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Current knowledge on PB1-F2 of influenza A viruses

Identifieur interne : 000F63 ( Main/Exploration ); précédent : 000F62; suivant : 000F64

Current knowledge on PB1-F2 of influenza A viruses

Auteurs : Andi Krumbholz [Allemagne] ; Anja Philipps [Allemagne] ; Hartmut Oehring [Allemagne] ; Katja Schwarzer [Allemagne] ; Annett Eitner [Allemagne] ; Peter Wutzler [Allemagne] ; Roland Zell [Allemagne]

Source :

RBID : ISTEX:C2B825E4C3115C97BB6808945C651CDFE8645055

English descriptors

Abstract

Abstract: Almost 10 years ago, an eleventh protein of influenza A viruses was discovered in a search for CD8+ T-cell epitopes. This protein was named PB1-F2 since it is encoded in the +1 reading frame of the PB1 gene segment. Various studies have shown that PB1-F2 has a pleiotropic effect: (1) The protein can induce apoptosis in a cell type-dependent manner, (2) PB1-F2 is able to promote inflammation, and (3) finally it up-regulates viral polymerase activity by its interaction with the PB1 subunit. These properties could contribute to an enhanced pathogenicity. However, the underlying mechanism is not fully understood yet. New data suggest that some effects of PB1-F2 are strain-specific and host-specific.

Url:
DOI: 10.1007/s00430-010-0176-8


Affiliations:


Links toward previous steps (curation, corpus...)


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<div type="abstract" xml:lang="en">Abstract: Almost 10 years ago, an eleventh protein of influenza A viruses was discovered in a search for CD8+ T-cell epitopes. This protein was named PB1-F2 since it is encoded in the +1 reading frame of the PB1 gene segment. Various studies have shown that PB1-F2 has a pleiotropic effect: (1) The protein can induce apoptosis in a cell type-dependent manner, (2) PB1-F2 is able to promote inflammation, and (3) finally it up-regulates viral polymerase activity by its interaction with the PB1 subunit. These properties could contribute to an enhanced pathogenicity. However, the underlying mechanism is not fully understood yet. New data suggest that some effects of PB1-F2 are strain-specific and host-specific.</div>
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