Revisiting Extrapulmonary Lesions in COVID-19

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6 2 月, 2026

On 6 2 月, 2026

Introduction:

Since December 2019, multiple cases of viral pneumonia have been identified in Wuhan, Hubei Province. Through related virus typing tests, it was confirmed to be caused by a novel coronavirus. On January 12, 2020, WHO temporarily named it “2019 Novel Coronavirus (2019-nCoV)”. Later, the Coronavirus Study Group of the International Committee on Taxonomy of Viruses officially named it “SARS-CoV-2”. On February 7, China’s National Health Commission named the pneumonia caused by this virus as “Novel Coronavirus Pneumonia (NCP)”, abbreviated as COVID-19.

On February 11, WHO officially named the disease caused by the novel coronavirus as “COVID-19”, which stands for Coronavirus Disease 2019. Its meaning extends beyond pneumonia and may better reflect the actual situation of SARS-CoV-2 infection, as the lesions caused by this virus are not limited to the lungs.

In the article “Several Suggestions for Autopsy Research on Novel Coronavirus Pneumonia—Also Discussing Extrapulmonary Organ Lesions” (February 19, 2020), the author, referencing autopsy results of SARS and MERS, speculated on possible extrapulmonary lesions in COVID-19 and recommended that autopsy examiners pay attention to them. According to preliminary reports from over 30 domestic COVID-19 autopsies, the disease primarily affects the lungs (see “Revisiting the Pathological Changes of Novel Coronavirus Pneumonia”, March 27, 2020), but there are indeed varying types and degrees of lesions outside the lungs.

The first to draw attention are lesions in the lymphoid and hematopoietic tissues. In COVID-19 autopsies, it was found that the spleen volume may shrink, lymphocyte count decreases, splenic sinus congestion, focal hemorrhagic necrosis, macrophage proliferation in the spleen with visible phagocytosis. Lymph nodes may show no significant changes, or decreased lymphocyte count, or histiocytic necrosis. Immunohistochemistry shows reduced CD4+ and CD8+ T cells in the spleen and lymph nodes, suggesting cellular immune function impairment, the mechanism of which remains to be further elucidated. These manifestations are similar to those seen in SARS.

During viremia, other organs also exhibit varying degrees of lesions. Currently discovered: ① Liver volume increases, dark red. Hepatocyte steatosis, hepatic sinus congestion, focal necrosis with neutrophil infiltration, mild inflammatory reaction in the portal area with lymphocyte and monocyte infiltration, or microthrombus formation. ② Myocardial cells show degeneration, necrosis, interstitial infiltration of a small number of monocytes, lymphocytes and/or neutrophils, also visible partial vascular endothelial cell detachment, endarteritis and thrombosis. ③ Proteinaceous exudate visible in the glomerular capsular space, renal tubular epithelial cell degeneration, necrosis, detachment, hyaline casts may form in renal tubules, interstitial congestion, sometimes microthrombi and focal fibrosis. ④ Other tissues also show varying degrees of lesions, such as cerebral congestion and edema, neuronal degeneration, adrenal focal necrosis, varying degrees of degeneration, necrosis, and detachment of esophageal and gastrointestinal mucosal epithelium. These lesions roughly correspond to interstitial inflammation caused by viral infection, and may also be drug reactions during treatment. The most direct and reliable evidence of viral pathogenicity is the in-situ detection of viral inclusion bodies, nucleic acids, or antigen components in the lesions. The target cells of SARS-CoV-2 outside the lungs remain undetermined and require verification in autopsy materials.

Whether COVID-19 has concurrent or secondary other infections, such as bacterial pneumonia, pulmonary aspergillosis, or cytomegalovirus infection seen in SARS autopsies, awaits further findings from autopsy data. Additionally, some lesions may be caused by underlying diseases, such as pulmonary interstitial fibrosis, myocardial infarction, glomerular lesions, etc., which need careful differentiation; not all lesions can be attributed solely to SARS-CoV-2 infection.

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