Virologists: Making Conclusions Not Justified by the Data

How do virologists back up the various claims they make regarding “viruses” and their variants? Are the reports of increased virulence and transmissibility confirmed by the data? What valid scientific evidence supports the statements they make publicly? Is there any or are virologists jumping to conclusions that clearly are not justified?

With all of this talk of “variants of concern,” the Delta variant, B.1.1.7, Lambda, etc., it is interesting to go back to the early days of this “pandemic” to see what virologists were saying about these variants back then and whether or not they were justified in making any of their claims. One such virologist that is very candid and forthcoming with his thoughts is Vincent Racaniello. He is a well-respected virologist with quite the resume. According to his Wikipedia page:

“Vincent R. Racaniello (born January 2, 1953 in Paterson, New Jersey) is a Higgins Professor in the Department of Microbiology and Immunology at Columbia University‘s College of Physicians and Surgeons.^[1] He is a co-author of a textbook on virology, Principles of Virology.^[2][3]

Racaniello has received the Irma T. Hirschl, Searle Scholars, Eli Lilly, Julius Younger and NIH Merit awards. He has also been a Harvey Society Lecturer at Rockefeller University, the Hilleman Lecturer at the University of Chicago, and University Lecturer at Columbia University. He is also the keynote speaker for the American Society for Virology, at its 2018 meeting.^[4] Racaniello has served on the editorial boards of scientific journals, including the Journal of Virology,^[5] and is a community editor for the open access journal PLOS Pathogens.^[6] He also served as the 2015 president of the American Society for Virology and keynote speaker for their 2017 annual meeting.^[7][8]

He is the host of the podcast, This Week in Virology.”

https://en.m.wikipedia.org/wiki/Vincent_Racaniello

This is a man who definitely knows his virology. While I disagree with Racaniello on many areas (such as the actual existence of “viruses”), there is a lot of common ground to be found in his writings. Much of what he says seems to line up very well with the warnings of virologist Dr. Charles Calisher and his 13 co-signers back in 2001. For a recap of Dr. Calishers warnings on the over-reliance of molecular technology in virology, see this post:

The Old Guard of Virology Warn About the Ways of the New Guard and Their Molecular Toys

Even though we may disagree, I can appreciate Racaniello’s critical eye towards his own profession and his willingness to be open about it. When I originally did a post about him back in March 2021, I only highlighted some of his thoughts on D614G. After reading a few of Racaniello’s other relevant posts, I figured it was best to share four of his writings in their entirety.

The first of these was written in July 2020 and deals with variant D614G and the lack of evidence for any increase in transmission. Like Calisher, Racaniello seems to share the same opinion that genomic data does not tell us much of anything and that virologists are making conclusions for which the data does not back up. He even takes a shot at the process of cell culture and its inability to say anything about human-to-human transmission:

No evidence for increased human transmission of SARS-CoV-2

“Don’t believe the headlines that SARS-CoV-2 is becoming more transmissible! Virologists are making conclusions that are not justified by the data.

SARS-CoV-2 virus isolates from many parts of the world have a single amino acid change in the spike protein, D614G. This observation in itself doesn’t mean very much. It could be that the change arose early in the outbreak and as this virus spread to other areas it was maintained because it has no fitness cost. We call this behavior ‘founder effect’. Whether the change has been selected for – what we would call ‘positive selection’, as claimed by many virologists, needs to be proven by experiments that have not been done.

The D614G change appears to make the virus more infectious in cells in culture. However, there are limitations to the conclusions that may be drawn from these data. First, cells that have been used are irrelevant to human transmission, such as a kidney cell line (VERO) from Vervet monkeys. I would like to see data from cultures of human respiratory epithelial cells, including airway-liquid cultures and lung organoids. Second, SARS-CoV-2 was not used for these experiments, but pseudotyped viruses – recombinant retroviruses or vesicular stomatitis virus with the SARS-CoV-2 spike glycoprotein gene inserted. The reason for this approach is that working with SARS-CoV-2 requires a BSL-3 laboratory which is not easy to come by. Nevertheless, even if all these issues were addressed, do we really think that results in cell culture tell us anything about human to human transmission? Seriously, virology colleagues? A monolayer of cells in culture in no way compares with the architecturally complex respiratory epithelium with mucus, antibodies, innate and adaptive responses.

