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.