Decoding the Scientific Jargon Used by Virologists

December 27, 2021
Science Magazine

In the light of the COVID-19 pandemic, the average person has been exposed to far more epidemiological and virological terms than before. Transmission, fitness, virulence, infectivity - to the layperson, it can be hard to pinpoint the actual differences in definitions of these words. Although these terms seem to be referring to very similar things, they actually have vastly different meanings from a virological standpoint. With the number of highly effective vaccines available, the AIDS epidemic seemingly under more control, and a lower number of COVID-19 cases in most parts of the US, it is easy for many people to see viruses as a threat of the past. However, if the past year and a half has shown us anything, it is that new pathogenic viruses are still emerging. With such formidable and omnipotent foes, it is important for everyone to have more of a baseline understanding of viruses. Specifically, how they function and spread through a population. In the first edition of Virology 101, I will be going through the definitions and significance of many terms that the average person without much virological experience has probably heard before. Hopefully, this article will leave you with a better understanding of these words and the exact biological properties they are referring to.

First of all, viruses are, in essence, genomic DNA or RNA encased within a membrane and proteins that must infect a cell to replicate. Because viruses don’t have a complete set of machinery necessary for replication, they must hijack the machinery of the cell to copy their genome, transcribe their genome, make proteins, and wrap themselves in a membrane. They are therefore not considered alive, as they don’t have their own metabolism.

Our first virological term is “transmission,” defined as “the process by which viruses spread between hosts” (7). Depending on the scientist, this word can have slightly different definitions, so it is important to understand them both. Some scientists, typically those studying the molecular biology of viruses, use it to refer to the actual mechanism by which a virus moves from one host to another (1). Such mechanisms include remaining stable on surfaces or in respiratory droplets for longer periods of time, withstanding higher levels of humidity, entering cells more efficiently, being able to spread through smaller aerosols and utilizing alternative modes of transmission (fecal/oral, direct physical contact, airborne, etc). An easy way to think about this is to imagine a single virus particle and compare the efficiency of that virus particle with a virus particle of another strain or variant, keeping all other factors constant. If one single particle can more efficiently infect a host, then it is more transmissible. On the other hand, transmission can also refer more broadly to the event of a microorganism or virus moving from one host to another and spreading through a population (3). Under this less strict definition, having higher transmission capabilities simply means that a pathogen can spread through a population better. This could be due to enhanced mechanisms of transmission, but it could also be due to immune escape (when a virus variant is able to escape the host’s immune system), an increase in the number of virus particles shed by an infected person, or fewer virus particles being necessary to establish an infection (i.e. infectivity): all examples of phenomena that can facilitate better spread of a virus through a population without altering the effectiveness of a virus’ intrinsic transmission process. This second definition is considered by some virologists to be the virus’ “fitness,” which will be discussed later (1). When virologists argue that something has higher transmissibility, they often support this claim with a value called an “R0 Number” (pronounced “R naught'').

The R0 number, or the baseline reproductive number, is defined as “the number of secondary infections that can arise in a large population of susceptible hosts from a single infected individual during their lifespan” (3). In other words, how many people, on average, an infected person can pass the virus to. At first glance, this sounds like the perfect way to determine how likely a pathogen is to cause an epidemic. However, the number has some limitations. Specifically, it assumes constant transmission capabilities during every season, does not incorporate differences in population density by location, and assumes that every person is susceptible and nobody is taking precautions to prevent the virus spread (2). In order to better account for these variables, other reproductive numbers are used, such as the time dependent reproductive number (Rt) and the effective reproductive number (Re). Rt incorporates seasonal differences in transmission (e.g. influenza being transmitted better during the winter months because of lower humidity) as well as any precautions people might take in order to avoid infection (e.g. masking in public spaces). Re takes the Rt value and multiplies it by the number of susceptible individuals in the population, and therefore tends to be the most useful during an epidemic (2). Because the different forms of the R number are accompanied with so much uncertainty, they are almost always presented as a range of values. Nevertheless, they can provide a valuable standard of measure for how well a virus can spread through a population.

