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Frank Bures: What we know -- and don't know -- about coronavirus reinfections

Frank Bures: What we know -- and don't know -- about coronavirus reinfections

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The possibility of COVID-19 virus reinfections has become a documented reality.

The SARS-CoV-2 (SC2) is dominating everyone’s lives with deleterious results, medically and economically. Can being infected with it once prevent reinfection? An infection with, even in asymptomatic people, leads to a detectable immune response via antibody levels of different sorts. How protective they are, and the susceptibility of previously infected individuals to reinfection is completely unknown.

The case of the first U.S. person documented was published in the Oct. 12, 2020, British journal Lancet. It was a 25-year-old male from Nevada, who had his first infection beginning on Mar. 25, 2020, with the viral symptoms of sore throat, cough, headache, nausea and diarrhea. He obtained a test on April 18 at a community testing center, which was positive. His symptoms resolved mostly by April 27. He had 2 negative tests on May 9 and 26. He felt fine until May 28, when he had cough, fever, headache, nausea, dizziness and diarrhea again. He was seen at an urgent care center, got a chest x-ray and was sent home. On June 5 he became short of breath, saw a primary doctor, who sent him to an ER, where he received oxygen — AND a new nasal swab test which was positive. It didn’t report whether he was hospitalized, but said this second episode was much worse than the first. He had developed positive SC2 antibodies from the second infection by June 6. Apparently he fully recovered. The genetic or genomic analysis or sequencing of both viral swabs identified two very distinct virus strains of SC2.

The Lancet paper cites four other published cases of reinfection to date, first from Hong Kong, then the Netherlands, Belgium and Ecuador. The Hong Kong patient was a 33-year-old man who contracted his second infection four months after the first. His genomic sequencing found two different strains as well. He had a worse case the second time around, as did the Ecuadorian patient, but not the others. A sixth case may be developing in Australia.

These are the ones we know of. If an infection produces no symptoms, how can you know if it is the first or second illness? The questions are legion about the whole immune response bloody mess, with few sensible answers yet. One conundrum is what viral strains can reinfect. The Wuhan strain was analyzed, and its sequence published in January. As of now all SC2 viruses are thought to have 30,000 little bits of amino acids in their gene chain. They seem to be constantly mutating by substituting one bit here or there. One paper found at least 12,000 mutations on that basis. The mutations’ individual viciousness or virulence is a mystery.

Another unknown factor is the number viruses needed to create an infection, and whether that is proportionate to the amount of symptoms or lack thereof? And, it takes two to tangle (no tangoing here), the viruses plus us. Our individual host response is the other part of the equation.

A study from the University of Vermont published in Clinical and Translational Immunology, Oct. 13, 2020, studied serum samples for antibodies from 32 hospitalized COVID-19 patients and from 17 asymptomatic subjects who had measurable antibodies to SC2. Contrary to expectations from early in the pandemic that assumed sicker patients would have lower antibody levels, the level of antibodies in these folks was higher with the disease severity. It implied they mirrored the severity, but didn’t protect from it, or were reactive but not protective!

In addition, they discovered no differences in a key type of antibody between men and women, even though men are more likely to die from COVID. Surprisingly, many elderly patients, 80 years and above, produced as vigorous an antibody response as 40-year-olds in the study. One researcher opined that this could infer that a vaccine would not need to elicit the highest antibody levels to be effective.

Other parts of our immune system are functioning along with the antibody producing white cells or B lymphocytes. T cells or lymphocytes create the memory of the invader for another time. We can’t measure their status yet. Trying to define such an incredibly complicated subject is futile in this space. As Ed Yong, a brilliant medical writer for The Atlantic magazine put it in an Aug. 5 article, “it’s an absurdly intricate network of cells and molecules that protect us from dangerous viruses and microbes. … Picture a thousand Rube Goldberg machines, some of which are aggressively smashing things to pieces.” Great image!

So, we don’t know how or why reinfections with SC2 can and do occur, but we keep looking and hoping for a vaccine, which won’t be 100% effective but will be a blessing as in other infections if developed correctly! I’ve thought it would be wonderful as well to develop a vaccine to keep our minds and hearts from being infected by the myriad viral like mutations of the truth we’ve heard from so many politicians during this election tsunami, like claiming you’re immune once you’ve had COVID-19.


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