hours on copper, up to 24 hours on cardboard and up to 2-3 days on plastic and stainless steel. HCoV-19 and SARS-CoV-1 exhibited similar half-lives in aerosols, with median estimates around 2.7 hours. Both viruses show relatively long viability on stainless steel and polypropylene compared to copper or cardboard: the median half-life estimate for HCoV-19 is around 13 hours on steel and around 16 hours on polypropylene. Our results indicate that aerosol and fomite transmission of HCoV-19 is plausible, as the virus can remain viable in aerosols for multiple hours and on surfaces up to days."
It's not peer reviewed yet so reader beware
A study from scientists at Princeton University, University of California and the National Institutes of Health indicated that the COVID-19 virus could remain viable in the air "up to 3 hours post aerosolization," while remaining alive on plastic and other surfaces for up to three days.
> A study awaiting peer review from scientists at Princeton University...
Also these things are probably a theoretically absolute best case scenario type thing. Not a practically viable mode of transmission.
I would not read a lot into the "awaiting peer review" bit. It normally takes at least a few months for an article to be reviewed, revised (if necessary) and re-reviewed. Things are undoubtedly fast-tracked for COVID-related stuff, but you can only do so much to speed it along.
Per their Table 1, the median halflife of an aerosol is about 3 hours, with a 95% credible interval of 1.81 of 5.45 hours, so it's not a a best (worst?) case number at all.
The plastic data in Figure 2 shows that it does decrease a lot by 48 hours (~1000x), but it's still above the limit of detection; they estimate the half-life to be 14.8 hrs. The 3 day claim is true, but is more of a best/worst case scenario
Don't forget that the traditional pre-publication peer review is more of a sanity check than a sacrament. All that happens is that ~3 people spend ~5-10 hours each reading the paper, thinking about it, and writing up their comments. This is often enough to flag major issues, especially in the interpretation of the data, but it's certainly possible for subtle errors to slip through.
Where are you getting that from?
This has been debunked on the This Week in Virology podcast[1]:
Vincent Racaniello: There are a series of articles here, where there have been some claims about different circulating lineages and what that means. Are you on this, Cathy?
Cathy Spindler: Right. So, there was an article that I first saw in the LA Times "Chinese Scientists Say Second Coronavirus Strain Is More Dangerous"[2]. But in that there's a link to virological.org, which we talked about another article posted there a couple of weeks ago[3], and they really debunk this and think even that this Chinese article about a second Coronavirus should be retracted. Two of the key claims that are reached by misunderstanding and overinterpreation of data and an additional analysis suffers from methodological limitations. So this long thing on virological.org goes in to the reasons why there's no real evidence for two different strains, a more severe strain and a less severe strain.
Rich Condit: It also provides a nice summary of this sort of variation in sequence that's being observed in the virus over time, which is good.
Vincent: Yeah, it's a good aritcle. We'll put a link. It's worth reading, but as everyone should know, when these [indistinct] viruses, every replication cycle they sustain mutations in their genomes and the lethal ones are gone, the viruses don't reproduce, but some of them stay and if they're neutral they remain. So they can be characteristic. So the virus introduced in to the Washington area is a single introduction and then it's spread and you can tell that because it has a unique set of mutations compared to say, the Chinese isolate, but it doesn't mean anything biologically. It's just markers.
Rich: And the markers are really interesting because they give you insight in to, I mean the insight that I got from observing what came out of the Washington cases is that from looking at the sequence of the virus they concluded that in fact it had been circulating for some time, and they could even get a very very rough estimate of how many cases might be out there based on the variation in sequence and the time at which the disease first showed up in a person.
Vincent: I think there are some emails later about this. People are concerned that, and people suggest in these papers, at least the one here, that we're being critical of that it could be evolved to be more virulent or more transmissible. There's no evidence for that whatsoever.
Rich: This is the kind of thing that... it just won't go away!
Vincent: Oh, it doesn't go away... new outbreak and it comes back.
Rich: Yeah, and there's no evidence. People have looked at this. We've gone over this for several.. Zika, Ebola, where's there's been variation and people point to a particular variation and they say, "This is going to make it more virulent" or something, and then the experiments ultimately get done and no. It hasn't made a difference.
Vincent: And also the issue of increased transmissibility, I think this virus is already very transmissible as it is, and I think the mutations that made it effectively transmissible among humans, which happened very early on, I don't know, either in animals or in humans early on, before we knew about it, they're done, and it's going to be hard to know what they were. MERS coronavirus has never acquired those high transmissibility changes and it keeps fizzling out and then you have another reintroduction from camels but this particular SARS-Cov-2 sustained them probably early on and it's a very good transmitter. It doesn't need to get better, at least from my anthropocentric view. We never really know what viruses are selected by, but I don't think there's eny evidence, and it's very hard to get that evidence. That paper tells you what you need to prove that mutations are doing something phenotypically. It's very hard to get that.
Rich: It has occurred to me that people who don't think about this stuff every day might be a little confused by this discussion relative to the discussion that goes on all the time about variation in influenza virus strains, and new strains coming up and having to change the vaccine and stuff. But that's different. That's variation in the influenza virus that makes it evade the existing immunity, and those sorts of variations arise so you get circulation of viruses that you don't have as good an immune response to, but that's different than a virus making mutations that make it more virulent. It's a different story.
[1] - at about 13 minutes in to episode 590 - http://www.microbe.tv/twiv/twiv-590/
[2] - https://www.latimes.com/science/story/2020-03-05/chinese-sci...
[3] - http://virological.org/t/response-to-on-the-origin-and-conti...