Alexander (Sasha) Gorbalenya is a virologist known for his work on how viruses are classified and named. He is Professor Emeritus of Medical Microbiology at Leiden University in the Netherlands, visiting professor at Lomonosov Moscow State University in Russia, and was lead author of the ICTV Coronavirus Study Group (CSG) statement that named SARS-CoV-2 and placed it within the official coronavirus classification system.
In July 2024, while I was drafting “The SARS-CoV-2 Name Game,” Dr. Gorbalenya answered questions I sent by email and later offered feedback on the article after it was published. I have since appended that feedback to the article itself, which can be read here:
We corresponded again in late 2025 and recently about his response to the article, the CSG consensus statement, SARS-CoV-2, and viruses more broadly.
What follows are excerpts from those exchanges, organized in Q&A format and published with his permission.
This was not a formal interview. My aim during each time we corresponded was simply to understand his perspective — with respect for his academic record, his contributions to his field, and his role in the COVID-19 event. The questions were intended to draw out his thinking in his own words, not to engage him in a debate.
Dr. Gorbalenya’s responses are unedited. He used brackets to clarify or qualify content in responses he had given in earlier emails, as he reviewed the final version.
Jessica Hockett/Sasha Gorbalenya: July 2024, November 2025, February 2026
Jessica Hockett:
You were commenting on a sentence in my introduction to “The SARS-CoV-2 Name Game” and suggested a change to “a goal of scientists who christened this virus.” Are you saying that the ICTV-CSG or some members thereof didn’t want the virus name to be connected to the disease name? Was that the case for you? (I don’t see it implied necessarily in the CSG emails.)
You then said, “As for WHO, there is no evidence that they would have favored departing from previous practice of marrying virus and disease names”. Did you mean there’s no evidence that the WHO wanted the name given to 2019-nCoV to be semantically disconnected from the disease name? I think it’s at least clear the WHO was wary of saying SARS.
Alexander (Sasha) Gorbalenya:
It is a bit complicated due to historical reasons dating back to the SARS pandemic. The ICTV-CSG derived SARS-CoV-2 name from the respective species name and its sibling SARS-CoV, which include reference to the disease (SARS). That might confuse some as implying causative connection between SARS-CoV-2 and SARS or that COVID-19 = SARS (it does not and that was articulated in the article). At the time, I expected the WHO would have come up with a disease name that differs from the virus name and includes attribute(s) of the disease, e.g. “acute respiratory” else. They decided differently and connected the disease to the virus family [coronavirus, after the family Coronaviridae] in the disease name [COVID-19, coronavirus disease 2019]. There is a long tradition to treat viruses as attributes of infectious diseases and [for] diseases defining viruses, which I hope will become part of the past.
I was not there when the disease name was discussed and decided. Right from the names introduction, the WHO promoted the use of “COVID-19 virus” or alike to refer to SARS-CoV-2 outside research. Based on this choice, it seems that the WHO favored the established tradition.
Was the WHO not comfortable with having two separate names for the virus and the disease due to either “SARS” in SARS-CoV-2 name or on general grounds or both? I don’t know. For sure, the introduced dichotomy in two names [one for the virus and another for the disease] complicated communication about pandemic with public and authorities (and that might have been of a concern to avoid for the WHO). To afford having two different names [for the virus and the disease), one needs to see benefits of this complexity (there are plenty!), and that realization required – another speculation! – a fresh look at the common practice and its pitfalls. On the other hand, it might be too much to have asked from the WHO at the time of main public distress. For further details, it might help to check this perspective https://doi.org/10.1371/journal.pbio.3002130
Hockett:
In that paper, you and Dr. Perlman make important distinctions between SARS-CoV-2 and COVID-19 (name of a virus versus the disease said to be caused by the virus). You define viruses generally by saying, “Viruses are the smallest known self-replicating entities that reproduce within cells of host organisms [4]. They were discovered as agents causing infectious diseases that spread through direct or indirect contact in a population. Within this traditional disease-centric framework, a virus is the sole etiology of a disease arising from infection.”
What is your understanding of when and how viruses were discovered as agents that cause infectious disease? In the paradigm you’ve articulated, all but the very fewest of millions of viruses can cause disease in some individuals. What is the best evolutionary explanation for that phenomenon, in your view?
Gorbalenya:
Discovery of first viruses is described in virology textbooks. Briefly, it happened during the last decade of the XIX century. Researchers were searching for mysterious causes of infectious diseases in plants and animals. Using filters with very small pores and clever experiments, they identified agents which were smaller than bacteria and capable of amplifying and causing disease in organisms. Later similar properties were described for agents causing disease in other cellular organisms, including humans or bacteria. Nowadays, they are known as viruses.
