New York - it was widespread well before anyone noticed.
This is inconsistent with the spread of a novel contagious pathogen causing a novel disease.
One of the most important aspects of our argument is that which is summarised by this comment of mine (click on the picture for the actual link to the comment):
What we are saying bears reiteration:
There is no evidence of either excess deaths or contemporaneous1 reports of clusters of unusual illnesses BEFORE the world was told there was something novel circulating, therefore the default hypothesis must be that it was the response to being told there was something novel afoot which caused the stigmata of “pandemic”2.
And yet it now seems uncontroversial to argue that whatever “it” was, “it” was spreading extensively for months before the “emergency”, apparently totally unnoticed. This should have been impossible. SARS-CoV-2 was - we are told - both highly contagious and deadly, causing a wide range of extremely characteristic clusters of symptoms with a high mortality rate, at least for certain groups.
One of the best examples to illustrate this is that of New York. The weirdness of the official data has been written about previously, and the questions raised therein remain unanswered.
Here, I report on some further weirdness in respect of New York in the form of strong evidence of extensive pre-pandemic spread3 as reported in 2 peer-reviewed papers, as well as antibody data from samples collected in spring 2020.
The first paper - out of NYU with contributions from the UK’s MRC based out of Imperial (yes, them!) - reports on sequencing of “the virus” during the “first wave”. This was published in Genome Research in Dec 2020.
It’s worth stating now that I personally believe that the utility of genomics and sequencing has been massively overstated. However, given that it has been used to drive the entire novel virus and variants narrative, it seems only fair to use it against that same narrative.
This paper basically reports on the results of sequencing 864 spring 2020 cases in New York City.
Here’s the abstract - with my highlighting using bold.
Effective public response to a pandemic relies upon accurate measurement of the extent and dynamics of an outbreak. Viral genome sequencing has emerged as a powerful approach to link seemingly unrelated cases, and large-scale sequencing surveillance can inform on critical epidemiological parameters. Here, we report the analysis of 864 SARS-CoV-2 sequences from cases in the New York City metropolitan area during the COVID-19 outbreak in spring 2020. The majority of cases had no recent travel history or known exposure, and genetically linked cases were spread throughout the region. Comparison to global viral sequences showed that early transmission was most linked to cases from Europe. Our data are consistent with numerous seeds from multiple sources and a prolonged period of unrecognized community spreading. This work highlights the complementary role of genomic surveillance in addition to traditional epidemiological indicators.
The authors presnt an estimate of the projected growth rate growth rate of the number of infected people derived from their data:
They also present an estimate of the “outbreak trajectory estimated from genetic data showing effective population size” (ie the estimated number of infected people):
They don’t seem to be able to ask themselves:
If it was a spreading pathogen, the growth rate can’t have just started that high on 1 March - it must have been building for some time beforehand, so “the virus” must have been spreading for weeks beforehand.
So why no cases at all (by their estimation) until 1 March? Didn’t it cause any cases before then?
And why - if it must have been spreading throughout February, and likely before - do excess deaths not show any signal whatsoever before 16 March?
Here’s the graph of total deaths in NYC for 2019-2020 courtesy of
There’s nothing cooking at all UNTIL 15 DAYS TO SLOW THE SPREAD
Really? This incredibly contagious and lethal virus spread for weeks throughout all of Feb (and likely before) WITHOUT CAUSING ANY EXCESS DEATHS?
Hmmm…forgive me for stating the obvious, but it looks to me more likely that it was “15 days to slow the spread” itself - or things done in association with that directive - which caused the mayhem4.
The authors admit that:
Our data are consistent with numerous seeds from multiple sources and a prolonged period of unrecognized community spreading.
Although our estimate of 109 introductions is thus likely to underestimate the total number of introductions, the genomic data are sufficiently informative to outline an unrecognized early spread in February that enabled rapid development of the outbreak in March.
The picture painted is one of quiet, stealthy spread, a sort of preparatory period where “the virus” is just waiting for its instruction to explode.
IS THIS HOW SPREADING RESPIRATORY VIRUSES ACT?
The second paper is a study out of New York published in the Clinical Infectious Diseases in Dec 2020 reporting on >46k patients tested by Northwell Health, NYC’s largest healthcare providor.
Most notably:
8 March through 10 April, a total of 26,735 of 46,793 persons (57.1%) tested positive for SARS-CoV-2.
Total hospitalization rate was thus 8174 persons (30.6% of positive persons).
They summarise this by stating:
"Our data reveal that SARS-CoV-2 incidence emerged rapidly and almost simultaneously across a broad demographic population in the region. These findings support the premise that SARS-CoV-2 infection was widely distributed prior to virus testing availability."
They even provide a time-lapse chronologic display of case accumulation per zip code:
This is not the picture of a pathogen being introduced into a few locations then growing in clusters which then branch out and form other clusters over time.
No, this is - as the authors admit - a picture of an explosion of testing finding cases of something which had already become widespread.
What about serology - testing for antibodies?
Pandemic-believers love to push the rise in antibodies as proof that something new and dangerous was circulating.
But data from NYC actually supports the idea that “it” was widespread well before anyone knew it was there.
This paper is a study of antibody levels in NYC:
From the abstract:
In this paper, we describe SARS-CoV-2 IgG antibody responses in 28,523 patients from the New York City metropolitan area and report a SARS-CoV-2 IgG positivity rate of 44%, indicating the widespread nature of the pandemic in the city and state of New York.