I don’t mention using an animal model to assess SARS-CoV-2 transmission potential because there are no good models (yet) for animal to animal transmission of the virus.

I can think of experiments that could be done to determine if viruses with D614G behave differently in humans, but they have not been done. One approach would be to determine if the change leads to higher shedding of infectious virus from the upper tract. One study reported higher levels of viral RNA in the upper tract of patients infected with 614G compared with patients infected with 614D. This observation is meaningless, because everyone knows that nucleic acids detected by PCR does not always mean that infectious virus is present. Increased RNA might be a consequence of a change in the viral RNA polymerase caused by another mutation that accompanies the spike change. What needs to be done is to measure the levels of INFECTIOUS VIRUS shed from the upper respiratory tract of humans infected with either variant. Even then I would argue that the results cannot be interpreted, because we do not know how much of an increase in virus shedding would lead to an increase in transmission. Would twofold more virus be enough? Fivefold? Tenfold? A thousand fold? Anyone who says they know is wrong.

We know that the dispersion factor, k, of SARS-CoV-2 is 0.1, which means that about 10% of cases lead to 80% of spread. Which virus are these individuals transmitting, 614D or 614G? The results would contribute to an understanding of the role of this amino acid change in transmission.

It’s unfortunate that during a serious outbreak, rigorous science appears to be relegated to the back seat. You might remember during the 2015 Ebolavirus outbreak in West Africa, a viruses with a single amino acid change in the spike protein arose early and predominated. This change made the virus more infectious in cells in culture in the laboratory, but was never shown to have any effect on human transmission. In a nonhuman primate model, the change actually reduced virulence of the virus. Whether the predominance of virus isolates with the amino acid change was a founder effect or positive selection was never determined.

An important consideration is to identify the selection pressure for SARS-CoV-2 viruses with increased transmission. By the time the virus was detected in China late in 2019, it was already very good at transmitting among humans. I fail to see what selection pressure would lead to the emergence of such a variant.

The D614 change does not appear to change the virulence of SARS-CoV-2, nor its ability to be neutralized by antibodies. Let’s toss all the above arguments aside and assume that D614G increases human transmission. What should we do? Wear face masks, avoid large gatherings of people, embrace physical distancing. All of which are already being done – or are they?”

No evidence for increased human transmission of SARS-CoV-2

In February 2021, Racaniello provided his thoughts on the incorrect usage by many in the MSM and the scientific community of three misunderstood virology terms: isolates, variants, and strains. He attempted to clarify the meanings of these words in order to clear up any confusion. His explanations provide some interesting insights into the lack of clear, universal definitions in virology as well as how these terms can be twisted:

Understanding virus isolates, variants, and strains

“Many virology terms are being used these days by people who do not understand their meaning. Included are journalists, medical doctors, scientists, lawyers, and people from all walks of life. In normal times this word mis-usage would be so rare that it would not matter. However, because we are in a viral pandemic that affects nearly everyone, I will attempt to explain the meaning of virus isolates, variants, and strains.

Many of the terms used in virology are ill-defined. They have no universally accepted definitions and there is no ‘bible’ with the correct meanings. As each of us are trained by other virologists, we hear them using terms in certain contexts and we copy their usage – whether or not it is correct. I learned many good things from my mentors but also many things that are wrong.

Nevertheless, certain terms should have specific meanings. Some of my colleagues will certainly disagree with some of my definitions, others will agree. Kudos to the latter. I also recognize that few will read this post and it will have little impact. Perhaps one day a high school student will search for some of the terms and come across it. It is mainly meant for me to put my thoughts down in an orderly manner.

