Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV
Autor(a) principal: | |
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Data de Publicação: | 2021 |
Outros Autores: | , , , , |
Tipo de documento: | Artigo |
Idioma: | eng |
Título da fonte: | The Journal of venomous animals and toxins including tropical diseases (Online) |
Texto Completo: | http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1678-91992021000100206 |
Resumo: | 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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Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBVCOVID-19GlomerulonephritisHepatitis BHepatitis CHIVInflammasomeSARS-COV-2Abstract 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.Centro de Estudos de Venenos e Animais Peçonhentos (CEVAP/UNESP)2021-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersiontext/htmlhttp://old.scielo.br/scielo.php?script=sci_arttext&pid=S1678-91992021000100206Journal of Venomous Animals and Toxins including Tropical Diseases v.27 2021reponame:The Journal of venomous animals and toxins including tropical diseases (Online)instname:Universidade Estadual Paulista (UNESP)instacron:UNESP10.1590/1678-9199-jvatitd-2020-0154info:eu-repo/semantics/openAccessMata,Gustavo Ferreira daFernandes,Danilo EuclidesLuciano,Eduardo de PaivaSales,Gabriel Teixeira MontezumaRiguetti,Michelle Tiveron PassosKirsztajn,Gianna Mastroiannieng2021-07-26T00:00:00Zoai:scielo:S1678-91992021000100206Revistahttp://www.scielo.br/jvatitdPUBhttps://old.scielo.br/oai/scielo-oai.php||editorial@jvat.org.br1678-91991678-9180opendoar:2021-07-26T00:00The Journal of venomous animals and toxins including tropical diseases (Online) - Universidade Estadual Paulista (UNESP)false |
dc.title.none.fl_str_mv |
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV |
title |
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV |
spellingShingle |
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV Mata,Gustavo Ferreira da COVID-19 Glomerulonephritis Hepatitis B Hepatitis C HIV Inflammasome SARS-COV-2 |
title_short |
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV |
title_full |
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV |
title_fullStr |
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV |
title_full_unstemmed |
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV |
title_sort |
Inflammation and kidney involvement in human viral diseases caused by SARS-CoV-2, HIV, HCV and HBV |
author |
Mata,Gustavo Ferreira da |
author_facet |
Mata,Gustavo Ferreira da Fernandes,Danilo Euclides Luciano,Eduardo de Paiva Sales,Gabriel Teixeira Montezuma Riguetti,Michelle Tiveron Passos Kirsztajn,Gianna Mastroianni |
author_role |
author |
author2 |
Fernandes,Danilo Euclides Luciano,Eduardo de Paiva Sales,Gabriel Teixeira Montezuma Riguetti,Michelle Tiveron Passos Kirsztajn,Gianna Mastroianni |
author2_role |
author author author author author |
dc.contributor.author.fl_str_mv |
Mata,Gustavo Ferreira da Fernandes,Danilo Euclides Luciano,Eduardo de Paiva Sales,Gabriel Teixeira Montezuma Riguetti,Michelle Tiveron Passos Kirsztajn,Gianna Mastroianni |
dc.subject.por.fl_str_mv |
COVID-19 Glomerulonephritis Hepatitis B Hepatitis C HIV Inflammasome SARS-COV-2 |
topic |
COVID-19 Glomerulonephritis Hepatitis B Hepatitis C HIV Inflammasome SARS-COV-2 |
description |
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. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-01-01 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article |
dc.type.status.fl_str_mv |
info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1678-91992021000100206 |
url |
http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1678-91992021000100206 |
dc.language.iso.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
10.1590/1678-9199-jvatitd-2020-0154 |
dc.rights.driver.fl_str_mv |
info:eu-repo/semantics/openAccess |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
text/html |
dc.publisher.none.fl_str_mv |
Centro de Estudos de Venenos e Animais Peçonhentos (CEVAP/UNESP) |
publisher.none.fl_str_mv |
Centro de Estudos de Venenos e Animais Peçonhentos (CEVAP/UNESP) |
dc.source.none.fl_str_mv |
Journal of Venomous Animals and Toxins including Tropical Diseases v.27 2021 reponame:The Journal of venomous animals and toxins including tropical diseases (Online) instname:Universidade Estadual Paulista (UNESP) instacron:UNESP |
instname_str |
Universidade Estadual Paulista (UNESP) |
instacron_str |
UNESP |
institution |
UNESP |
reponame_str |
The Journal of venomous animals and toxins including tropical diseases (Online) |
collection |
The Journal of venomous animals and toxins including tropical diseases (Online) |
repository.name.fl_str_mv |
The Journal of venomous animals and toxins including tropical diseases (Online) - Universidade Estadual Paulista (UNESP) |
repository.mail.fl_str_mv |
||editorial@jvat.org.br |
_version_ |
1748958541004144640 |