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Modulation of Host Immune Response Is an Alternative Strategy to Combat SARS-CoV-2 Pathogenesis
The novel SARS-CoV-2virus that caused the disease COVID-19 is currently a pandemic worldwide. The virus requires an alveolar type-2 pneumocyte in the host to initiate its life cycle. The viral S1 spike protein helps in the attachment of the virus on toACE-2 receptors present on type-2 pneumocytes, a...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8296981/ https://www.ncbi.nlm.nih.gov/pubmed/34305892 http://dx.doi.org/10.3389/fimmu.2021.660632 |
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author | Singh, Lakhveer Bajaj, Sakshi Gadewar, Manoj Verma, Nitin Ansari, Mohd Nazam Saeedan, Abdulaziz S. Kaithwas, Gaurav Singh, Manjari |
author_facet | Singh, Lakhveer Bajaj, Sakshi Gadewar, Manoj Verma, Nitin Ansari, Mohd Nazam Saeedan, Abdulaziz S. Kaithwas, Gaurav Singh, Manjari |
author_sort | Singh, Lakhveer |
collection | PubMed |
description | The novel SARS-CoV-2virus that caused the disease COVID-19 is currently a pandemic worldwide. The virus requires an alveolar type-2 pneumocyte in the host to initiate its life cycle. The viral S1 spike protein helps in the attachment of the virus on toACE-2 receptors present on type-2 pneumocytes, and the S2 spike protein helps in the fusion of the viral membrane with the host membrane. Fusion of the SARS-CoV-2virus and host membrane is followed by entry of viral RNA into the host cells which is directly translated into the replicase-transcriptase complex (RTC) following viral RNA and structural protein syntheses. As the virus replicates within type-2 pneumocytes, the host immune system is activated and alveolar macrophages start secreting cytokines and chemokines, acting as an inflammatory mediator, and chemotactic neutrophils, monocytes, natural NK cells, and CD8+ T cells initiate the local phagocytosis of infected cells. It is not the virus that kills COVID-19 patients; instead, the aberrant host immune response kills them. Modifying the response from the host immune system could reduce the high mortality due to SARS-CoV-2 infection. The present study examines the viral life cycle intype-2 pneumocytes and resultant host immune response along with possible therapeutic targets. |
format | Online Article Text |
id | pubmed-8296981 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82969812021-07-23 Modulation of Host Immune Response Is an Alternative Strategy to Combat SARS-CoV-2 Pathogenesis Singh, Lakhveer Bajaj, Sakshi Gadewar, Manoj Verma, Nitin Ansari, Mohd Nazam Saeedan, Abdulaziz S. Kaithwas, Gaurav Singh, Manjari Front Immunol Immunology The novel SARS-CoV-2virus that caused the disease COVID-19 is currently a pandemic worldwide. The virus requires an alveolar type-2 pneumocyte in the host to initiate its life cycle. The viral S1 spike protein helps in the attachment of the virus on toACE-2 receptors present on type-2 pneumocytes, and the S2 spike protein helps in the fusion of the viral membrane with the host membrane. Fusion of the SARS-CoV-2virus and host membrane is followed by entry of viral RNA into the host cells which is directly translated into the replicase-transcriptase complex (RTC) following viral RNA and structural protein syntheses. As the virus replicates within type-2 pneumocytes, the host immune system is activated and alveolar macrophages start secreting cytokines and chemokines, acting as an inflammatory mediator, and chemotactic neutrophils, monocytes, natural NK cells, and CD8+ T cells initiate the local phagocytosis of infected cells. It is not the virus that kills COVID-19 patients; instead, the aberrant host immune response kills them. Modifying the response from the host immune system could reduce the high mortality due to SARS-CoV-2 infection. The present study examines the viral life cycle intype-2 pneumocytes and resultant host immune response along with possible therapeutic targets. Frontiers Media S.A. 2021-07-08 /pmc/articles/PMC8296981/ /pubmed/34305892 http://dx.doi.org/10.3389/fimmu.2021.660632 Text en Copyright © 2021 Singh, Bajaj, Gadewar, Verma, Ansari, Saeedan, Kaithwas and Singh https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Singh, Lakhveer Bajaj, Sakshi Gadewar, Manoj Verma, Nitin Ansari, Mohd Nazam Saeedan, Abdulaziz S. Kaithwas, Gaurav Singh, Manjari Modulation of Host Immune Response Is an Alternative Strategy to Combat SARS-CoV-2 Pathogenesis |
title | Modulation of Host Immune Response Is an Alternative Strategy to Combat SARS-CoV-2 Pathogenesis |
title_full | Modulation of Host Immune Response Is an Alternative Strategy to Combat SARS-CoV-2 Pathogenesis |
title_fullStr | Modulation of Host Immune Response Is an Alternative Strategy to Combat SARS-CoV-2 Pathogenesis |
title_full_unstemmed | Modulation of Host Immune Response Is an Alternative Strategy to Combat SARS-CoV-2 Pathogenesis |
title_short | Modulation of Host Immune Response Is an Alternative Strategy to Combat SARS-CoV-2 Pathogenesis |
title_sort | modulation of host immune response is an alternative strategy to combat sars-cov-2 pathogenesis |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8296981/ https://www.ncbi.nlm.nih.gov/pubmed/34305892 http://dx.doi.org/10.3389/fimmu.2021.660632 |
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