The virology terms I have in mind all have to do with attempts to place order on the huge varieties of viruses in the virosphere. Most of them today derive their meaning from the viral genome: the DNA or RNA that encodes the production of new virus particles. This reliance on the genome is relatively recent: until the 1980s we had no genome sequences; hence most categories were based on other properties, such as the size of the virus particle, whether or not it has a membrane, its type of symmetry, and much more. Today it’s all about the genome. Whether or not you think this myopia is a good idea is not the topic of this post.

Let’s start with the term virus isolate, because it’s the easiest to define. An isolate is the name for a virus that we have isolated from an infected host and propagated in culture. The first isolates of SARS-CoV-2 were obtained from patients with pnemonia in Wuhan in late 2019. A small amount of fluid was inserted into their lungs, withdrawn, and placed on cells in culture. The virus in the fluid reproduced in the cells and voila, we had the first isolates of the virus.

Virus isolate is a very basic term that implies nothing except that the virus was isolated from an infected host. An isolate comes from a single host. We can have my virus isolate, or yours, or the neighbor’s down the street. Most patients do not get to have virus isolates taken from them. Even though SARS-CoV-2 has infected millions, we do not have millions of isolates, probably just thousands. We do have genome sequences from many people, and those can be inferred to represent the isolate from each person – however in most cases infectious virus is not isolated from individual patients.

Isolates are given names so that their origin is known. For example, one of the early isolates of SARS-CoV-2 is called BetaCoV/Wuhan/WIV04/2019. This isolate name consists of the genus, Betacoronavirus, followed by the city of origin, the isolate number, and the year. SARS-CoV-2 is the name of the virus; it is not an isolate name. Isolates of other viruses are also precisely named. I’m a big fan of the very detailed influenza virus nomenclature, which is as follows: Virus name/antigenic type/host of origin if other than human/geographical origin/serial number/last two digits (or all four digits) of year of isolation/hemagglutinin subtype neuraminidase subtype. Examples include influenza A virus A/duck/Germany/1868/68 (H6N1) or influenza A virus A/chicken/Vietnam/NCVD- 404/2010 (H5N1).

A virus variant is an isolate whose genome sequence differs from that of a reference virus. No inference is made about whether the change in genome sequence causes any change in the phenotype of the virus. The meaning of variant has become clouded in the era of whole viral genome sequencing, because nearly every isolate may have a slightly different genome sequence. Such is the case for SARS-CoV-2: nearly every sequence from a different person is slightly different. Up until the end of 2020, any SARS-CoV-2 sequences from any two individuals differed by about ten nucleotide changes out of 30,000. They are all variants, but the term is rarely used in this context. However since then viral genomes with many more changes have been identified. These have been called ‘variants of concern’ (VOC) because it is thought that the changes confer new phenotypic properties such as increased fitness. British scientists did a good deed by calling them VOCs, because now the press must call them variants.

Unfortunately mainstream media, following in the footsteps of scientists who really should know better, have been using the term ‘strain’ to describe what are actually variants. This practice emerges in every viral outbreak: there is a new, more (fill in the blank with your favorite phenotype) strain of Ebolavirus, of Zika virus, and now of SARS-CoV-2. It began early in 2020 with the finding of variants with a single amino acid change in the spike protein, from D to G at position 614. The press called this a new strain that was more transmissible. But the use of strain was incorrect: it is a variant and remains so to this day.

A virus strain is a variant that possesses unique and stable phenotypic characteristics. Such characteristics can only be ascertained by the results of experiments done in the laboratory, in cells in culture and in animals, coupled with observations made in infected humans. The name strain is not easily earned: certainly it cannot simply be given by journalists! As Jens Kuhn has written, “The designation of a virus variant as a strain would be the responsibility of international expert groups”. No such designation of strain has been given more than once to SARS-CoV-2: there is one, and only one strain of this virus. No incorrect usage of that term will change this fact. As you might imagine, it can take some time for an international group of experts to agree on anything.

