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A cohort autopsy study defines COVID-19 systemic pathogenesis #MMPMID34135479
Yao XH; Luo T; Shi Y; He ZC; Tang R; Zhang PP; Cai J; Zhou XD; Jiang DP; Fei XC; Huang XQ; Zhao L; Zhang H; Wu HB; Ren Y; Liu ZH; Zhang HR; Chen C; Fu WJ; Li H; Xia XY; Chen R; Wang Y; Liu XD; Yin CL; Yan ZX; Wang J; Jing R; Li TS; Li WQ; Wang CF; Ding YQ; Mao Q; Zhang DY; Zhang SY; Ping YF; Bian XW
Cell Res 2021[Aug]; 31 (8): 836-846 PMID34135479show ga
Severe COVID-19 disease caused by SARS-CoV-2 is frequently accompanied by dysfunction of the lungs and extrapulmonary organs. However, the organotropism of SARS-CoV-2 and the port of virus entry for systemic dissemination remain largely unknown. We profiled 26 COVID-19 autopsy cases from four cohorts in Wuhan, China, and determined the systemic distribution of SARS-CoV-2. SARS-CoV-2 was detected in the lungs and multiple extrapulmonary organs of critically ill COVID-19 patients up to 67 days after symptom onset. Based on organotropism and pathological features of the patients, COVID-19 was divided into viral intrapulmonary and systemic subtypes. In patients with systemic viral distribution, SARS-CoV-2 was detected in monocytes, macrophages, and vascular endothelia at blood-air barrier, blood-testis barrier, and filtration barrier. Critically ill patients with long disease duration showed decreased pulmonary cell proliferation, reduced viral RNA, and marked fibrosis in the lungs. Permanent SARS-CoV-2 presence and tissue injuries in the lungs and extrapulmonary organs suggest direct viral invasion as a mechanism of pathogenicity in critically ill patients. SARS-CoV-2 may hijack monocytes, macrophages, and vascular endothelia at physiological barriers as the ports of entry for systemic dissemination. Our study thus delineates systemic pathological features of SARS-CoV-2 infection, which sheds light on the development of novel COVID-19 treatment.