The China Health Authority alerted the World Health Organization (WHO) on December 31 2019, to several cases of pneumonia of unknown aetiology in Wuhan City in Hubei Province in central China. Since December 8, 2019, these cases had been reported, worked at or lived around the local Huanan Seafood Market.

Radiology finding may vary with patients age, disease progression, immunity status, comorbidity, and initial medical intervention. In a study describing 41 of the initial cases of 2019-nCoV infection, all 41 patients had pneumonia with abnormal findings on chest computed tomography (CT-scan). Abnormalities on chest CT-scan were also seen in another study of 6 cases, in which all of them showed multifocal patchy ground-glass opacities notably nearby the peripheral sections of the lungs.

Complete autopsy studies were almost nonexistent in the initial phases of the outbreak; reasonably so, due to concerns related to infectivity, transmission rates, and biosafety. The few reports initially published were limited to postmortem biopsies in COVID-19–positive patients or from lobectomy specimens initially resected for lung adenocarcinoma, but patients were later found to be COVID-19–positive (7). Pathologic features of exudative and proliferative phases of diffuse alveolar damage (DAD) were noted in these initial reports and overlapping features with SARS were also noted. Later complete autopsies performed in United States further supported the presence of DAD.

The predominant pattern of lung lesions in COVID-19 patients is DAD, as described for the other two coronavirus that infect humans, SARS-CoV and MERSCoV. Hyaline membrane formation and pneumocyte atypical hyperplasia are frequently found. The main relevant finding is the presence of platelet-fibrin thrombi in small arterial vessels; this important observation fits into the clinical context of coagulopathy which dominates in these patients and which is one of the main targets of therapy.

The macroscopic features of COVID-19 are likely to be in the chest and may include pleurisy, pericarditis, lung consolidation and pulmonary oedema. Lung weight may be increased above normal. It should be noted a secondary infection may be superimposed on the viral infection that can lead to purulent inflammation more typical of bacterial infection.

The pulmonary histologic characteristics of COVID-19 resembled those observed in diseases caused by other Betacoronavirus infections such as severe acute respiratory syndrome4 and Middle East respiratory syndrome.

Histopathology of the lungs showed diffuse alveolar damage, consistent with early acute respiratory distress syndrome in 8 cases. Predominant findings were hyaline membranes, activated pneumocytes, microvascular thromboemboli, capillary congestion, and proteinenriched interstitial edema. As described by Wang and colleagues, a moderate degree of inflammatory infiltrates concurred with clinically described leukopenia in patients with COVID-19 and predominant infiltration of lymphocytes fit the picture of a viral pathogenesis.