期刊
JOURNAL OF VIROLOGY
卷 81, 期 2, 页码 548-557出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.01782-06
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- NATIONAL CANCER INSTITUTE [R24CA095823] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI059443, F32AI066542] Funding Source: NIH RePORTER
- NCI NIH HHS [5R24 CA095823-04, R24 CA095823] Funding Source: Medline
- NCRR NIH HHS [1 S10 RR0 0145-01] Funding Source: Medline
- NIAID NIH HHS [F32 AI066542, P01 AI059443-01A1, F32 AI66542, P01 AI059443] Funding Source: Medline
- PHS HHS [T32 A1007645] Funding Source: Medline
The severe acute respiratory syndrome coronavirus (SARS-CoV) is highly pathogenic in humans, with a death rate near 10%. This high pathogenicity suggests that SARS-CoV has developed mechanisms to overcome the host innate immune response. It has now been determined that SARS-CoV open reading frame (ORF) 3b, ORF 6, and N proteins antagonize interferon, a key component of the innate immune response. All three proteins inhibit the expression of beta interferon (IFN-beta), and further examination revealed that these SARS-CoV proteins inhibit a key protein necessary for the expression of IFN-beta, IRF-3. N protein dramatically inhibited expression from an NF-kappa B-responsive promoter. All three proteins were able to inhibit expression from an interferon-stimulated response element (ISRE) promoter after infection with Sendai virus, while only ORF 3b and ORF 6 proteins were able to inhibit expression from the ISRE promoter after treatment with interferon. This indicates that N protein inhibits only the synthesis of interferon, while ORF 3b and ORF 6 proteins inhibit both interferon synthesis and signaling. ORF 6 protein, but not ORF 3b or N protein, inhibited nuclear translocation but not phosphorylation of STAT1. Thus, it appears that these three interferon antagonists of SARS-CoV inhibit the interferon response by different mechanisms.
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