The discovery of virus genome presence so early in Spain, if confirmed, would imply the disease may have appeared much earlier than the scientific community thought.
The University of Barcelona team, who had been testing waste water since mid-April this year to identify potential new outbreaks, decided to also run tests on older samples.
They first found the virus was present in Barcelona on Jan. 15, 2020, 41 days before the first case was officially reported there.
Then they ran tests on samples taken between January 2018 and December 2019 and found the presence of the virus genome in one of them, collected on March 12, 2019.
“The levels of SARS-CoV-2 were low but were positive,” research leader Albert Bosch was quoted as saying by the university.
The research has been submitted for a peer review.
Dr Joan Ramon Villalbi of the Spanish Society for Public Health and Sanitary Administration told Reuters it was still early to draw definitive conclusions.
“When it’s just one result, you always want more data, more studies, more samples to confirm it and rule out a laboratory error or a methodological problem,” he said.
There was the potential for a false positive due to the virus’ similarities with other respiratory infections.
Bosch, who is president of the Spanish Society of Virologists, said that an early detection even in January could have improved the response to the pandemic. Instead, patients were probably misdiagnosed with common flu, contributing to community transmission before measures were taken.
Prof. Gertjan Medema of the KWR Water Research Institute in the Netherlands, whose team began using a coronavirus test on waste water in February, suggested the Barcelona group needs to repeat the tests to confirm it is really the SARS-CoV-2 virus.
Spain has recorded more than 28,000 confirmed deaths and nearly 250,000 cases of the virus so far.
That “levels of SARS-CoV-2 were low but were positive,” in a single sample is suggestive of contamination, and rtPCR testing is quite prone to false positives because any amount of genetic material is replicated whether it is active virus or just residual fragments that can be introduced by many sources of laboratory contamination. Given how rapidly the virus spread post-discovery, the idea that it was circulating around in Europe in early 2019 is just inconsistent with reality.
Also note, this article was from June 2020 and we discussed it a bit back with the same conclusion, that a false positive was the most likely explanation.
And given the lack of news since then, I suspect the result was not confirmed.
Or it could be a small degree of community transmission before the transmission speeds up in late 2019. This might also be the actual cause of the atypical pneumonitis (which turned out to be SARS CoV 2) happening in late 2019. A lot of people fell sick with something weird in late 2019. Remember that.
The 2019-2020 influenza season had already slightly exceeded the epidemic threshold before SARS-CoV-2 was recognized in China in December 2019, and given how rapidly contagion spread once it entered populations in Spain, Italy, and later the US and Northern and Central Europe, there is no plausible rationale for “a small degree of community transmission before the transmission speeds up”. The anecdota that people caught a “strange” respiratory illness in late 2019 (which did not produce excess mortality or the specific features of the COVID-19 syndrome) is only evidence of some other mild respiratory illness passing around which is quite normal in the fall and winter in the Northern Hemisphere, coming as it does with people moving to indoor activities. All cats may seem black at midnight because one does not turn on the light, but it doesn’t mean they are actually the same cat, just that one lacks the evidence to distinguish between them.
We periodically hear about new variants, some of which are more easily transmitted, and some of which can cause more serious illness than Covid Classic.
Is it plausible that the SARS-CoV-2 variant detected in March 2019 was a far less virulent and less transmissible strain* than the ones extant in December 2019 and beyond?
Couldn’t that account for the Barcelona discovery and also explain why it avoided detection at the time and didn’t cause many (any?) symptomatic illnesses?
Why should the serious and quite obvious early cases in Wuhan necessarily be caused by the very earliest versions of the virus? Wouldn’t it make sense that weaker and less obvious variants would proliferate undetected first?
*I don’t think this is quite the correct usage of ‘strain’. Forgive me for essentially using ‘variant’ and ‘strain’ as synonyms.
it has to be minimally infectious, otherwise it would have flared and there would be other clinical records in Spain or before end 2019 in Europe
BUT not so minimally infectious that it died out
AND it would have had to make its way to Wuhan [which is probably not hard in 1-2-3 steps] without significant infection beyond a carrier.
Stranger things have happened, but its relying on a Lemony Snicket-sized chain of unfortunate events, rather than a much more parsimonious false positive as is known to be a frequent occurrence.
That’s really it. Just because something could possibly have happened, doesn’t mean that it’s at all likely that it did actually happen, and the explanation that is simpler and more likely to have actually happened is the right one.
(aside- that seems to be what conspiracy theorists don’t get; their whole existence seems to be based on the plausibility of the “could have happened” part, not the “likely to have actually happened” part)
Again, this news is a year old. If it had been confirmed in Barcelona, or found in other cities, don’t you think we’d be hearing more about that and less about the lab leak theory?
These types of outbreaks are due to a series of unlikely events. Just like a plane crash, it’s never one thing that went wrong, but a series of things going wrong that leads to disaster.
I’m not an expert on zoonosis by any means, so some of these steps may be wrong, and there are probably many more that I’m missing.
First a virus has to get from some animal host to a human.
Then the virus has to be able to actually infect the human, rather than just sit there and do nothing.
Once infected, the human needs to start making new viruses.
Those new viruses have to get from that human to other humans.
The first step is going to happen anytime humans and animals are in close contact, but the second step is going to be much, much rarer. If I handle a sick cat I could get FCV on me, and maybe transmit it to another cat, but it isn’t going to make me sick.
The concern that has been raised for decades is that habitat destruction (and other practices) cause humans to come into more frequent contact with animals they are not usually in contact with. This results in many more exposures of humans to animal viruses. So even if the chances of the second step (humans getting infected) is one in millions, it is still beneficial to limit the number of times we make that dice roll.
Exactly this. There are lots of cases of zoonosis including coronaviruses. There are seven well-known human coronaviruses that came from animals. There have probably been many more, but they usually die out without strong human-to-human transmission. So even if they cause serious disease, they’re not likely to be identified as a coronavirus because a serious outbreak never occurs.
Corona viruses have been around for a long time. Corona viruses are a common cause of the common cold.
It was possible that the test procedure used in Barcelona detected some other corona virus due to lab technique. It was possible that it detected some not-very-important Barcelona variant corona virus due to lab technique. I haven’t seen any discussion of what they thought went wrong.
Lab’s aren’t the only place where this confusion can happen: it is thought that the partial immunity some children seem to have to COV-19 may be due to just having had a number of recent colds.