Viral strains are few and far between: it is a designation highly desired but given sparingly. A retrovirologist recently assured me that there is only one strain of HIV-1. The Lansing strain of poliovirus is derived from a human isolate that was passaged 99 times in mice until it acquired the ability to infect that species. That strain has demonstrably different properties from the human strain.

There are other terms to describe viruses but they are more confusing than contentious, and they are not used universally. The term serotype is used to describe viruses of the same species that are antigenically different. There are three serotypes of poliovirus; if you are infected with type 1, then immunity you generate will not protect you against infection with types 2 or 3. Same for the four serotypes of dengue virus, and the hundreds of rhinovirus serotypes. These days, the genome sequence of the virus is used to infer whether isolates are serologically different. The term genotype is used to describe the genetic makeup of a virus. For example, hepatitis C viruses are placed in different genotypes depending on the overall identity of their genomes. For other viruses, the term clade is used. A clade is a group of organisms composed of an ancestor and its descendants, as illustrated by the phylogenetic tree below. SARS-CoV-2 isolates and HIV-1 isolates are placed in clades based on phylogenetic trees constructed from their genome sequences.

I believe that the terms of virology should be used accurately and consistently. The terms isolate, strain, and variant have been frequently and incorrectly misused during the pandemic, which generates confusion. I have little faith that either the general public or the scientists will agree on any nomenclature. Rest assured that if you misuse isolate, variant, or strain, I will correct you according to my lexicon.”

Understanding virus isolates, variants, and strains

In April 2020, Racaniello broke down the lack of evidence for the claims of increased virulence of variant B.1.1.7. He briefly discusses a few studies which show no association with severe disease yet the MSM still rolled with unfounded and unsubstantiated fear-based headlines:

SARS-CoV-2 variant B.1.1.7 is not more virulent

“When the B.1.1.7 variant of SARS-CoV-2 was first detected in the UK in December 2020 it was accompanied by unsubstantiated claims of increased transmissibility and virulence. The results of a hospital-based study in London reveals no association of the variant with severe disease in this cohort.

In a note published by NERVTAG on 21 January 2021, the panel concluded that ‘there is a realistic possibility that infection with VOC B.1.1.7 is associated with an increased risk of death compared to infection with non-VOC viruses.’ The death risk ratio for VOC infected individuals compared with non-VOC infected individuals was 1.65. This conclusion was based on analysis of COVID-19 related deaths at several hospitals in the UK. The authors noted in this report that ‘The data set used in the LSHTM, Imperial, Exeter and PHE analyses is based on a limited subset of the total deaths. This includes approximately 8% of the total deaths occurring during the study period’.

In the present study, SARS-CoV-2 PCR-positive samples from hospitalized patients were analyzed that had been collected between 9 November and 20 December 2020 in London. Of these, 341 (58%) were infected with B.1.1.7 and 143 (42%) were infected with an ancestral virus. Results of statistical models showed no association between severe disease and death and the B.1.1.7 lineage.

I hope that these results can begin to reverse the disturbing narrative advanced by some that B.1.1.7 is 50% more virulent than its ancestor. This conclusion was never firmly grounded, yet it has been echoed by mainstream media as if it were dogma.

Unfortunately the authors of this paper continue to promote the idea that B.1.1.7 viruses are more transmissible. Their conclusion is based on increased levels of viral RNA in patient samples as determined by RT-PCR (cycle threshold 28.8 in VOC infected patients versus 32.0 in non-VOC infected patients) and genomic reads by sequencing (1280 vs 831). Increased viral load determined by these methods might be an indication of increased viral fitness, but it does not prove increased transmission. It is not known if VOC-infected patients shed more infectious virus, which might be consistent with increased transmission. Until such experiments are done, it can only be speculated that B.1.1.7 and other VOC have increased transmissibility.“

SARS-CoV-2 variant B.1.1.7 is not more virulent

Finally, in June 2021, Racaniello looked at variant 20E which was said to have spread from Spain due to its increased transmissibility. However, he once again goes after the lack of concrete scientific evidence for these claims and instead points his finger at increased travel and a lack of safety measures for any perceived increase in transmission. Instead of unsubstantiated hyped up claims of increased transmissibility, Racaniello argues it is the overall fitness level of the “virus” variant which makes all the difference. Obviously, 20E can do more pull-ups than the other variants.

