Abstract

Patients suffering from viral respiratory disease are often infected with several unrelated viruses, known as co-infection; however, it is unclear how viral co-infections influence disease pathogenesis. Our lab previously established a respiratory viral co-infection mouse model to answer this question. Mice were inoculated with a mild respiratory virus (rhinovirus, RV1B) two days before a virus that causes severe disease (influenza A virus, PR8; or pneumonia virus of mice, PVM). Co-infection with RV1B reduced severity of both PR8 and PVM infections, determined by mortality, weight loss, and clinical signs of disease. Bronchoalveolar lavage (BAL) samples were collected from lungs of mice infected with PR8 or PVM alone or those that were co-infected with RV1B. BAL samples were used to quantify leukocyte subtypes present in the airways of infected mice. Lung tissues were paraffin-embedded for staining and further analysis. Histology slides were stained with Masson’s trichrome stain and a hematoxylin and eosin (H&E) stain to evaluate inflammation and tissue damage, and immunohistochemistry was used to show localization of virus and immune cells. These analyses will inform how respiratory viral co-infection alters lung pathology compared to single infections, including mechanisms responsible for RV1B-mediated protection.

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Histopathological Analyses of Respiratory Viral Co-infections in Mice.

Patients suffering from viral respiratory disease are often infected with several unrelated viruses, known as co-infection; however, it is unclear how viral co-infections influence disease pathogenesis. Our lab previously established a respiratory viral co-infection mouse model to answer this question. Mice were inoculated with a mild respiratory virus (rhinovirus, RV1B) two days before a virus that causes severe disease (influenza A virus, PR8; or pneumonia virus of mice, PVM). Co-infection with RV1B reduced severity of both PR8 and PVM infections, determined by mortality, weight loss, and clinical signs of disease. Bronchoalveolar lavage (BAL) samples were collected from lungs of mice infected with PR8 or PVM alone or those that were co-infected with RV1B. BAL samples were used to quantify leukocyte subtypes present in the airways of infected mice. Lung tissues were paraffin-embedded for staining and further analysis. Histology slides were stained with Masson’s trichrome stain and a hematoxylin and eosin (H&E) stain to evaluate inflammation and tissue damage, and immunohistochemistry was used to show localization of virus and immune cells. These analyses will inform how respiratory viral co-infection alters lung pathology compared to single infections, including mechanisms responsible for RV1B-mediated protection.