And:
While we do not have detailed symptom history for all patients, many of the members of our patient population were asymptomatic (at least 50%) and never reported SARS-CoV-2 symptoms, which implies that the spread of SARS-CoV-2 in New York City may be more extensive than previously suspected. Further, our data show that the highest rates of prior infection are seen in patients aged 11–20 years, however it is formally possible that part of the explanation for this is a more robust immune response in this generally young, healthy age group.
NYC officials actually did a lot of antibody testing, and notwithstanding that it’s not entirely clear who was tested and in what circumstances, what it found was still surprising - very high levels of seropositivity - especially as is it generally assumed that it takes several weeks from exposure to testing positive5. Here’s a graph generated by
from official data sources
Part of NY State’s antibody testing drive included 3,000 people selected at random at grocery and big-box stores, including 1,300 in the City itself. Over one fifth of the NYC tests came back positive according to this article dated 23 April 2020 (click on image for link):
To quote from the transcript of the April 23rd press conference, Governor Cuomo says:
We did 3,000 surveys in about 19 counties, 40 localities across the state. The surveys were collected at grocery stores, box stores, et cetera.
These are people who were out and about shopping.
What we found, so far, is the statewide number is 13.9% tested positive for having the antibodies. What does that mean? It means these are people who were infected and who developed the antibodies to fight the infection. They were infected three weeks ago, four weeks ago, five weeks ago, six weeks ago, but they had the virus, they developed the antibodies, and they are now, quote, unquote, recovered, 13.9%, just about 14%.
Regionally, Long Island at 16.7, New York City at 21.2, Westchester/Rockland 11.7, and rest of state 3.6.
If the infection rate is 13.9%, then it changes the theories of what the death rate is if you get infected. 13% of the population is about 2.7 million people who have been infected.
It gets even more complicated because, in California, they’re now finding deaths that go back to last December or January that they believe were COVID-related, and people didn’t even know about COVID at that time.
How can so many millions of people have come into contact with this supposedly highly lethal and contagious pathogen without noticing? And by what mechanism did something so innocuous become so lethal, as described by Dr Kory here:
Accommodating the inconvenient points made in this article into the pandemic narrative involves advancing all sort of complex, entirely untested and unevidenced assumptions about seasonal triggers, viral mutations, or other fantastical mechanisms.
However, the simplest explanation should always be regarded as the most likely6, and hence the default, hypothesis; the burden of proof rests on the believers of more complex explanations7.
As the late, great, man said:
Why did I and my family go down with something really weird in late 2019 then?
This is a postscript I have added following some comments. I really should have included it before publishing:
This article is receiving a number of comments along the lines of “I had a weird / the worst illness ever in Dec 2019” (or similar), so I thought I would add some commentary to that claim, since it has been voiced so many times to me before:
The fact remains that even if these observations WERE representative of a true biological phenomenon:
No reports of clusters of unusual illness were writen about at the time8 - so whatever “it” was it had minimal impact anywhere.
Whatever “it” was, it wasn’t capable of causing a congruent signal in terms of excess deaths.
So if - and it’s a big if in my view - there was something novel around, it was harmless until those behind the pandemic narrative efforts decided to tell us all about it and test for it in a frenzy. So, under this paradigm it would be wrong to regard this purportedly novel thing as the cause of “the pandemic”, since the harms which people regard as the constituent elements of “the pandemic” resulted from the response to the idea of something novel circulating, not the (purportedly) novel thing itself.
Put differently, Jon Snow’s “pump handle”9 is a narrative, not “a virus”.
However, I would question what is really meant by “something novel”. Illnesses regarded as viral in nature have always manifested in weird and wonderful ways. The question “did you have that weird bug going around recently” did not hitherto raise the question of whether humanity was under bioattack.
It’s worth thinking of these things as we do with climate and weather. The latter is changing all the time. Ask people to shout out if they have recently experienced the most extreme weather they have ever known and at any time many people will say “yeah, last week it was X, Y or Z”.
But does that (alone) mean the climate is changing? No. It means that in an incredibly variable system it is virtually inevitable that observation and confirmation bias will give the impression that something is changing, when that change is actually illusory.
That is to say written at the time and not moulded by experience and post-hoc rationalisation.
Meaning the features which people associate with the term “pandemic” - we don’t believe anything which can reasonably be termed a pandemic happened and every aspect of it is fake.
Meaning before “15 days to slow the spread”. Absolutely no admsission to the pandemic narrative is intended here.
I’m using a word there which is neutral in terms of whether the deaths claimed happened - either at all or on the days claimed.
Bear in mind also that many people will fight off a respiratory virus in the mucosal immune layer in the lungs without generating antibodies.
AKA Occam’s Razor - which is also an exemplar of something which is no less true for being cliche.
Everyone knows that in court proceedings, massive weight is applied by judges and juries to contemporaneous evidence - ie evidence written or spoken at the time of an event, before post-hoc rationalisation can mould people’s view of events. In relation to all this unusual illness apparently circulating in late 2019, I have yet to find anything written at the time about it. It’s not that it didn’t happen, it’s just that if it did it wasn’t notable enough to merit anyone mentioning it, so it would seem to have little relevance to a global lethal pandemic.
See: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7150208/
In my very first post about Covid, in May of 2020, I wrote the following: “There is a pandemic, but it is a pandemic of testing and not of any disease….”
1. Respiratory viruses do not necessarily elicit antibody response. 2. Antibodies are famously unspecific.