Abstract
ABSTRACTH9N2 avian influenza virus has been continuously circulating among poultry and can infect mammals, indicating that this virus is a potential pandemic strain. During influenza pandemics, secondary bacterial (particularly pneumococcal) pneumonia usually contributes to excessive mortality. In the present study, we observed the dynamic effect of H9N2 virus infection on host defense against secondary pneumococcal infection in mice. BALB/c mice were intranasally inoculated with 1.2 × 105 PFU of H9N2 virus followed by 1 × 106 CFU of Streptococcus pneumoniae at 7, 14, or 28 days post-H9N2 infection (dpi). The bacterial load, histopathology, body weight, and survival were assessed after pneumococcal infection. Our results showed that H9N2 virus infection had no significant impact on host resistance to secondary pneumococcal infection at 7 dpi. However, H9N2 virus infection increased pulmonary pneumococcal clearance and reduced pneumococcal pneumonia-induced morbidity after secondary pneumococcal infection at 14 or 28 dpi, as reflected by significantly decreased bacterial loads, markedly alleviated pulmonary histopathological changes, and significantly reduced weight loss in mice infected with H9N2 virus followed by S. pneumoniae compared with mice infected only with S. pneumoniae. Further, the significantly decreased bacterial loads were observed when mice were previously infected with a high dose (1.2 × 106 PFU) of H9N2 virus. Also, similar to the results obtained in BALB/c mice, improvement in pulmonary pneumococcal clearance was observed in C57BL/6 mice. Overall, our results showed that pulmonary pneumococcal clearance is improved after resolution of H9N2 virus infection in mice.
Highlights
H9N2 avian influenza virus has been continuously circulating among poultry and can infect mammals, indicating that this virus is a potential pandemic strain
The overall architecture of the lungs of H9N2-infected mice was similar to those of mock-infected mice at 14 and 28 dpi (Fig. 1C). In line with these observations, the percentage of lung areas affected, determined by semiquantitative measurement of histopathological alterations, was significantly increased in H9N2-infected mice compared with mock-infected mice at 7 dpi but was not significantly different between the two groups at 14 and 28 dpi (Fig. 1D). These data showed that H9N2 virus infection caused obvious respiratory diseases in BALB/c mice and that mice infected with H9N2 virus had recovered by 14 dpi
Our results showed that a nonlethal dose (1.2 Â 105 PFU) of H9N2 virus infection caused obvious signs of illness and significantly decreased body weight from 3 to 7 dpi in BALB/c mice
Summary
H9N2 avian influenza virus has been continuously circulating among poultry and can infect mammals, indicating that this virus is a potential pandemic strain. Secondary bacterial ( pneumococcal) pneumonia usually contributes to excessive mortality. We observed the dynamic effect of H9N2 virus infection on host defense against secondary pneumococcal infection in mice. Our results showed that H9N2 virus infection had no significant impact on host resistance to secondary pneumococcal infection at 7 dpi. H9N2 virus infection increased pulmonary pneumococcal clearance and reduced pneumococcal pneumonia-induced morbidity after secondary pneumococcal infection at 14 or 28 dpi, as reflected by significantly decreased bacterial loads, markedly alleviated pulmonary histopathological changes, and significantly reduced weight loss in mice infected with H9N2 virus followed by S. pneumoniae compared with mice infected only with S. pneumoniae. Mechanisms of increased susceptibility to secondary bacterial infections following influenza virus infection have been widely studied since the 1918 pandemic [22, 23]. Defects in lung innate immune response, including the loss and dysfunction of alveolar macrophages [29, 30] and neutrophils [31, 32] and the dysregulation of cytokine productions [33], could play a key role in promoting secondary bacterial pneumonia
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