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Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV

Gustavo Ferreira da Mata1, Danilo Euclides Fernandes1, Eduardo de Paiva Luciano1, Gabriel Teixeira Montezuma Sales1, Michelle Tiveron Passos Riguetti1 , Gianna Mastroianni Kirsztajn1 [ + show more ]

J Venom Anim Toxins incl Trop Dis, 2021, 27:e20200154
Received: 17 November 2020 | Accepted: 01 March 2021 | Published online: 28 July 2021
Collection: Inflammation: from bench to bedside


Inflammation is closely related to renal diseases. This is particularly true for renal diseases caused by infections as in viral diseases. In this review, we highlight the inflammatory mechanisms that underlie kidney dysfunction in SARS-CoV-2, human immunodeficiency (HIV), hepatitis C (HCV), and hepatitis B (HBV) infections. The pathophysiology of renal involvement in COVID-19 is complex, but kidney damage is frequent, and the prognosis is worse when it happens. Virus-like particles were demonstrated mostly in renal tubular epithelial cells and podocytes, which suggest that SARS-CoV-2 directly affects the kidneys. SARS-CoV-2 uses the angiotensin-converting enzyme 2 receptor, which is found in endothelial cells, to infect the human host cells. Critical patients with SARS-CoV-2-associated acute kidney injury (AKI) show an increase in inflammatory cytokines (IL-1β, IL-8, IFN-γ, TNF-α), known as cytokine storm that favors renal dysfunction by causing intrarenal inflammation, increased vascular permeability, volume depletion, thromboembolic events in microvasculature and persistent local inflammation. Besides AKI, SARS-CoV-2 can also cause glomerular disease, as other viral infections such as in HIV, HBV and HCV. HIV-infected patients present chronic inflammation that can lead to a number of renal diseases. Proinflammatory cytokines and TNF-induced apoptosis are some of the underlying mechanisms that may explain the virus-induced renal diseases that are here reviewed.


Keywords: COVID-19; Glomerulonephritis; Hepatitis B; Hepatitis C; HIV; Inflammasome; SARS-CoV-2.

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