Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2021 Jul 28:27:e20200154.
doi: 10.1590/1678-9199-JVATITD-2020-0154. eCollection 2021.

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

Affiliations
Review

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

Gustavo Ferreira da Mata et al. J Venom Anim Toxins Incl Trop Dis. .

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.

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

PubMed Disclaimer

Conflict of interest statement

Competing interests: The authors declare that they have no competing interests.

Figures

Figure 1.
Figure 1.. Article selection flow chart. HIV: human immune deficiency virus; HBV: hepatitis B virus; HCV: hepatitis C virus.

References

    1. Andrade-Oliveira V, Foresto-Neto O, Watanabe IKM, Zatz R, Câmara NOS. Inflammation in renal diseases: new and old players. Front Pharmacol. 2019;10:1192. - PMC - PubMed
    1. Xiong W, Meng X-F, Zhang C. Inflammasome activation in podocytes: a new mechanism of glomerular diseases. Inflamm Res. 2020;69(8):731–743. - PubMed
    1. Chi K, Geng X, Liu C, Cai G, Hong Q. Research progress on the role of inflammasomes in kidney disease. Mediators Inflamm. 2020;2020:1–9. - PMC - PubMed
    1. Gu Y-Y, Liu X-S, Huang X-R, Yu X-Q, Lan H-Y. Diverse role of TGF-β in kidney disease. Front Cell Dev Biol. 2020;8:123. - PMC - PubMed
    1. Zhu N, Zhang D, Wang W, Li X, Yang B, Song J, et al. A novel Coronavirus from patients with pneumonia in China, 2019. N Engl J Med. 2020;382(8):727–733. - PMC - PubMed

LinkOut - more resources