Table 2.

Most important histological lesions observed during autopsy of patients who died from SARS-CoV-2 infection.

Lung	References
Diffuse alveolar damage (histological hallmark of SARS-CoV-2 infection)	[15,16,17,18,19,20,21,22,23,24]
Focal vasculitis and capillaritis associated to microthrombosis as direct viral effect
Thrombosis of large and medium-size pulmonary, related to SARS-COV-2-associated coagulopathy (likely secondary to an endothelial damage related to direct viral infection of the endothelial cells) or deriving from the deep veins of the lower extremities. Superimposed bronchopneumonia as result of bacterial superinfection
Heart
Myocardial damage and myocarditis associated with increase in troponin levels, related to (a) direct myocardial infection by SARS-CoV-2 (b) hypoxemia due to respiratory failure and (c) inflammatory response correlated to the severe systemic inflammation status. Acute vasculitis of the intramyocardial vessels	[25,26,27,28,29,30]
Kidney
Acute tubular injury involving mainly the proximal tubules, probably related to direct infection of kidney by SARS-CoV-2	[30,32]
Skin
Urticarial rashes and papulovesicular exanthems (cause not yet known)	[33,34,35,36,37,38,39,40]
Livedoid purple lesions and acrocyanosis
Kawasaki disease
Central Nervous System
Aspecific acute hypoxic damage in the brain and cerebellum (molecular test in sections of brain tissue were positive for the virus, but not immunohistochemistry)	[41]
Liver
Sinusoidal dilatation with lymphocytic infiltration and steatosis (cause not yet known)	[20]
Adrenal
Acute fibrinoid necrosis of arterioles (cause not yet known)	[42]
Testis
Seminiferous tubular injury, mild lymphocytic inflammation (cause not yet known)	[43]