Holiday travel explains spread of a SARS-CoV-2 variant

“The emergence and spread throughout Europe of a SARS-CoV-2 variant, 20E (EU1) in the summer of 2020 illustrates how a virus may become dominant not by increased transmissibility but through travel and lack of effective containment and screening.

The SARS-CoV-2 variant 20E (EU1) emerged in Spain in the summer of 2020 and spread to multiple European countries. By the fall of 2020 most of the sequences in Europe were from 20E (EU1). The variant bears a number of amino acid changes including A222V in the N-terminal domain of the spike protein (pictured).

Results of binding and neutralization assays revealed that the A222V change did not affect interaction of the spike protein with polyclonal or monoclonal antibodies. Lentivirus particles bearing the spike with A222V did not reproduce with higher efficiency in cells in culture. Authors conclude that these observations are not consistent with increased transmissibility of the 20E (EU1) variant. However, I would argue that studying the infectivity of a pseudotyped virus – in this case a lentivirus bearing the SARS-CoV-2 spike – in 293 cells (possibly human embryonic kidney) has virtually no relevance to what occurs in humans. At the very least, authentic SARS-CoV-2 infection of human respiratory tract cells must be examined. Even then, the results may have no direct bearing on what occurs in humans.

In contrast, epidemiological evidence explains the spread of 20E (EU1). This variant arose first in Spain in early summer 2020. It then spread extensively in Spain and also spread to other European countries. Results of modeling indicate that the spread of the variant can be explained by holiday travel-associated transmission (many EU countries opened their borders to travel on 15 June), and human behaviors such as failure to distance, mask, restrict gatherings, and adequately test for infections.

It seems likely that human behavior might also account for the global spread of other SARS-CoV-2 variants (e.g. alpha and beta). Authors believe that such spread is due to increased inherent transmission of the viruses, but the data in support of this conclusion are not convincing. Increased reproduction of pseudotyped viruses in cells in culture, as pointed out above, is likely irrelevant. Increased shedding of viral RNA from the nasopharynx, detected by PCR, is also irrelevant as it does not represent infectious virus. In no case has shedding of infectious virus from the nasopharyngeal tract been studied to address potential mechanisms of increased transmission. It is claimed that the reproductive index of variants is increased, but these calculations are flawed. The reproductive index is determined by a formula that includes both viral and host factors. However, host factors are never included when this index is determined for individual variants. As the study above indicates, human activities can substantially affect predominance of a virus in a population.

Why do variants out-compete and displace other viruses? It is because the variants have increased fitness, the ability of a virus to reproduce in the host. Fitness can be altered in many ways, including evasion of antibody responses, increased particle stability, and even person to person transmission. No experiments have been done to explain the increased fitness of variants. Fitness is not the same as transmission.

Variants of influenza virus arise frequently, and these variants displace existing viruses because they have a fitness advantage. For influenza virus, a fitness advantage is often conferred by HA amino acid changes that allow escape from antibody neutralization. Antigenic variants can infect a slightly larger number of hosts and that is enough natural selection advantage for the new variants to outcompete the older ones. No one ever says that these influenza virus variants have increased transmission.

Unfortunately the narrative that the variants have increased transmission is dominating the media. This situation has arisen because virologists, epidemiologists, and evolutionary biologists are not talking to one another. In addition, what we know about other viruses, as illustrated here for influenza virus, is also ignored.”

