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SARS-CoV-2 proteins and anti-COVID-19 drugs induce lytic reactivation of an oncogenic virus
An outbreak of the novel coronavirus SARS-CoV-2, the causative agent of Coronavirus Disease-2019 (COVID-19), a respiratory disease, has infected almost one hundred million people since the end of 2019, killed over two million, and caused worldwide social and economic disruption. Because the mechanis...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8175744/ https://www.ncbi.nlm.nih.gov/pubmed/34083759 http://dx.doi.org/10.1038/s42003-021-02220-z |
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author | Chen, Jungang Dai, Lu Barrett, Lindsey James, Jennifer Plaisance-Bonstaff, Karlie Post, Steven R. Qin, Zhiqiang |
author_facet | Chen, Jungang Dai, Lu Barrett, Lindsey James, Jennifer Plaisance-Bonstaff, Karlie Post, Steven R. Qin, Zhiqiang |
author_sort | Chen, Jungang |
collection | PubMed |
description | An outbreak of the novel coronavirus SARS-CoV-2, the causative agent of Coronavirus Disease-2019 (COVID-19), a respiratory disease, has infected almost one hundred million people since the end of 2019, killed over two million, and caused worldwide social and economic disruption. Because the mechanisms of SARS-CoV-2 infection of host cells and its pathogenesis remain largely unclear, there are currently no antiviral drugs with proven efficacy. Besides severe respiratory and systematic symptoms, several comorbidities increase risk of fatal disease outcome. Therefore, it is required to investigate the impacts of COVID-19 on pre-existing diseases of patients, such as cancer and other infectious diseases. In the current study, we report that SARS-CoV-2 encoded proteins and some currently used anti-COVID-19 drugs are able to induce lytic reactivation of Kaposi’s sarcoma-associated herpesvirus (KSHV), one of major human oncogenic viruses, through manipulation of intracellular signaling pathways. Our data indicate that those KSHV + patients especially in endemic areas exposure to COVID-19 or undergoing the treatment may have increased risks to develop virus-associated cancers, even after they have fully recovered from COVID-19. |
format | Online Article Text |
id | pubmed-8175744 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-81757442021-06-07 SARS-CoV-2 proteins and anti-COVID-19 drugs induce lytic reactivation of an oncogenic virus Chen, Jungang Dai, Lu Barrett, Lindsey James, Jennifer Plaisance-Bonstaff, Karlie Post, Steven R. Qin, Zhiqiang Commun Biol Article An outbreak of the novel coronavirus SARS-CoV-2, the causative agent of Coronavirus Disease-2019 (COVID-19), a respiratory disease, has infected almost one hundred million people since the end of 2019, killed over two million, and caused worldwide social and economic disruption. Because the mechanisms of SARS-CoV-2 infection of host cells and its pathogenesis remain largely unclear, there are currently no antiviral drugs with proven efficacy. Besides severe respiratory and systematic symptoms, several comorbidities increase risk of fatal disease outcome. Therefore, it is required to investigate the impacts of COVID-19 on pre-existing diseases of patients, such as cancer and other infectious diseases. In the current study, we report that SARS-CoV-2 encoded proteins and some currently used anti-COVID-19 drugs are able to induce lytic reactivation of Kaposi’s sarcoma-associated herpesvirus (KSHV), one of major human oncogenic viruses, through manipulation of intracellular signaling pathways. Our data indicate that those KSHV + patients especially in endemic areas exposure to COVID-19 or undergoing the treatment may have increased risks to develop virus-associated cancers, even after they have fully recovered from COVID-19. Nature Publishing Group UK 2021-06-03 /pmc/articles/PMC8175744/ /pubmed/34083759 http://dx.doi.org/10.1038/s42003-021-02220-z Text en © The Author(s) 2021 https://creativecommons.org/licenses/by/4.0/Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Article Chen, Jungang Dai, Lu Barrett, Lindsey James, Jennifer Plaisance-Bonstaff, Karlie Post, Steven R. Qin, Zhiqiang SARS-CoV-2 proteins and anti-COVID-19 drugs induce lytic reactivation of an oncogenic virus |
title | SARS-CoV-2 proteins and anti-COVID-19 drugs induce lytic reactivation of an oncogenic virus |
title_full | SARS-CoV-2 proteins and anti-COVID-19 drugs induce lytic reactivation of an oncogenic virus |
title_fullStr | SARS-CoV-2 proteins and anti-COVID-19 drugs induce lytic reactivation of an oncogenic virus |
title_full_unstemmed | SARS-CoV-2 proteins and anti-COVID-19 drugs induce lytic reactivation of an oncogenic virus |
title_short | SARS-CoV-2 proteins and anti-COVID-19 drugs induce lytic reactivation of an oncogenic virus |
title_sort | sars-cov-2 proteins and anti-covid-19 drugs induce lytic reactivation of an oncogenic virus |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8175744/ https://www.ncbi.nlm.nih.gov/pubmed/34083759 http://dx.doi.org/10.1038/s42003-021-02220-z |
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