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Acute lung injury induced by H9N2 virus in mice

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Background H9N2 avian influenza viruses (AIVs) have repeatedly caused infections in mammals even humans in many countries. The purpose of our study was to evaluate the acute lung injury (ALI) caused by H9N2 viral infection in mice. Methods Six- to eight- week-old female SPF C57BL/6 mice were infected intranasally with 1×104 MID50 of A/HONG KONG/2108/2003 [H9N2 (HK)] virus. Clinical signs, pathological changes, virus titration in tissues of mice, arterial blood gas, and cytokines in bronchoalveolar lavage fluid (BALF) and serum were observed at different time points after AIV infection. Results H9N2-AIV-infected mice exhibited severe respiratory syndrome, with a mortality rate of 50%. Lung histopathological changes in infected mice included diffuse pneumonia, alveolar damage, inflammatory cellular infiltration, interstitial and alveolar edema, and hemorrhage. In addition, H9N2 viral infection resulted in severe progressive hypoxemia, lymphopenia, and a significant increase in interleukin 1, interleukin 6, tumor necrosis factor, and interferon in BALF and serum. Conclusions The results suggest that H9N2 viral infection induces a typical ALI in mice that resembles the common features of ALI. Our data may facilitate the future studies of potential avian H9N2 disease in humans.
Title: Acute lung injury induced by H9N2 virus in mice
Description:
Background H9N2 avian influenza viruses (AIVs) have repeatedly caused infections in mammals even humans in many countries.
The purpose of our study was to evaluate the acute lung injury (ALI) caused by H9N2 viral infection in mice.
Methods Six- to eight- week-old female SPF C57BL/6 mice were infected intranasally with 1×104 MID50 of A/HONG KONG/2108/2003 [H9N2 (HK)] virus.
Clinical signs, pathological changes, virus titration in tissues of mice, arterial blood gas, and cytokines in bronchoalveolar lavage fluid (BALF) and serum were observed at different time points after AIV infection.
Results H9N2-AIV-infected mice exhibited severe respiratory syndrome, with a mortality rate of 50%.
Lung histopathological changes in infected mice included diffuse pneumonia, alveolar damage, inflammatory cellular infiltration, interstitial and alveolar edema, and hemorrhage.
In addition, H9N2 viral infection resulted in severe progressive hypoxemia, lymphopenia, and a significant increase in interleukin 1, interleukin 6, tumor necrosis factor, and interferon in BALF and serum.
Conclusions The results suggest that H9N2 viral infection induces a typical ALI in mice that resembles the common features of ALI.
Our data may facilitate the future studies of potential avian H9N2 disease in humans.

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