Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons production
<p>Abstract</p> <p>Background</p> <p>Recent studies have revealed that Mitochondrial Antiviral Signaling (MAVS) protein plays an essential role in the inhibition of viral infection through type I interferon (IFN) pathway. It has been shown that 3C (pro) cysteine proteas...
| Main Authors: | , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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BMC
2012-12-01
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| Series: | Virology Journal |
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| Online Access: | http://www.virologyj.com/content/9/1/312 |
| _version_ | 1818066353954750464 |
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| author | Zhang Qing-Meng Song Wu-Qi Li Yu-Jun Qian Jun Zhai Ai-Xia Wu Jing Li Ai-Mei He Jun-Ming Zhao Jin-Yun Yu Xin Wei Lan-Lan Zhang Feng-Min |
| author_facet | Zhang Qing-Meng Song Wu-Qi Li Yu-Jun Qian Jun Zhai Ai-Xia Wu Jing Li Ai-Mei He Jun-Ming Zhao Jin-Yun Yu Xin Wei Lan-Lan Zhang Feng-Min |
| author_sort | Zhang Qing-Meng |
| collection | DOAJ |
| description | <p>Abstract</p> <p>Background</p> <p>Recent studies have revealed that Mitochondrial Antiviral Signaling (MAVS) protein plays an essential role in the inhibition of viral infection through type I interferon (IFN) pathway. It has been shown that 3C (pro) cysteine protease of coxsackievirus B3 (CVB3) cleaves MAVS to inhibit type I IFNs induction. Other workers also found that MAVS knock-out mice suffered CVB3 susceptibility and severe histopathological change. Accordingly,our experiments were designed to explore the protection of over-expressing MAVS against CVB3 infection and the possible mechanism.</p> <p>Results</p> <p>In this study, HeLa cells (transfected with MAVS constructs pre- or post- exposure to CVB3) were used to analyze the function of exogenous MAVS on CVB3 infection. The results revealed that though CVB3 infection induced production of type I IFNs, viral replication and cell death were not effectively inhibited. Similarly, exogenous MAVS increased type I IFNs moderately. Morever, we observed robust production of type I IFNs in CVB3 post-infected HeLa cells thereby successfully inhibiting CVB3 infection, as well formation of cytopathic effect (CPE) and cell death. Finally, introduction of exogenous MAVS into CVB3 pre-infected cells also restricted viral infection efficiently by greatly up-regulating IFNs.</p> <p>Conclusions</p> <p>In summary, exogenous MAVS effectively prevents and controls CVB3 infection by modulating and promoting the production of type I IFNs. The IFNs level in MAVS over-expressing cells is still tightly regulated by CVB3 infection. Thus, the factors that up-regulate MAVS might be an alternative prescription in CVB3-related syndromes by enhancing IFNs production.</p> |
| first_indexed | 2024-12-10T15:06:27Z |
| format | Article |
| id | doaj.art-38209414e91b4d61928df945638ce338 |
| institution | Directory Open Access Journal |
| issn | 1743-422X |
| language | English |
| last_indexed | 2024-12-10T15:06:27Z |
| publishDate | 2012-12-01 |
| publisher | BMC |
| record_format | Article |
| series | Virology Journal |
| spelling | doaj.art-38209414e91b4d61928df945638ce3382022-12-22T01:44:02ZengBMCVirology Journal1743-422X2012-12-019131210.1186/1743-422X-9-312Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons productionZhang Qing-MengSong Wu-QiLi Yu-JunQian JunZhai Ai-XiaWu JingLi Ai-MeiHe Jun-MingZhao Jin-YunYu XinWei Lan-LanZhang Feng-Min<p>Abstract</p> <p>Background</p> <p>Recent studies have revealed that Mitochondrial Antiviral Signaling (MAVS) protein plays an essential role in the inhibition of viral infection through type I interferon (IFN) pathway. It has been shown that 3C (pro) cysteine protease of coxsackievirus B3 (CVB3) cleaves MAVS to inhibit type I IFNs induction. Other workers also found that MAVS knock-out mice suffered CVB3 susceptibility and severe histopathological change. Accordingly,our experiments were designed to explore the protection of over-expressing MAVS against CVB3 infection and the possible mechanism.</p> <p>Results</p> <p>In this study, HeLa cells (transfected with MAVS constructs pre- or post- exposure to CVB3) were used to analyze the function of exogenous MAVS on CVB3 infection. The results revealed that though CVB3 infection induced production of type I IFNs, viral replication and cell death were not effectively inhibited. Similarly, exogenous MAVS increased type I IFNs moderately. Morever, we observed robust production of type I IFNs in CVB3 post-infected HeLa cells thereby successfully inhibiting CVB3 infection, as well formation of cytopathic effect (CPE) and cell death. Finally, introduction of exogenous MAVS into CVB3 pre-infected cells also restricted viral infection efficiently by greatly up-regulating IFNs.</p> <p>Conclusions</p> <p>In summary, exogenous MAVS effectively prevents and controls CVB3 infection by modulating and promoting the production of type I IFNs. The IFNs level in MAVS over-expressing cells is still tightly regulated by CVB3 infection. Thus, the factors that up-regulate MAVS might be an alternative prescription in CVB3-related syndromes by enhancing IFNs production.</p>http://www.virologyj.com/content/9/1/312Mitochondrial antiviral signaling proteinCoxsackievirus B3InterferonAntiviral response |
| spellingShingle | Zhang Qing-Meng Song Wu-Qi Li Yu-Jun Qian Jun Zhai Ai-Xia Wu Jing Li Ai-Mei He Jun-Ming Zhao Jin-Yun Yu Xin Wei Lan-Lan Zhang Feng-Min Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons production Virology Journal Mitochondrial antiviral signaling protein Coxsackievirus B3 Interferon Antiviral response |
| title | Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons production |
| title_full | Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons production |
| title_fullStr | Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons production |
| title_full_unstemmed | Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons production |
| title_short | Over-expression of mitochondrial antiviral signaling protein inhibits coxsackievirus B3 infection by enhancing type-I interferons production |
| title_sort | over expression of mitochondrial antiviral signaling protein inhibits coxsackievirus b3 infection by enhancing type i interferons production |
| topic | Mitochondrial antiviral signaling protein Coxsackievirus B3 Interferon Antiviral response |
| url | http://www.virologyj.com/content/9/1/312 |
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