Coronavirus III: What is to be done?

We live in evolutionary competition with microbes — bacteria and viruses.  There is no guarantee that we will be the survivors. The aphorism from Joshua Lederberg, a founder of molecular biology, is remarkable for its humility and for the challenge it defines. Before the germ theory of disease, which appeared in the second half of the 19th century, medicine was helpless against infection. We have since become good at preventing and treating many infections, so it is galling that we remain stymied in our battle with COVID-19.

The natural world creates new viral genomes by mutation or exchange between two viruses. Some of these viruses escape the surveillance of human immune systems and spread as epidemics or pandemics. What the natural world can mount in the way of threats is greater than anything we could build ourselves, but when a new disease appears, we have an innate tendency to blame other humans, as if nature could not be so clever.  Thus, President Trump and Secretary Pompeo have been blaming the Chinese. But Chinese virologists did not make SARS-CoV2. 

The genome of SARS-CoV2 is almost 30,000 nucleotides long and is arranged in a code that can be translated into the proteins of SARS-CoV2.  On Jan. 9, Chinese virologists deposited the sequence in GenBank, the NIH-sponsored resource for the world’s scientific and medical communities. It had taken them 10 days to sequence and analyze the genome. From that sequence, skilled virologists can make vaccines and begin other studies. Two and a half months into the pandemic, the flow of scientific reports on COVID-19 has become a reassuring flood. 

That the Wuhan Institute of Virology deposited the sequence so fast is not the act of people hiding information. Perhaps the more regressive and suspicious functionaries of the Chinese Government, who had already chastised Dr. Li Wenliang (who described the syndrome and then died from it), probably knew nothing about GenBank. Perhaps (purely my guess) the critical sequence information slipped by them, like a fastball low and away.

How did the pandemic develop? Imagine a person with COVID-19 who infects between two and three other people. Thus R naught is 2-3, compared to flu at 1.3 to 1.4. If everyone is taking maximum precautions, they are both much less. Social distancing, hand washing and staying at home reduce R naught. A good vaccine could reduce it to nearly zero, but that is months away. 

The COVID-19 coronavirus produces many copies of itself that exit a lung cell in little blisters. If replication of the virus is not slowed, the inflammation and cellular destruction that result cause the blood vessels around the alveoli of the lungs to leak. Liquid and the defensive cells of the immune system fill these air sacs and breathing becomes difficult without supplemental oxygen and often a ventilator. Some people recover, but ventilation is often a long haul.

Between now and the appearance of new vaccines, the best we can do, beyond isolation, is to find drugs that slow the virus infection and protect front-line medical staff. There will probably be a new surge of virus in the fall and it would be criminal to ask nurses, doctors and others to return to emergency rooms without much better protection than they have had. 

Drugs that slow viruses similar to SARS-CoV2 exist, and are entering clinical trials quickly. Some, like hydroxyquinoline, don’t work and have been abandoned. Remdesivir blocks the production of the RNA genomes for new viruses. More trials are necessary according to Dr. Anthony Fauci, for whom this is familiar territory from the battle against HIV. Tests of dosage and early use in the course of an infection may make remdesivir more effective. Another drug, baricitinib, blocks the cytokine storms and inflammation that occur days after infection. The NIH is beginning a clinical trial that asks whether the two drugs have additive benefits. Many such experimental treatments with other drugs are being done around the world (see 

Prof. Arturo Casadevall of The Johns Hopkins Bloomberg School of Public Health speaks of layered defenses. What he has in mind is the convalescent antisera of people who have recovered from COVID-19. Francis Collins, Director of the NIH, has noted that almost all patients who have recovered from COVID-19 have circulating antibodies to the virus. This approach to stopping the virus by supplying such antibodies to the circulation has entered clinical trials in the United Kingdom and will soon be in double-blind trials in the United States. Anecdotal evidence (a scientific oxymoron) says that Italian patients benefited. 

It is good to use a layered defense, trying all therapies because there will be a COVID-25, a pandemic flu strain, or a respiratory form of Ebola virus in our future. In this pandemic, we have not performed brilliantly up to now. Science and organization count and we should reinforce them — a lot.

Richard Kessin is Professor Emeritus of Pathology and Cell Biology at the Columbia University Irving Medical Center. He lives in Norfolk and can be reached at

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