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DIESEL EXHAUST PARTICLES ENHANCE INFLUENZA VIRUS INFECTIVITY BY INCREASING VIRUS ATTACHMENT
Citation:
JASPERS, I., J. CIENCEWICKI, L. E. BRIGHTON, W. ZHANG, J. L. CARLSON, AND M. C. MADDEN. DIESEL EXHAUST PARTICLES ENHANCE INFLUENZA VIRUS INFECTIVITY BY INCREASING VIRUS ATTACHMENT. Presented at American Thoracic Society Meeting, San Diego, CA, May 20 - 25, 2005.
Description:
Despite vaccination and antiviral therapies, influenza infections continue to cause large scale morbidity and mortality every year. Several factors, such as age and nutritional status can affect the incidence and severity of influenza infections. Moreover, exposure to air pollutants, such as diesel exhaust (DE), can also affect respiratory virus infections. Previous studies have demonstrated that chronic DE-exposures enhanced influenza virus replication in mice by decreasing interferon-dependent antiviral defense responses. However, it is not known how acute exposures affect influenza infections. In this study we exposed differentiated human nasal and bronchial epithelial cells, as well as A549 cells, to DE particles (DEP) for 2 hours and subsequently infected the cells with influenza A/Bangkok/1/79. Exposure to DEP enhanced influenza virus replication, as assessed by influenza hemagglutinin (HA) RNA levels, viral protein levels, and the number of influenza-infected cells. This response was not caused by suppressed IFNb levels or IFN-dependent antiviral mediator production, since influenza-induced mRNA levels for IFNb and MxA, an IFN-inducible antiviral mediator, were also enhanced by exposure to DEP. However, exposure to DEP increased influenza virus attachment within 2 hours post-infection. Furthermore, exposure to DEP enhanced markers of oxidative stress and addition of glutathione ethylester (GSH-ET), reversed the effects of DEP on influenza virus replication and number of infected cells. These data suggest that oxidative stress induced by DEP creates and cellular environment which favors influenza virus attachment and uptake. Taken together, the results presented here indicate that exposure to DE can have significant impact on influenza infections in human respiratory epithelial cells.