There were articles in the news and some videos about it.
One of the most intriguing is a
study from Lombardy, northern Italy, by measles researchers who had spotted that
Covid could cause a measles-like syndrome. They tested hundreds of stored samples taken during 2018-20 for both antibodies and viral RNA. The researchers found
11 samples positive for viral RNA from August 2019 to February 2020, including one from September, five from October, one from November and two from December. Four of these were also positive for antibodies, including the earliest sample from
September 12th 2019 (both IgG and IgM). Note that these samples were from ill people so estimates cannot be made from them of community prevalence.
The positive samples were
genetically sequenced to reveal mutation information, reducing the chances of them being false positives. None of the 100 samples from August 2018 to July 2019 showed strong evidence of infection, further validating the methods used and suggesting to the researchers that the
virus emerged around July 2019.
A separate
study in northern Italy tested waste water from 2019 for viral RNA and found samples in Milan and Turin positive
from December 18th, though negative prior to that, which is in contrast to the results of the first study. The samples were again genetically sequenced, adding to their reliability.
A Brazilian
sewage study found SARS-CoV-2 RNA in samples from late November and December 2019, but not in two earlier samples from October and early November. The samples were taken from one site in the southern Brazilian city of Florianópolis and were genetically sequenced for confirmation.
Testing of sewage in Florianópolis, Brazil for SARS-CoV-2 RNA
An antibody study of
archived Red Cross blood conducted by the U.S. CDC found
39 antibody-positive serum samples collected December 13th-16th 2019 in California, Washington and Oregon. Overall, 2% of blood samples collected from these states and for these dates tested positive for antibodies. The full results can be viewed in the table below.
A 2% antibody prevalence in mid-December suggests significant community spread across America during November 2019. However, there were no earlier samples for comparison and no testing or sequencing of viral RNA for confirmation.
A study of stored blood samples in France looked at routinely collected samples in a population cohort and found around 2% prevalence of antibodies in November, rising prevalence in December and around 5% prevalence in January. These figures do seem on the high side when compared to the above studies, and the lack of testing and sequencing of viral RNA and the absence of samples from earlier periods suggest this may be
less reliable evidence.
Another
Italian study tested blood samples from lung cancer screening for SARS-CoV-2 antibodies and
found 14% of those from September 2019 were positive for SARS-CoV-2 antibodies. But again, this lacked testing and sequencing of viral RNA and negative controls from earlier periods. A
Spanish study detected SARS-CoV-2 viral RNA in a sample of waste water from
Barcelona on March 12th 2019; however, all the other historic samples up to January 2020 were negative and it is
suspected that this is a false positive due to contamination or cross-reaction (it wasn’t sequenced).
What about early spread in China? It’s hard to get reliable data for this country. However, a
leaked Chinese Government report found hospital patients (recognised retrospectively) admitted in Wuhan as early as
November 17th, suggesting the virus was spreading there during November and probably October.
A molecular clock
study estimating the date at which the common ancestor of early viral samples was around
put the emergence of SARS-CoV-2 as early as July, in China. A separate
molecular clock study estimated the emergence between
mid-October and mid-November in Hubei province, China.
So the evidence is clear that the virus was circulating both in China and internationally by November 2019 at the latest. We can also say with strong confidence that it was not circulating prior to July 2019, and it may not have been around before October 2019, depending on how reliable the European data from the early autumn are.
Some argue that all this evidence of early spread – despite coming from multiple sources and using robust validation methods such as sequencing – must be faulty in some way, as the
lack of excess deaths prior to March 2020 makes it impossible for the virus to have been spreading widely over the autumn and winter.
(ER: And excess deaths in March-April 2020, a sudden spike which quickly declined, can be accounted for by other causes, including shutting up carehomes and injecting residents with drugs like midazolam.)
My view is that
this argument is insufficient to overcome the clear evidence of early spread. I don’t deny that there is something of a ‘
mystery‘ that must be resolved, in that the wave of excess deaths did not begin until March 2020. Some sceptics resolve this ‘mystery’ by arguing that the virus must therefore be no more deadly than other similar viruses, and thus that any excess deaths since March 2020 must all have been caused by interventions such as lockdowns, faulty treatment protocols and vaccines. However, I agree with
Dr. Pierre Kory that we have undeniable evidence of
waves of severe pneumonia with a common clinical profile that began in March 2020 and that are best explained by the novel respiratory virus to which most of the deceased tested positive.
So how to explain the lack of excess deaths during the autumn and winter of 2019-20?
The most important point to be made is that
while SARS-CoV-2 was clearly circulating during that winter, it does not appear to have been the dominant virus either in the community or in care homes and hospitals. Thus while, say, 2% of the population may have contracted the virus during the winter, because it was competing with other, milder viruses and wasn’t running rampant among the high risk population, its impact was limited and it did not cause noticeable excess deaths.
The early-spread-sceptic’s objection to this point is that the virus is clearly highly infectious so if it was present and circulating, it’s simply not possible for it to have remained at a low level and not run rampant in, say, care homes, causing havoc.
Several mentions of it prior to Dec/Jan when it first came to light.