Nonprofit, nonpartisan journalism. Supported by readers.


A COVID-19 primer: How viruses work and spread

COVID-19 isolation room
Antara Foto/Rahmad/ via REUTERS
A medical officer is seen inside an isolation room prepared for patient affected by COVID-19 at Cut Meutia hospital in Aceh, Indonesia.

In case you haven’t heard, there’s a new viral sensation sweeping the globe and it’s called COVID-19. Viruses are complicated, and epidemics even more so, but if you understand the basics of how a virus works and spreads, the more complicated details will make sense.

First, this from the CDC about how this coronavirus got its name:

The new name of this disease is coronavirus disease 2019, abbreviated as COVID-19. In COVID-19, ‘CO’ stands for ‘corona,’ ‘VI’ for ‘virus,’ and ‘D’ for disease. Formerly, this disease was referred to as “2019 novel coronavirus” or “2019-nCoV”.

Here’s a little COVID-19 primer for you.

What, exactly, IS a virus?

A virus isn’t “alive” in a typical sense. It doesn’t need to eat, drink, or breathe. It’s just a collection of genetic material (DNA or RNA) and a small toolbox of proteins. Most flu and cold viruses — including COVID-19 — are contained in a shell called a capsid.

A virus uses its proteins to perform two critical tasks: to get inside the cells of its animal host; and then to hijack that cell’s own genetic machinery in order to produce thousands and thousands of copies of itself. It’s as if it jumps up on a cell’s internal printer, selects “millions” on the number of copies, and then hits the “print” button.

How do viruses travel?

Given its nearly inert state, a virus must hitchhike its way across the universe. It makes sense that respiratory viruses travel primarily through respiratory secretions — the dribbling nose, yes, but more forcefully via the sneeze or the cough. Our country’s premier cough-and-sneezologist might be Lydia Bourouiba, the director of the Fluid Dynamics of Disease Transmission Laboratory at MIT. As her title suggests, a kerchoo is more complicated than we ever imagined. Bourouiba’s research shows that a cough or a sneeze produces what she describes as a “multiphase, turbulent puff cloud” that boils and expands as it spreads. Because exhaled air is typically warmer and moister than room air, it billows up to the ceiling, carrying with it a continuum of different-sized snot particles.

Some of these airborne particles can either be directly inhaled or end up in the eyes (which connect to the nose and respiratory tract via our tear ducts). Given the virus’ ‘freshness’ in this wham-bam scenario, this is the most direct and contagious way of catching a viral bug. By the way, a surgical mask seems to be a more effective deterrent when worn by the infected, not the healthy.

Once the particles fall from the cloud and settle on public surfaces like door handles, countertops, keyboards etc., they must depend on human hands to provide any further transportation. Because handwashing is neither perfect nor perpetual, you can avoid inoculating yourself by keeping your hands away from your eyes, nose, and mouth.

How long can a virus survive on its own?

Respiratory viruses can sometimes survive inside their little mucus condo for a number of days, but their infectivity tails off sharply after a few hours. Some of that depends on where they land. Non-porous surfaces like stainless steel and plastic slow the drying process and give the virus added time. Luckily, human skin is very hostile to flu and cold viruses, which are usually dead 20 minutes after landing there.

How do the lungs protect themselves?

We need to breathe every 5-6 seconds, and each time we do, we allow the atmospheric environment — including bacteria and viruses — to enter deep into our body. Not surprisingly, the respiratory tract is heavily fortified with … mucus and brooms. Goblet cells lining the airways produce a thick mucus that traps particulates (dust, smoke, etc.), viruses, and bacteria. Cilia cells have hairs that rhythmically sweep this mucus out of the lung, where it is either coughed up, or unconsciously swallowed and dumped into the acid bath of the stomach.

How does a virus actually get inside the human body?

If a virus somehow gets past the mucus and brooms, it still needs to find a particular protein (a “receptor”) on the cells that line the human respiratory tract. Like a computer being hacked, carrying the right protein to bind to the right cell receptor is the “password” that will allow the virus to enter the host cell. These proteins exist to allow the cell to interact with its surroundings, but the virus takes advantage of them for its own purposes.

A virus’ ability to enter the human body has two key variables: the anatomical location of that receptor, and how strongly the virus binds to the receptor. If the required binding site is only found deep in the lung, and not in the upper respiratory tract, that will make it harder for the virus to be passed to a new host. If the virus binds tightly to its preferred receptor, the victim only needs to be exposed to a small number of viral particles to get infected. The 2003 coronavirus named SARS bound primarily to the “ACE-2” receptor deep in the lung, which may explain why the infection seemed to require particularly close contact, and perhaps why the virus flashed out in 2003 and hasn’t been heard from since.  Meanwhile MERS, the other most common coronavirus, seems to have had more staying power: It appeared in 2012, spiked in 2014, but has hung around at low levels ever since.

