Abstract:
:Vertebrates mount a strong innate immune response against viruses, largely by activating the interferon system. Double-stranded RNA (dsRNA), a common intermediate formed during the life cycle of many viruses, is a potent trigger of this response. In contrast, no general inducible antiviral defense mechanism has been reported in any invertebrate. Here we show that dsRNA induces antiviral protection in the marine crustacean Litopenaeus vannamei. When treated with dsRNA, shrimp showed increased resistance to infection by two unrelated viruses, white spot syndrome virus and Taura syndrome virus. Induction of this antiviral state is independent of the sequence of the dsRNA used and therefore distinct from the sequence-specific dsRNA-mediated genetic interference phenomenon. This demonstrates for the first time that an invertebrate immune system, like its vertebrate counterparts, can recognize dsRNA as a virus-associated molecular pattern, resulting in the activation of an innate antiviral response.
journal_name
J Viroljournal_title
Journal of virologyauthors
Robalino J,Browdy CL,Prior S,Metz A,Parnell P,Gross P,Warr Gdoi
10.1128/JVI.78.19.10442-10448.2004subject
Has Abstractpub_date
2004-10-01 00:00:00pages
10442-8issue
19eissn
0022-538Xissn
1098-5514pii
78/19/10442journal_volume
78pub_type
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/JVI.31.2.376-388.1979
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doi:10.1128/JVI.72.4.3185-3195.1998
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journal_title:Journal of virology
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abstract::Infection of human dermal microvascular endothelial (HMVEC-d) cells and human foreskin fibroblast (HFF) cells in vitro by Kaposi's sarcoma-associated herpesvirus (KSHV) provides an excellent in vitro model system to study viral latency. KSHV infection is characterized by the induction of preexisting host signal cascad...
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pub_type: 杂志文章
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pub_type: 杂志文章
doi:10.1128/JVI.44.2.752-754.1982
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pub_type: 杂志文章
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pub_type: 杂志文章
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journal_title:Journal of virology
pub_type: 杂志文章
doi:10.1128/JVI.66.4.2495-2504.1992
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abstract::Superinfection exclusion is the ability of an established viral infection to interfere with a second viral infection. Using West Nile virus (WNV) as a model, we show that replicating replicons in BHK-21 cells suppress subsequent WNV infection. The WNV replicon also suppresses superinfections of other flaviviruses but ...
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pub_type: 杂志文章
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