The non-pathogenic Henipavirus Cedar paramyxovirus phosphoprotein has a compromised ability to target STAT1 and STAT2.

Autor: Lieu KG; Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia., Marsh GA; CSIRO Biosecurity Flagship, Australian Animal Health Laboratory, Geelong, Australia., Wang LF; CSIRO Biosecurity Flagship, Australian Animal Health Laboratory, Geelong, Australia; Program in Emerging Infectious Diseases, Duke-NUS Graduate Medical School, Singapore., Netter HJ; Infection and Immunity Program, Monash Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton, Victoria, Australia. Electronic address: hans.netter@monash.edu.
Jazyk: angličtina
Zdroj: Antiviral research [Antiviral Res] 2015 Dec; Vol. 124, pp. 69-76. Date of Electronic Publication: 2015 Oct 23.
DOI: 10.1016/j.antiviral.2015.09.017
Abstrakt: Immune evasion by the lethal henipaviruses, Hendra (HeV) and Nipah virus, is mediated by its interferon (IFN) antagonist P gene products, phosphoprotein (P), and the related V and W proteins, which can target the signal transducer and activator of transcription 1 (STAT1) and STAT2 proteins to inhibit IFN/STAT signaling. However, it is not clear if the recently identified non-pathogenic Henipavirus, Cedar paramyxovirus (CedPV), is also able to antagonize the STAT proteins. We performed comparative studies between the HeV P gene products (P/V/W) and CedPV-P (CedPV does not encode V or W) and demonstrate that differences exist in their ability to engage the STAT proteins using immunoprecipitation and quantitative confocal microscopic analysis. In contrast to HeV-P gene encoded proteins, the ability of CedPV-P to interact with and relocalize STAT1 or STAT2 is compromised, correlating with a reduced capacity to inhibit the mRNA synthesis of IFN-inducible gene MxA. Furthermore, infection studies with HeV and CedPV demonstrate that HeV is more potent than CedPV in inhibiting the IFN-α-mediated nuclear accumulation of STAT1. These results strongly suggest that the ability of CedPV to counteract the IFN/STAT response is compromised compared to HeV.
(Copyright © 2015 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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