Ehrlich J P, Burleson G R
Department of Environmental Medicine, New York University Medical School, A. J. Lanza Laboratory, Tuxedo.
J Toxicol Environ Health. 1991 Oct;34(2):259-73. doi: 10.1080/15287399109531565.
Animal infectivity models have been important in the demonstration of enhanced susceptibility to viral and bacterial infection as a result of low-level toxicant exposure. This study demonstrated an enhanced and prolonged viral infection using an influenza virus infectivity model in the rat following exposure to the toxicant gas phosgene. Fischer-344 rats exposed to either air or a sublethal concentration of phosgene demonstrated peak pulmonary influenza virus titers 1 d after infection. Virus titers in rats exposed to air declined rapidly falling below detectable levels by 4 d after infection. However, a significantly enhanced and prolonged pulmonary influenza virus infection was observed on d 3 and 4 after infection in rats exposed to phosgene. Virus was cleared below detectable limits on d 5 after infection in animals exposed to phosgene. Thus, inhalation of sublethal concentrations of phosgene resulted in an increased severity of pulmonary influenza virus infection. This study provides a demonstration of the effective use of a rat viral infectivity model to detect the immunotoxicity of inhaled pollutants. This model will allow future studies to focus on the immunological mechanism(s) responsible for the enhanced and prolonged pulmonary influenza virus infection.
动物感染性模型在证明低水平毒物暴露导致对病毒和细菌感染易感性增强方面一直很重要。本研究利用大鼠流感病毒感染性模型，证明了暴露于有毒气体光气后，病毒感染增强且持续时间延长。暴露于空气或亚致死浓度光气的Fischer-344大鼠在感染后1天出现肺部流感病毒滴度峰值。暴露于空气的大鼠病毒滴度迅速下降，在感染后4天降至可检测水平以下。然而，在感染后第3天和第4天，观察到暴露于光气的大鼠肺部流感病毒感染显著增强且持续时间延长。在暴露于光气的动物中，感染后第5天病毒清除至可检测限度以下。因此，吸入亚致死浓度的光气会导致肺部流感病毒感染的严重程度增加。本研究证明了有效利用大鼠病毒感染性模型来检测吸入污染物的免疫毒性。该模型将使未来的研究能够专注于导致肺部流感病毒感染增强和持续时间延长的免疫机制。
