Views on the things called viruses (including SARS-CoV-2)

I am guessing that my previous conception of viruses is similar to most people’s— including that of my own daughter: Viruses are very, very small things that are “out there,” can be “caught,” and can make people sick.

Until more recently, I hadn’t given much thought to whether virology is a legitimate scientific discipline, or whether virologists have been misled about their object of study. Working on an article last summer about how SARS-CoV-2 was named gave me a glimpse into how virologists think and talk amongst themselves.

The SARS-CoV-2 Name Game (Long Read)

Much of the article content was drawn from batch of emails I obtained from the University of North Carolina which chronicled the speedy deliberations of an international committee that did the naming.

Poring over those exchanges, other documents, and the timeline left me with scientifically and medically important questions like What are the things called viruses? Are they causal of illness? “Where” are viruses? Do they transmit? How do we know/why do we say so?¹

The emails made clear that the committee of virologists charged with giving 2019-nCoV a new name did not consider the “coronavirus” novel and wasn’t responsible for determining or verifying a cause-effect relationship between virus and disease.

Winston

As I pieced things together, I reached out to one of the virologists involved in the naming who is employed by a public research university. To keep the focus on what was said versus who said it, I’ll refer to him by the pseudonym “Winston.”

My correspondence with Winston was professional, courteous, and centered largely on questions about the sequence of events and differences between the pre-preprint and published versions of the naming committees’s papers.²

In one exchange, I asked Winston more specifically about the following:

• the difference between viral “spread” and viral “circulation”

• viral spread from animal to human or between humans

• evidence for human-to-human transmission of SARS-CoV-2

• ideas in this article https://journals.plos.org/plospathogens/article?id=10.1371/journal.ppat.1009318³

Reacting to the above queries and comments, Winston said: [emphasis mine]

Spread refers to transmission expansion of some sort, commonly host- or geography-wise. In contrast, circulation is transmission constrained by host or geography or both.

Nowadays, researchers use next generation genome sequencing (NGS) for virus detection and discovery in any sample and regardless of syndromes or diseases.

When SARS-CoV-2 was detected for the first time in humans in the ever-increasing number of countries in early 2020, it became clear that there is human-to-human transmission. (There is no other sensible explanation for this pattern). The detection of this virus in sick & dead people, whose number grew fast, implicated this virus into the disease. That evidence was substantiated and expanded over numerous studies that used different methods. Due to a sheer number of infected in many hundred millions and considerable diversity of human population, symptoms of SARS-CoV-2 infection may include other than respiratory illness in some of the infected.

The advent of NGS changed virology forever (it was what I called “huge advancements in appreciation of the virosphere in recent years that are yet to be accepted universally”).⁴ Most viruses we know now have no known connection to diseases and they were named accordingly.

In our papers, we provided a line of reasoning to treat known (human) pathogens in the same way. This logic approaches viruses as biological entities first and pathogens second. All human beings and other cellular entities live in the virosphere which may be the largest part of the biosphere by diversity.

I fully understand when people have difficulties to accept this grand view which has no connection to their everyday experience. But if accepted, it provides a vantage point to look at pandemics and associated events with less biased approach that may have informed current communication.⁵

Observations and Questions

It may surprise readers to learn that my emails with Winston left me with a better impression of academic virologists than I had prior to the correspondence. I found him sincere, knowledgeable, and well-versed in the assumptions of the field. It would be difficult for any scholar of any discipline - especially one with an impressive publication record - to do an “about face” after having been entrenched in certain conclusions for so long. Nevertheless, I take issue with a number of things he asserted and offer my reactions as a way of showing what I think about viruses and SARS-CoV-2.

Nature/Detection of Viruses

Winston’s statement about viruses being biological entities comprising a vast virosphere is at-odds with the position Viruses don’t exist/There is no such thing as viruses. Either viruses are biological entities with unique properties and structure or they are not. I don’t see an “in between” view on that score. I agree with distinctions Katherine Watt and Jonathan Engler have made, respectively, in that if viruses are not what we have been “taught” they are, then it’s fair to say there is no evidence for their “existence.”

Winston observing that Next Generation Sequencing (NGS) has “changed virology forever” via “virus detection and discovery in any sample and regardless of syndromes or diseases” is concerning when, despite most viruses having “no known connection to disease,” we are asked to accept on faith that causality has been established for the precious few that purportedly do.

I can more readily accept that some biological entity within living things is being detected and sorted into patterns - one about which we have little to no idea regarding its role or function - than I can the notion of a sky full of stars field full of viruses, only a few of which cause respiratory illness.