Since that, we have learned a lot about viruses and beyond virus size and its link to disease. Using this knowledge and tremendous advancement of technology, especially spectacular during the XXI century, researchers now identify viruses using very sensitive and fast genome-based methods (see below). These methods were broadly used during the last pandemic to sequence SARS-CoV-2 genomes. The fact that many healthy humans were found to be infected with SARS-CoV-2 show that the development of COVID-19 upon SARS-CoV-2 infection is conditional on other factors (e.g. advanced age). Within this framework, the identification (discovery) of new viruses in literally every biological species tested may look less surprising. Although there may be no evidence for most currently known viruses causing disease, this does not mean that they may not cause disease under certain circumstances in some organisms.
Generally speaking, humans and other animals or plants, bacteria and other life forms live in the world full of viruses and got sick only occasionally.
Hockett:
How do you see the difference between viral “spread” and “circulation”?
Gorbalenya:
Spread refers to transmission expansion of some sort, commonly host- or geography-wise. In contrast, circulation is transmission [in population] 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. [While many infected individuals may stay healthy, see above].
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”). 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 [without stressing connection to disease]. This logic approaches viruses as biological entities first and pathogens second. All human[s] being 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 [they don’t see viruses flying around]. But if accepted, it provides a vantage point to look at pandemics and associated events with [the] less biased approach that may have informed current communication.
Hockett:
With SARS-CoV-2, do you think it’s possible that the virus being detected (via testing) was already in humans or the environment long before detection, and that what appeared to be “transmission” and “spread” was, in reality, the launch of a test that shined a light on what was previously hidden in the dark (so to speak)?
Gorbalenya:
Good questions. Indeed, we know that some viruses may be present (persist) in organisms for many years without evident effect on the infected individuum. On the other hand, there are many viruses that cause so-called acute infection, when they enter organism, produce progeny and then cleared from the infected organism over several days or weeks. Like other coronaviruses, SARS-CoV-2 belong to the second group.
SARS-CoV-2 was discovered in humans following a spike in the number of sick individuals whose conditions could not be linked to infection by agents known at the time.
Hockett:
Have you written recently as to your individual position regarding whether SARS-CoV-2 emerged from a zoonotic event (so to speak) or was adulterated and escaped/was released from a lab?
Gorbalenya:
No.
Hockett:
You signed the so-called “Lancet letter” in 2020, indicating that you subscribed to a natural-origins viewpoint. Has your view changed? If so, how? If not, why not?
Gorbalenya:
That Letter was written at the beginning of the pandemic in a very different knowledge and communication environment, compared to subsequent months and years. At that time, I considered only natural vs engineered origins of SARS-CoV-2. Based on my knowledge and experience, the choice was trivial. However, that aspect was not on my mind. Rather I was thinking about brave medical doctors who were with COVID-19 patients and may have paid the ultimate price for their assistance. It was the primary reason why I signed that Letter.
Hockett:
In the Consensus paper acknowledgments, researchers who released SARS-CoV-2 genomic sequences are thanked—and the authors of the GenBank sequence thanked in particular.
Gorbalenya:
That was to thank colleagues for their generosity in making genome sequences public. As a token of appreciation, we listed (acknowledged) all authors of the sequence used in our analysis.
Hockett:
The six sequences [listed in the acknowledgements] were those listed in Marion Koopmans’ Virological post here, yes? https://virological.org/t/initial-assessment-of-the-ability-of-published-coronavirus-primers-sets-to-detect-the-wuhan-coronavirus/321
Gorbalenya:
I don’t recall how many full genome sequences became available while we conducted our analysis and wrote the paper.
Hockett:
Can you speak to why the F. Wu sequence was regarded as superior? In emails from January 2020, Dr. Koopmans refers to the diversity across the six samples but said the diversity likely reflects the use of different platforms. Was the GenBank sequence considered most informative because of the platform used?
Gorbalenya:
If I am not mistaken, that genome sequence was the first publicly available; it came from respected colleagues and thus could be trusted, time was of immense importance.
Hockett:
The ICTV-CSG was looking at all six sequences for its discussion, yes? Was there a way to know if these sequences were causal of a disease and/or any way to check if the sequences were irrelevant to disease?
Gorbalenya:
I don’t recall discussion of genome sequence variation. I am not aware about methods to predict disease determinants in a [new] virus. That has not been extensively studied in this respect.
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