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

Abstract 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)...

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Bibliographic Details
Published in:Journal of Venomous Animals and Toxins including Tropical Diseases
Main Authors: Gustavo Ferreira da Mata, Danilo Euclides Fernandes, Eduardo de Paiva Luciano, Gabriel Teixeira Montezuma Sales, Michelle Tiveron Passos Riguetti, Gianna Mastroianni Kirsztajn
Format: Article in Journal/Newspaper
Language:English
Published: SciELO 2021
Subjects:
COVID-19
Glomerulonephritis
Hepatitis B
Hepatitis C
HIV
Inflammasome
SARS-COV-2
Arctic medicine. Tropical medicine
RC955-962
Toxicology. Poisons
RA1190-1270
Zoology
QL1-991
Arctic
Online Access:https://doi.org/10.1590/1678-9199-jvatitd-2020-0154
https://doaj.org/article/851657c3808b438a803693a4caddb7b7
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Summary:Abstract 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.

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