Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner.
Junín virus (JUNV), an arenavirus, is the causative agent of Argentine hemorrhagic fever, an infectious human disease with 15-30% case fatality. The pathogenesis of AHF is still not well understood. Elevated levels of interferon and cytokines are reported in AHF patients, which might be correlated t...
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ftdoajarticles:oai:doaj.org/article:f483370b4ed0431aa15c643db0501333 2023-05-15T15:13:10+02:00 Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner. Cheng Huang Olga A Kolokoltsova Nadezdha E Yun Alexey V Seregin Allison L Poussard Aida G Walker Allan R Brasier Yingxin Zhao Bing Tian Juan Carlos de la Torre Slobodan Paessler 2012-01-01T00:00:00Z https://doi.org/10.1371/journal.pntd.0001659 https://doaj.org/article/f483370b4ed0431aa15c643db0501333 EN eng Public Library of Science (PLoS) http://europepmc.org/articles/PMC3358329?pdf=render https://doaj.org/toc/1935-2727 https://doaj.org/toc/1935-2735 1935-2727 1935-2735 doi:10.1371/journal.pntd.0001659 https://doaj.org/article/f483370b4ed0431aa15c643db0501333 PLoS Neglected Tropical Diseases, Vol 6, Iss 5, p e1659 (2012) Arctic medicine. Tropical medicine RC955-962 Public aspects of medicine RA1-1270 article 2012 ftdoajarticles https://doi.org/10.1371/journal.pntd.0001659 2022-12-31T05:44:55Z Junín virus (JUNV), an arenavirus, is the causative agent of Argentine hemorrhagic fever, an infectious human disease with 15-30% case fatality. The pathogenesis of AHF is still not well understood. Elevated levels of interferon and cytokines are reported in AHF patients, which might be correlated to the severity of the disease. However the innate immune response to JUNV infection has not been well evaluated. Previous studies have suggested that the virulent strain of JUNV does not induce IFN in human macrophages and monocytes, whereas the attenuated strain of JUNV was found to induce IFN response in murine macrophages via the TLR-2 signaling pathway. In this study, we investigated the interaction between JUNV and IFN pathway in human epithelial cells highly permissive to JUNV infection. We have determined the expression pattern of interferon-stimulated genes (ISGs) and IFN-β at both mRNA and protein levels during JUNV infection. Our results clearly indicate that JUNV infection activates the type I IFN response. STAT1 phosphorylation, a downstream marker of activation of IFN signaling pathway, was readily detected in JUNV infected IFN-competent cells. Our studies also demonstrated for the first time that RIG-I was required for IFN production during JUNV infection. IFN activation was detected during infection by either the virulent or attenuated vaccine strain of JUNV. Curiously, both virus strains were relatively insensitive to human IFN treatment. Our studies collectively indicated that JUNV infection could induce host type I IFN response and provided new insights into the interaction between JUNV and host innate immune system, which might be important in future studies on vaccine development and antiviral treatment. Article in Journal/Newspaper Arctic Directory of Open Access Journals: DOAJ Articles Arctic Argentine PLoS Neglected Tropical Diseases 6 5 e1659 |
institution |
Open Polar |
collection |
Directory of Open Access Journals: DOAJ Articles |
op_collection_id |
ftdoajarticles |
language |
English |
topic |
Arctic medicine. Tropical medicine RC955-962 Public aspects of medicine RA1-1270 |
spellingShingle |
Arctic medicine. Tropical medicine RC955-962 Public aspects of medicine RA1-1270 Cheng Huang Olga A Kolokoltsova Nadezdha E Yun Alexey V Seregin Allison L Poussard Aida G Walker Allan R Brasier Yingxin Zhao Bing Tian Juan Carlos de la Torre Slobodan Paessler Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner. |
topic_facet |
Arctic medicine. Tropical medicine RC955-962 Public aspects of medicine RA1-1270 |
description |
Junín virus (JUNV), an arenavirus, is the causative agent of Argentine hemorrhagic fever, an infectious human disease with 15-30% case fatality. The pathogenesis of AHF is still not well understood. Elevated levels of interferon and cytokines are reported in AHF patients, which might be correlated to the severity of the disease. However the innate immune response to JUNV infection has not been well evaluated. Previous studies have suggested that the virulent strain of JUNV does not induce IFN in human macrophages and monocytes, whereas the attenuated strain of JUNV was found to induce IFN response in murine macrophages via the TLR-2 signaling pathway. In this study, we investigated the interaction between JUNV and IFN pathway in human epithelial cells highly permissive to JUNV infection. We have determined the expression pattern of interferon-stimulated genes (ISGs) and IFN-β at both mRNA and protein levels during JUNV infection. Our results clearly indicate that JUNV infection activates the type I IFN response. STAT1 phosphorylation, a downstream marker of activation of IFN signaling pathway, was readily detected in JUNV infected IFN-competent cells. Our studies also demonstrated for the first time that RIG-I was required for IFN production during JUNV infection. IFN activation was detected during infection by either the virulent or attenuated vaccine strain of JUNV. Curiously, both virus strains were relatively insensitive to human IFN treatment. Our studies collectively indicated that JUNV infection could induce host type I IFN response and provided new insights into the interaction between JUNV and host innate immune system, which might be important in future studies on vaccine development and antiviral treatment. |
format |
Article in Journal/Newspaper |
author |
Cheng Huang Olga A Kolokoltsova Nadezdha E Yun Alexey V Seregin Allison L Poussard Aida G Walker Allan R Brasier Yingxin Zhao Bing Tian Juan Carlos de la Torre Slobodan Paessler |
author_facet |
Cheng Huang Olga A Kolokoltsova Nadezdha E Yun Alexey V Seregin Allison L Poussard Aida G Walker Allan R Brasier Yingxin Zhao Bing Tian Juan Carlos de la Torre Slobodan Paessler |
author_sort |
Cheng Huang |
title |
Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner. |
title_short |
Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner. |
title_full |
Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner. |
title_fullStr |
Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner. |
title_full_unstemmed |
Junín virus infection activates the type I interferon pathway in a RIG-I-dependent manner. |
title_sort |
junín virus infection activates the type i interferon pathway in a rig-i-dependent manner. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2012 |
url |
https://doi.org/10.1371/journal.pntd.0001659 https://doaj.org/article/f483370b4ed0431aa15c643db0501333 |
geographic |
Arctic Argentine |
geographic_facet |
Arctic Argentine |
genre |
Arctic |
genre_facet |
Arctic |
op_source |
PLoS Neglected Tropical Diseases, Vol 6, Iss 5, p e1659 (2012) |
op_relation |
http://europepmc.org/articles/PMC3358329?pdf=render https://doaj.org/toc/1935-2727 https://doaj.org/toc/1935-2735 1935-2727 1935-2735 doi:10.1371/journal.pntd.0001659 https://doaj.org/article/f483370b4ed0431aa15c643db0501333 |
op_doi |
https://doi.org/10.1371/journal.pntd.0001659 |
container_title |
PLoS Neglected Tropical Diseases |
container_volume |
6 |
container_issue |
5 |
container_start_page |
e1659 |
_version_ |
1766343755722391552 |