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Porcine IFITM1 is a host restriction factor that inhibits pseudorabies virus infection
Interferon-inducible transmembrane proteins (IFITMs) restrict infection by several viruses, such as influenza A virus, West Nile virus and dengue virus. It has not been determined whether porcine IFITMs (pIFITMs) inhibit infection by pseudorabies virus (PRV), an enveloped, double-stranded DNA virus,...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Authors. Published by Elsevier B.V.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102536/ https://www.ncbi.nlm.nih.gov/pubmed/31743714 http://dx.doi.org/10.1016/j.ijbiomac.2019.10.162 |
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author | Wang, Jiang Wang, Chun-Feng Ming, Sheng-Li Li, Guo-Li Zeng, Lei Wang, Meng-Di Su, Bing-Qian Wang, Qi Yang, Guo-Yu Chu, Bei-Bei |
author_facet | Wang, Jiang Wang, Chun-Feng Ming, Sheng-Li Li, Guo-Li Zeng, Lei Wang, Meng-Di Su, Bing-Qian Wang, Qi Yang, Guo-Yu Chu, Bei-Bei |
author_sort | Wang, Jiang |
collection | PubMed |
description | Interferon-inducible transmembrane proteins (IFITMs) restrict infection by several viruses, such as influenza A virus, West Nile virus and dengue virus. It has not been determined whether porcine IFITMs (pIFITMs) inhibit infection by pseudorabies virus (PRV), an enveloped, double-stranded DNA virus, which is the etiological agent of Aujeszky’s disease in pigs. Here, we report that PRV infection elicited pIFITM1 expression in PK15 porcine kidney epithelial cells and 3D4/21 alveolar macrophages. pIFITM2 and pIFITM3 expression was only elevated in PK15 cells during PRV infection. Depletion of pIFITM1 using RNA interference, either in PK15 or in 3D4/21 cells, enhanced PRV infection while overexpression of pIFITM1 had the opposite effect. Knockdown of pIFITM2 and pIFITM3 did not influence PRV infection, suggesting that pIFITM2 and pIFITM3 are independent of PRV infection. PRV-induced pIFITM1 expression was dependent on the cGAS/STING/TBK1/IRF3 innate immune pathway and interferon-alpha receptor-1, suggesting that pIFITM1 is up-regulated by the type I interferon signaling pathway. The anti-PRV role of pIFITM1 was inhibited upon PRV entry. Our data demonstrate that pIFITM1 is a host restriction factor that inhibits PRV entry that may shed light on a strategy for prevention of PRV infection. |
format | Online Article Text |
id | pubmed-7102536 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | The Authors. Published by Elsevier B.V. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71025362020-03-31 Porcine IFITM1 is a host restriction factor that inhibits pseudorabies virus infection Wang, Jiang Wang, Chun-Feng Ming, Sheng-Li Li, Guo-Li Zeng, Lei Wang, Meng-Di Su, Bing-Qian Wang, Qi Yang, Guo-Yu Chu, Bei-Bei Int J Biol Macromol Article Interferon-inducible transmembrane proteins (IFITMs) restrict infection by several viruses, such as influenza A virus, West Nile virus and dengue virus. It has not been determined whether porcine IFITMs (pIFITMs) inhibit infection by pseudorabies virus (PRV), an enveloped, double-stranded DNA virus, which is the etiological agent of Aujeszky’s disease in pigs. Here, we report that PRV infection elicited pIFITM1 expression in PK15 porcine kidney epithelial cells and 3D4/21 alveolar macrophages. pIFITM2 and pIFITM3 expression was only elevated in PK15 cells during PRV infection. Depletion of pIFITM1 using RNA interference, either in PK15 or in 3D4/21 cells, enhanced PRV infection while overexpression of pIFITM1 had the opposite effect. Knockdown of pIFITM2 and pIFITM3 did not influence PRV infection, suggesting that pIFITM2 and pIFITM3 are independent of PRV infection. PRV-induced pIFITM1 expression was dependent on the cGAS/STING/TBK1/IRF3 innate immune pathway and interferon-alpha receptor-1, suggesting that pIFITM1 is up-regulated by the type I interferon signaling pathway. The anti-PRV role of pIFITM1 was inhibited upon PRV entry. Our data demonstrate that pIFITM1 is a host restriction factor that inhibits PRV entry that may shed light on a strategy for prevention of PRV infection. The Authors. Published by Elsevier B.V. 2020-05-15 2019-11-16 /pmc/articles/PMC7102536/ /pubmed/31743714 http://dx.doi.org/10.1016/j.ijbiomac.2019.10.162 Text en © 2019 The Authors Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Wang, Jiang Wang, Chun-Feng Ming, Sheng-Li Li, Guo-Li Zeng, Lei Wang, Meng-Di Su, Bing-Qian Wang, Qi Yang, Guo-Yu Chu, Bei-Bei Porcine IFITM1 is a host restriction factor that inhibits pseudorabies virus infection |
title | Porcine IFITM1 is a host restriction factor that inhibits pseudorabies virus infection |
title_full | Porcine IFITM1 is a host restriction factor that inhibits pseudorabies virus infection |
title_fullStr | Porcine IFITM1 is a host restriction factor that inhibits pseudorabies virus infection |
title_full_unstemmed | Porcine IFITM1 is a host restriction factor that inhibits pseudorabies virus infection |
title_short | Porcine IFITM1 is a host restriction factor that inhibits pseudorabies virus infection |
title_sort | porcine ifitm1 is a host restriction factor that inhibits pseudorabies virus infection |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102536/ https://www.ncbi.nlm.nih.gov/pubmed/31743714 http://dx.doi.org/10.1016/j.ijbiomac.2019.10.162 |
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