Holiday travel explains spread of a SARS-CoV-2 variant

In Summary:

• Virologists are making conclusions that are not justified by the data
• “SARS-CoV-2 virus” isolates from many parts of the world have a single amino acid change in the spike protein, D614G, yet this observation in itself doesn’t mean very much
• Positive selection (the process by which new advantageous genetic variants sweep a population) as claimed by many virologists, needs to be proven by experiments that have not been done
• Cell culture experiments seem to show D614G as more infectious, however there are limitations to the conclusions that may be drawn from these data
• First, cells that have been used are irrelevant to human transmission, such as a kidney cell line (VERO) from Vervet monkeys
• Second, “SARS-CoV-2” was not used for these experiments, but pseudotyped “viruses” – recombinant retroviruses or vesicular stomatitis “virus” with the “SARS-CoV-2” spike glycoprotein gene inserted
• Nevertheless, even if all these issues were addressed, do we really think that results in cell culture tell us anything about human to human transmission?
• A monolayer of cells in culture in no way compares with the architecturally complex respiratory epithelium with mucus, antibodies, innate and adaptive responses
• There are no good models for animal to animal transmission of the “virus”
• One study reported higher levels of “viral” RNA in the upper tract of patients infected with 614G compared with patients infected with 614D, however, this observation is meaningless because everyone knows that nucleic acids detected by PCR does not always mean that infectious “virus” is present
• Racaniello states that what needs to be done is to measure the levels of “infectious virus” shed from the upper respiratory tract of humans infected with either variant
• Even then, he argues that the results cannot be interpreted, because they do not know how much of an increase in “virus” shedding would lead to an increase in transmission and anyone who says they know is wrong
• He laments that it is unfortunate that during a serious outbreak, rigorous science appears to be relegated to the back seat
• During the 2015 Ebolavirus outbreak in West Africa,”viruses” with a single amino acid change in the spike protein arose early and predominated, however while this change made the “virus” more infectious in cells in culture in the laboratory, it was never shown to have any effect on human transmission
• In a nonhuman primate model, the change actually reduced virulence of the “virus”
• The D614 change does not appear to change the virulence of “SARS-CoV-2,” nor its ability to be neutralized by antibodies
• Journalists, medical doctors, scientists, lawyers, and people from all walks of life are misusing certain virology terms
• Many of the terms used in virology are ill-defined and they have no universally accepted definitions nor a ‘bible’ with the correct meanings
• Most of them today derive their meaning from the “viral” genome: the DNA or RNA that encodes the production of new “virus” particles
• This reliance on the genome is relatively recent: until the 1980s there were no genome sequences
• Today it’s all about the genome
• “Virus” Isolate:
  1. An isolate is the name for a “virus” isolated from an infected host and propagated in culture
  2. Very basic term that implies nothing except that the “virus” was isolated from an infected host
  3. We do have genome sequences from many people, and those can be inferred to represent the isolate from each person – however in most cases infectious “virus” is not isolated from individual patients
• “Virus” Variants:
  1. An isolate whose genome sequence differs from that of a reference “virus”
  2. No inference is made about whether the change in genome sequence causes any change in the phenotype of the “virus”
  3. The meaning of variant has become clouded in the era of whole “viral” genome sequencing, because nearly every isolate may have a slightly different genome sequence
  4. Such is the case for “SARS-CoV-2:” nearly every sequence from a different person is slightly different
  5. They are all variants, but the term is rarely used in this context
  6. Unfortunately mainstream media, following in the footsteps of scientists who really should know better, have been using the term ‘strain’ to describe what are actually variants
  7. D614G is a variant which the press called a new strain that was more transmissible but the use of strain was incorrect: it is a variant and remains so to this day
• “Virus” Strain:
  1. A variant that possesses unique and stable phenotypic characteristics
  2. Such characteristics can only be ascertained by the results of experiments done in the laboratory, in cells in culture and in animals, coupled with observations made in infected humans
  3. The name strain is not easily earned: certainly it cannot simply be given by journalists
  4. No such designation of strain has been given more than once to “SARS-CoV-2:” there is one, and only one strain of this “virus” (with over 4.25 million variants as of 10/12/2021)