Spread/Transmission

For me, the core lie involved in the staging of a pandemic in early 2020 is less about the existence of a virus - or (more accurately) the “discovery” of an existing thing classified as a “virus” - than it is about human-to-human transmission of a pathogen and propaganda about slowing the spread. There was never evidence of transmission, despite the WHO claiming otherwise.

The distinction Winston makes between spread and circulation seems dependent on time and mechanism. Although left undefined, I infer transmission has to do with a virus being “passed” with integrity from one living thing to another. On the respiratory illness/virus front, much is inferred about the passage between living things and asserted despite repeated, unsuccessful attempts to make people “catch” colds and flu from one another.

A March 2021 review “Transmissibility and transmission of respiratory viruses” doesn’t make the case either. A PhD isn’t needed to spot the kind of cautious language that all academics are (rightly) taught to use when findings don’t permit certitude:

• …can be transmitted via..

• Traditionally, it is believed that..

• …can be recovered from…

• …may spread via…

• …suggesting respiratory viruses might also be…

In other words we don’t know and nothing has been proven.

SARS-CoV-2

The most fascinating part of Winston’s response regards SARS-CoV-2. He apparently does not see how the deployment of mass testing can be used to create the illusion of spread — or recognize that this was done with relative success in 2003 with SARS-1 and 2009 with H1N1. Instead, he interprets the appearance of positive tests as evidence of human to human transmission and can see “no other sensible explanation for this pattern,” possibly due to what he believes about what and where viruses are - and what they do. The idea of viruses being an endogenous phenomenon (as Ben Marten put it) doesn’t cross his mind…or if it does, he didn’t say so.

Like far too many scientists, doctors, officials, and commoners, Winston accepts that

• a new disease/new form of pneumonia came on the scene in late 2019,

• a “found” sequence from some specimen was the causal agent,

• tests developed for that casual agent were mostly reliable, valid, and medically meaningful.

Borrowing from what Jonathan Engler wrote in a recent article, can I allow for there being things inside the human body which can be detected by tests more often when people are ill than when they are well? Sure. But what those things are and whether they are causes or effects is another matter altogether.

Consider a study from Chinese scientists published in an NEJM study on 29 January 2020, Early Transmission Dynamics in Wuhan, China, of Novel Coronavirus-Infected Pneumonia. Essentially, incidence of positive tests for a nonspecific thing run at high cycle thresholds among loosely-associated people with unremarkable symptoms is characterized as transmission.

There is no presentation of “cases” in the context of all pneumonia cases, either at the time or as compared to previous years, and no sense of whether this “novel coronavirus” was impacting respiratory disease or all-cause mortality.

There is the fact that the study was published shortly after the WHO claimed evidence of transmission and the day before the WHO declared a PHEIC (which, among other things, “requires” evidence of spread/transmission).

Was there spread?

So, as Winston suggested, it seems pretty clear that we have genomic sequencing and “seek & find” testing to thank blame for telling us about a “silently-spreading threat” on the verge of becoming a “pandemic”.

• Have he and other virologists grappled with data from New York City showing that the thing and a committee named SARS-CoV-2 was already out there well before the naming process began?

• Have they cross-checked two studies that strongly suggest the “first” person-to-person transmission in the U.S. (between a wife and husband) was no such thing?

• Have they watched the February 2020 interview in which Nobel prize winner Michael Levitt observed that “cases” [positive tests] inside Hubei peaked at the same time as cases outside of Hubei and said “it’s almost like…it’s almost like there’s been no spreading”?

• Are they aware that Christian Drosten - who also participated in naming SARS-CoV-2, in addition to helping create a PCR protocol for “it” - said, on 13 March 2020, “you have to be clear that if we didn't test then in many countries we wouldn't even know that this virus even exists”?

• Do they have good explanations for why the virus dropped like a bomb in spring 2020 on Bergamo and New York City but not on Venice or Los Angeles?⁶

I don’t know.

I do know that, whatever viruses are, the formula for staging sudden spread is very straightforward— and is one of the many reasons the truth about 2020 needs to be exposed.

1. See also On dividing a resistance, the existence of viruses, 'the COVID response', & spreading-non-deadly threats

2. Key differences summarized well in SARS-CoV-2: What’s in a Name? Everything and mentioned in Virus Origins and Gain (Claim) of Function Research

3. Regarding the article, I wrote, One challenge I see is the presumption of a causal link between SARS-CoV-2 and COVID-19. The three papers cited (ref 21-23) do not establish causality whatsoever. At best, they are examples of co-incidence. Two of the three papers are even titled cautiously (“associated with”).

4. Quoting self from email earlier in the chain.

5. I quoted a portion of this in COVID-19 Did Not Come from a Lab

6. John Ioannidis is not a virologist, but his explanation is insufficient.