Where did COVID come from and how does a virus “jump” species?

SARS, MERS, and COVID-19 are all thought to have originated in bats, but then moved to humans via another animal: perhaps civet cats in SARS, camels in MERS and in the case of COVID-19, a scaly anteater called a pangolin.

Viruses can alter their genetic profile — and whom they can infect — in two primary ways. Errors made during the replication process are called mutations, and RNA viruses in particular are bungling replicators. They make a lot of mutations, and most of them are “losers” — of no benefit or even a detriment; but because viruses reproduce in such massive numbers, eventually a “winning” combination comes up and a new viral strain is born.

The second way that viruses can acquire new infective capabilities is known as “reassortment.” When a mammal has the misfortune of being infected with two (or more) respiratory viruses at once, as the viruses replicate, the two genetic decks can be shuffled together and then redealt. The predecessor to the 2009 H1N1 pandemic virus had been sitting in pigs (swine) since the 1930s until 1998 when it exchanged information with a contemporary human influenza virus and an avian influenza (called a “triple reassortment”). When that virus went back and incestuously mingled with its predecessor, the standard swine H1N1, a pandemic was born.

Could COVID 19 be stopped by warmer weather?

We still don’t understand why respiratory infections like colds and the flu typically start in the winter and tend to fizzle out by late spring. There are many different theories to explain this, but one key component might be that the dryness of winter air makes it difficult for the lung to defend itself. If you don’t have winter to dry out your schnoz, just get on an airplane, where average humidity is about 12% — drier than most deserts (because the engineering required to humidify an airplane is exceedingly complicated).

We can hope that COVID-19 will tail off with the coming of spring. The 2003 SARS outbreak peaked in March and April and was all but over by May. MERS appeared in 2012, spiked in the spring of 2014, and has just simmered since. It’s been isolated primarily to the Arabian Peninsula, which lacks what most people would recognize as winter.

How infective is COVID-19?

Pretty infective. The latest evidence from China suggests each infected patient is passing the virus on to two or three others. There are two major factors that affect infectivity. As noted previously, the first factor has to do with the virus’ innate ability to infect a host: How capable is it of finding and binding tightly to a suitable cellular receptor in the lung? The second has to do with the virus’ ability to reproduce but not sicken the host (example: An English house sparrow can be infected by millions of West Nile virus particles and not be ill). A healthy-but-infected host is a Trojan horse ridden by Typhoid Mary, going to work, school, meetings, traveling, and interacting with people, all the while unwittingly spreading the virus.

How lethal is COVID-19?

Mortality is calculated by dividing the number of patients who died (the numerator) by the number who have been infected (the denominator). Of those two numbers, the denominator is typically much more difficult to define.

Mortality rates tend to range higher early on in an outbreak, because the denominator is falsely low. Without accurate diagnostic testing, the number of patients infected only includes those with obvious symptoms. This seems to be the case with COVID-19. When the West Nile virus first hit the U.S., it seemed quite lethal, until wider testing showed that 80% of people who became infected had no symptoms at all.

Since symptoms alone make for a sketchy denominator, public health officials rely on lab verification of infection, but historically, viruses have been difficult to detect. Because they are hard to grow (“culture”) in a lab, the next best step was to look for antibodies against the virus. Unfortunately that was clunky and inaccurate, and it often missed early infections because the body had yet to even mount an antibody response.

Doctors and scientists have had the ability to look for viral genetic material in various body fluids for some time, but recently this technology — Reverse Transcription-Polymerase Chain Reaction (RT-PCR) — has become much more widely and quickly available. In a head-spinning combination of genetics, virology, laboratory science, computer power, and international data-sharing, scientists outside of China developed a RT-PCR for COVID-19 without even having a sample of the virus.

When Germany flew 126 of its citizens out of the Hubei province on Feb. 1, they isolated 10 of the group for either symptoms or exposure concerns. On arrival to Frankfurt, the isolated 10 tested negative for COVID-19. All others were quarantined and screened. One had signs and symptoms consistent with a respiratory infection but tested negative. All of the remaining 115 people were asymptomatic, but two tested positive for COVID-19. They were hospitalized but developed only minimal symptoms.

Here in the U.S., initially only the CDC had COVID-19 RT-PCR testing capability, but this is now expanding into the state health departments, which should add speed and quantity to what we know about this virus’ true whereabouts.