  5. “Viral” strains are few and far between: it is a designation highly desired but given sparingly
• There are other terms to describe “viruses” but they are more confusing than contentious, and they are not used universally
• The genome sequence of the “virus” is used to infer whether isolates are serologically different
• The terms isolate, strain, and variant have been frequently and incorrectly misused during the pandemic, which generates confusion
• When the B.1.1.7 variant of “SARS-CoV-2” was first detected in the UK in December 2020 it was accompanied by unsubstantiated claims of increased transmissibility and virulence
• The results of a hospital-based study in London reveals no association of the variant with severe disease in this cohort
• Results of statistical models showed no association between severe disease and death and the B.1.1.7 lineage
• The conclusion that B.1.1.7 is 50% more virulent than its ancestor was never firmly grounded, yet it has been echoed by mainstream media as if it were dogma
• Increased “viral” load determined by PCR might be an indication of increased “viral” fitness, but it does not prove increased transmission
• It is not known if VOC-infected patients shed more infectious “virus,” which might be consistent with increased transmission
• Until such experiments are done, it can only be speculated that B.1.1.7 and other VOC have increased transmissibility
• Racaniello believes that the spread of 20E (EU1) in the summer of 2020 illustrates how a “virus” may become dominant not by increased transmissibility but through travel and lack of effective containment and screening
• Neutralization tests and the lack of efficiency of cell culture spread led authors to conclude that these observations are not consistent with increased transmissibility of the 20E (EU1) variant
• Racaniello argues that studying the infectivity of a pseudotyped “virus” – in this case a lentivirus bearing the “SARS-CoV-2” spike – in 293 cells (possibly human embryonic kidney) has virtually no relevance to what occurs in humans
• At the very least, authentic “SARS-CoV-2” infection of human respiratory tract cells must be examined but even then, the results may have no direct bearing on what occurs in humans
• He believes the results of modeling indicate that the spread of the variant can be explained by holiday travel-associated transmission and human behaviors such as failure to distance, mask, restrict gatherings, and adequately test for infections
• Racaniello also believes that it seems likely that human behavior might also account for the global spread of other “SARS-CoV-2” variants (e.g. alpha and beta)
• Authors believe that such spread is due to increased inherent transmission of the “viruses,” but the data in support of this conclusion are not convincing
• Increased reproduction of pseudotyped “viruses” in cells in culture is irrelevant
• Increased shedding of “viral” RNA from the nasopharynx, detected by PCR, is also irrelevant as it does not represent infectious “virus”
• In no case has shedding of infectious “virus” from the nasopharyngeal tract been studied to address potential mechanisms of increased transmission
• It is claimed that the reproductive index of variants is increased, but these calculations are flawed
• Racaniello believes it is because the variants have increased fitness, the ability of a “virus” to reproduce in the host, which allows them to spread
• No experiments have been done to explain the increased fitness of variants
• Fitness is not the same as transmission
• Variants of influenza “virus” arise frequently, and these variants displace existing “viruses” because they have a fitness advantage
• No one ever says that these influenza “virus” variants have increased transmission
• Unfortunately the narrative that the variants have increased transmission is dominating the media

Like Charles Calisher before him, Vincent Racaniello admonishes those within the scientific community and the media for making unsubstantiated claims based on genomic data. The MSM headlines screaming about increased virulence and transmissibility of these variants have no concrete scientific evidence to back them up. The scientific community has become over-reliant on genomics and is not doing the neccessary studies with properly purified/isolated particles and valid controls to make any specific claims about any “virus,” let alone variants of them. However, even as the genomic data does not tell us anything about supposed “viruses,” nor too does the cell culture method championed by the old guard of virology. As Racaniello himself stated:

“Nevertheless, even if all these issues were addressed, do we really think that results in cell culture tell us anything about human to human transmission? Seriously, virology colleagues? A monolayer of cells in culture in no way compares with the architecturally complex respiratory epithelium with mucus, antibodies, innate and adaptive responses.”

I would love to see his colleagues respond.