The next term on our list is “infectivity,” which is thought of as the “capacity of a virus to enter a host cell and effectively produce progeny infectious virus particles” (5). This property is measured by something called a “particle to pfu ratio,” where “pfu'' stands for “plaque forming units” (4). A plaque forming unit is a congregation of dead or deformed cells that forms when a cell monolayer is infected with a specific concentration of virus (called the “viral titer”). As long as one virus particle is sufficient to initiate an infection, each plaque can be assumed to be caused by one infectious virus particle. Therefore, when the number of plaques is counted and compared to the total number of virus particles inoculated into a cell culture, the particle/pfu ratio can be determined (3). But does that mean that every virus particle cannot initiate an infection? That is correct. Different viruses have different fractions of their “population” that can actually initiate infection because of missing components in some virus particles or mutations in regions of the genome that must remain constant. That ratio of infective viruses to non-infectious virus particles compared across virus types is the essence behind the infectivity of a virus.

Our next term, “virulence,” has a very straightforward definition, but its significance is a bit harder to understand. Virologists define it as “the ability of a virus to cause disease” (3). However, one cannot compare one virus’ virulence with that of another virus, because virulence is a relative property and has no scale through which it can be quantified and compared (3). It is also influenced by many factors that are difficult to control in a clinical trial, including the viral dose, the route of infection, a person’s age, a person’s sex and even the species the virus is infecting. A particularly fascinating and important field of research is looking for virulence factors: viral genes that directly result in host pathogenesis, or the development of disease. To find genes that specifically affect the virulence of a virus, the virus should still be able to replicate normally in cell culture when the gene is silenced or removed (3). However, in vivo (i.e. in animal models) the host should exhibit decreased pathogenesis. Examples of virulence factors are genes that encode proteins that act as toxins to humans and gene products that intercept the normal functions of the immune system.

It is only fitting that our final word is “fitness,” a term that broadly encompasses many characteristics of a virus. The word is typically used when comparing two or more variants (viruses of the same species with slight differences in genotype) or strains (variants with significant differences in phenotype). One virus is more fit than another if it displaces or “outcompetes” the other in a population, indicating that mutation and natural selection are at work (1). Consistent with the relationship between mutation and natural selection in all organisms, viruses are constantly mutating, yielding mutations that confer debilitating, advantageous, and neutral or nonexistent effects on the virus. Naturally, only the advantageous and neutral mutations are carried on to progeny viruses. An advantageous mutation will increase the fitness of the virus, whether that is through increased transmission, immune escape, infectivity, and so forth, resulting in this virus outcompeting a virus without the advantageous mutation.

In this article, I have hardly scratched the surface of the concepts that govern our interactions with viruses. To make any conclusion about how a virus interacts with a host or with a population as a whole, scientists of many different disciplines must collaborate to study the replication cycle, fitness, transmission capabilities, immune escape, virulence, and other qualities of a virus. With such formidable and omnipotent foes, this work never ceases to be vital. However, it is equally important for the general population to have more of a baseline understanding of viruses and how they function and transmit through a population. Not only will this information aid in understanding many facets of this pandemic, but a stronger baseline understanding could also help stop the spread of misinformation surrounding future outbreaks. After reading this article, I hope you have begun to see that viruses are vastly complex, and that their ability to cause disease is dictated by many different qualities.  


  1. Barker, V. R. K. S. (2021a, July 8). TWiV 777: SARS-CoV-2 fitness with Ron Fouchier. Microbe.TV.
  2. Barker, V. R. K. S. (2021b, August 12). TWiV 792: Transmission with Jeffrey Shaman. Microbe.TV.
  3. Flint, S. J., Enquist, L. W., Racaniello, V. R., Rall, G. F., & Skalka, A. M. (2015). Principles of Virology: 2 Vol set - Bundle (4th ed.). American Society for Microbiology.
  4. Norkin, L. C. (2009). Virology: Molecular biology and pathogenesis (Norkin, Ed.). American Society for Microbiology.
  5. Rodríguez-Lázaro, D., Kovac, K., & Hernández, M. (2013). Molecular detection of viruses in foods and food-processing environments. In Viruses in Food and Water (pp. 49–78). Elsevier.
  6. Sanjuán, R. (2017). Collective infectious units in viruses. Trends in Microbiology, 25(5), 402–412.
  7. Viral transmission. (2021, September 30). Nature.Com.
Kaeden Hill

Kaeden (Trinity '25) is from Atlanta, Georgia, and is majoring in biology with a concentration in molecular and cell biology. He is specifically interested in DNA tumor viruses and how their “cellular hijacking” can drive cells towards cancer, and he is a member of the Luftig Lab, studying Epstein-Barr virus and the cancers that it causes. Outside of academics, he loves to hike, travel, ski, scuba dive, collect minerals, and make jewelry.

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