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Postmortem on COVID-19 patients shows extensive alveolar lung damage and scarring, thromboses, viral RNA in lung cells, and syncytial dysmorphism: Lancet

sars-cov-2 virions by EM: NIAID

Lancet, on Nov 3, 2020, published an autopsy report with 41 patients who died of COVID-19 pneumonia. This is a highly technical pathology report that describes new findings in virus-infected tissues.

The autopsies showed lungs with thromboses and a few infarctions, viral RNA in pneumocytes and endotheliocytes, and “a large number of dysmorphic pneumocytes, often forming syncytial elements”– besides extensive scarring. Examination of non-lung tissues showed little or no virus infection in most cases.

The presence of thromboses has been widely reported. Scarring and widespread destruction of alveoli were also universally seen. These features have come to be expected in COVID-19. The severe scarring could account for symptoms of persistent shortness of breath in people who appear to have recovered from the infection.

Dysmorphism and syncytia have not been noted, however. The presence of neovascularization and similar signs of new growth was reported previously, but syncytia are a new and troubling finding. This suggests that the reactive process that occurs in virus-infected tissue includes new growth and abnormal cells.

Another troubling finding is the persistence of viral RNA in the lungs, long after the infection has come under attack by the immune system. Continued production of intact virus and shedding into the airways could mean these patients are still contagious even as they have been ill for weeks and are on the point of expiration.

Here is the “findings” section of the abstract:

COVID-19 is characterized by extensive alveolar damage (41/41 of patients) and thrombosis of the lung micro- and macro-vasculature (29/41, 71%). Thrombi were in different stages of organization, consistent with their local origin. Pneumocytes and endothelial cells contained viral RNA even at the later stages of the disease. An additional feature was the common presence of a large number of dysmorphic pneumocytes, often forming syncytial elements (36/41, 87%). Despite occasional detection of virus-positive cells, no overt signs of viral infection were detected in other organs, which showed non-specific alterations.

In the body of the paper, the authors state that: “They [the findings] support the concept that, different from other forms of interstitial pneumonia and ARDS, the clinical features of COVID-19 patients are not [solely] attributable to extensive DAD, but rather derive from the persistence of infected and dysfunctional cells in the lung.”

In other words, diffuse alveolar damage (DAD) doesn’t explain all the clinical features of COVID-19 pneumonia. Rather, infected, dysfunctional endothelial cells (that form the lung’s inner lining) are causing additional symptoms that account for long-term complications.

The authors say that the dysfunctional cells may explain the development of localized thrombi (blood clots) within the lungs. They blame the syncytial cells on the influence of the “fusogenic S-protein”– that is, the spike protein may cause cells to fuse together.

The paper states that virus-infected or altered cells are largely absent from the rest of the body, despite the findings of studies that showed gastrointestinal (GI) and kidney involvement with at least transient presence of viral RNA in stool and urine.

They propose that the highly inflammatory response that continues in severe infection may be due to the persistence for several weeks of virus-infected, dysfunctional cells in the lungs alone.

The picture that they describe in autopsies suggests that persistence of infection and severe alterations in the lungs, by themselves, can cause the persistence of inflammation and systemic dysfunction through-out the body.

This report is another advance in our understanding of the pathological features of infection with SARS-COV-2 that helps to explain the prolonged nature of the disease in severe cases.

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