Journal
JOURNAL OF IMMUNOLOGY
Volume 180, Issue 4, Pages 2385-2395Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.4.2385
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Funding
- NCRR NIH HHS [P51 RR 11069, P51 RR000169] Funding Source: Medline
- NIAID NIH HHS [U01 AI057264-03, U01 AI 57264, U01 AI057264, U01 AI 5726] Funding Source: Medline
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To determine the relationship between influenza A virus replication and innate antiviral immune responses, rhesus monkeys were given oseltamivir before influenza A/Memphis/7/01 (H1N1) challenge. We found that oseltamivir treatment significantly reduced viral replication in the trachea (p < 0.029). Further, in the trachea of both treated and untreated monkeys the mRNA levels of most innate antiviral molecules in the IFN-alpha beta pathway were dramatically increased by 24 h postinfection. However, the mRNA level of a single IFN-stimulated gene, MxA (myxovirus resistance A), the IFN-stimulated gene known to be critical in blocking influenza virus replication, was significantly lower in the tracheal lavages of untreated monkeys than in the oseltamivir-treated monkeys (p = 0.05). These results demonstrate for the first time that uncontrolled influenza A virus replication actively suppresses MxA gene expression and emphasize the critical role of innate immunity in controlling influenza virus replication in vivo.
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