But you want to know a mortality number, right? According to a Feb. 28 New England Journal of Medicine editorial by Dr. Anthony Fauci, head of the National Institute of Allergy and Infectious Diseases, the most current mortality rate is calculated to be 1.4%, but it might be “considerably less than 1%” if wider, population-based testing shows high numbers of asymptomatic or minimally symptomatic individuals. If so, Fauci writes, “the overall clinical consequences of Covid-19 may ultimately be more akin to those of a severe seasonal influenza (which has a case fatality rate of approximately 0.1%) or a pandemic influenza (similar to those in 1957 and 1968).”

May it be even less so.

Dr. Craig Bowron is a Twin Cities internist and writer.

Comments (12)

  1. Submitted by Bob Barnes on 03/06/2020 - 10:03 am.

    From my reading up on this it appears that covid19 is most likely spread via fecal matter which is why it is more prevalent in 3rd world nations and places where sanitation isn’t that great (like a nursing home where many have bowel issues). That doesn’t mean it isn’t also spread via coughs, sneezes and direct personal contact (kissing your spouse etc).

    • Submitted by Alan Nilsson on 03/06/2020 - 03:15 pm.

      The NHS; the Mayo Clinic; WebMD – These are all sites offering reliable information. NO. The primary source of infection is not fecal material.
      “Like the flu, COVID-19 is spread primarily via respiratory droplets—little blobs of liquid
      released as someone coughs, sneezes, or talks. Viruses contained in these droplets
      can infect other people via the eyes, nose, or mouth—either when they land directly on
      somebody’s face or when they’re transferred there by people touching their face with
      contaminated hands.”

      This is also one of the most common means of transmitting the most often encountered corona virus: The common cold.

    • Submitted by Craig Bowron on 03/07/2020 - 06:52 am.

      PCR for coronavirus detects genetic fragments of the virus. Finding coronavirus fragments in the stool is a sign of infection, but it doesn’t guarantee infectivity. One can only get infected by an intact, functioning virus, not viral debris.

  2. Submitted by Rachel Kahler on 03/06/2020 - 01:04 pm.

    While the mortality rate might end up being low, depending on how many of the population are susceptible to infection but maybe not susceptible to the illness, probably more important is the mortality rate among those who actually get ill. It would appear that, when you’re old and frail, if you get ill with the disease, you have a VERY high chance of dying. We know less about the young and immunologically/physically impaired. But I am not certain that the humane approach is to do nothing (or excuse administrative incompetence) because only people who are already sick die.

    It doesn’t take much to be considered “already sick” in this instance. Those with chronic respiratory or cardiovascular disease appear to be at greater risk of both getting sick and dying. Both respiratory illness and cardiovascular disease are co-morbidities that vastly increase the risk of death if you get sick. According to the CDC, in the US, heart disease is the #1 cause of death and chronic respiratory disease is the #4 cause of death. That is, we have a LOT of chronically sick people, enough of whom are already fated to die of the disease WITHOUT Covid-19 for those diseases to be 2 of the top 4 ways to die. In fact, 60% of Americans have at least one condition that increases their risk of death–from 0.9% in those without co-morbidities to 5% and more for those with them (see,

    So, no, we should not panic because panic solves nothing. But we shouldn’t pretend that this isn’t a big deal. Other coronaviruses fizzled out because they were SO deadly (among other reasons), and they didn’t spread like this one. The 1918 Spanish flu is thought to have had a mortality rate of about 2.5% (although, it could have been lower since there were no PCR tests back then to determine how many were actually infected and showed no symptoms), and it killed between 1% and 6% of the population at the time. 1-6% of the population might not sound like much, but the mortality rate and the propensity of the disease to kill young people may have been important in deciding the outcome of WWI, and there’s evidence that the disease stunted the educational and economic achievement of people whose mothers pregnant with them during the pandemic. We don’t know what this new disease might do, but it very well could have an impact greater than the standard annual flu, which we largely just shrug at, yet costs the US, on average, over $11 billion PER YEAR (

  3. Submitted by Gene Dorio on 03/08/2020 - 10:16 am.

    Very good review of Covid-19 Craig!

    I believe we should wear masks…especially if we are in susceptible public areas.

    The CDC does not recommend them in most circumstances, but what is their justification, and is it worthy? I believe most people wear masks around the world, and by not doing this in the U.S. might make the spread worse. Doesn’t common sense say “wear a mask”?


    Gene Uzawa Dorio, M.D.
    Santa Clarita, CA

    • Submitted by Rachel Kahler on 03/09/2020 - 01:00 pm.

      Masks are probably more important to wear for those who are infected rather than by those who want to avoid being infected. This is because infected people are more likely to transmit by coughing or sneezing–virus exits through the nose and mouth. And, while the viral particles are small and some might pass through the mask, it reduces the amount that actually is accessible by people who are not yet infected because it does manage to capture SOME of the viral particles on their way out.

      On the other hand, because viral particles are small, they CAN pass through the mask, so it’s of limited use to those who might eventually be exposed. It might be a layer of defense for those who are at high risk of exposure, such as medical personnel who are treating patience, but not so much for the average joe. As an MD, you might consider wearing a mask when you are working with high risk patients–but not all the time. Not only will it not help, but you create an environment of fear where people are often quite stressed already.

      Furthermore, once the viral particles are out and about, you’re probably just as likely to touch your eyes with hands that have viral particles on them, thus getting infected anyway. As a result, you are only getting a false sense of safety (putting public health at risk) AND reducing the availability of masks to people who need them more. So, don’t.

      Importantly, your beliefs are better of supported by good science and good sense. As an MD, your medical opinion has influence, for good or bad. It does not mean that your opinion is gospel, especially if counter to public health.

      Here’s a good piece of info on who should wear masks and when:

  4. Submitted by James Mickelson on 03/10/2020 - 07:03 pm.

    Thanks for an enlightening article on the virus. Can someone provide answers for these questions?
    -Define incubation period and what is the incubation period for the virus?
    -How long after being exposed to the virus would we show symptoms?
    -How long after exposure would the test kit detect the virus?
    -What does the patient have to do to produce a sample for the test kit?
    -How long does it take to process the sample and get the results back to the patient?

    • Submitted by Rachel Kahler on 03/13/2020 - 09:15 am.

      Incubation period is the time between exposure and onset of symptoms.

      We don’t yet know the true incubation period for this virus. The 14 day quarantine period is supposed to encompass the incubation period. The average estimated incubation period is about 5 days, and those that get sick typically do so within 12 days. However, this estimation is based mostly on severe cases, and there’s some evidence to suggest that people can still be infectious for several days after recovering.

      I can’t definitively answer the question on how long after you’ve been exposed that the kit would be able to detect exposure. There’s more than one way to test for the virus. The “official” test kit is a PCR test, which is very sensitive–and prone to more prone to false results–but should be able to detect viral load very quickly after exposure (maybe less than a day given the 5 day incubation period in severe cases). It simply takes a sample from your nose (just a swab), or sputum (stuff you cough up). This kit requires special equipment and reagents to get results. Theoretically, the results should be available within hours, however depending on how backed up the lab is and whether the reagents are back ordered, it could take longer to get the results than it takes you to get sick.

      Another test kit measures immune response (, which would provide fewer false results, but requires an amount of time after exposure for the immune system to figure out something’s wrong–and that depends on your immune system (a day or two…or more…you might already be showing symptoms, if you’re going to show symptoms at all). This kit requires blood (probably just a prick of the finger), but you probably will get results literally before your eyes–like a pregnancy test (

  5. Submitted by Jeomoan Kurian on 03/12/2020 - 02:38 pm.

    Thank you Dr Craig for such an informative article. I am pretty sure a lot of people are searching the web to understand how Covid-19 is actually entering and infecting our body but the information is is hard to find. Excellent narration of a complex topic.

  6. Submitted by Zabrae Valentine on 03/13/2020 - 10:20 pm.

    Presumably the idea of social distancing, as it relates to slowing transmission of Covid-19, is to deny the virus the opportunity to transfer to a new host, where it gets to start making trouble all over again. Does a virus have a life cycle of sorts, particularly in one host, if denied the chance to move to another? If a person is infected and stays away from others for some number of days, can he/she sort of terminate the virus in their body? Catch and kill in a sense?? (ha) And if so, do we know how long a virus lasts in a host? (vs on a surface outside of a host — lots written on this, looking for info on the above however). thanks!

  7. Submitted by Tillman Eddy on 03/22/2020 - 05:15 am.

    Is there any infectivity study on the number of viral particles that will cause infection?

    My ancient memory recalls that infectivity, pathogen quantity and frequency of exposure are the trilogy that result in an infection.

  8. Submitted by Jules Grossi on 03/25/2020 - 09:42 am.


    I have a question regarding the relation between number if viral particles inhaled and impact on the symptoms.

    In other words, while good hygiene is obviously reducing the infection probability, would it also have a positive impact on the disease symptoms ? (Less viral particles could lead to a slower development in the host body, leading to more time for the host to develop defenses)

    Sorry if my question is silly.

    Thank you

Leave a Reply