• Acute lung injury;
  • H5N1 avian influenza A virus;
  • oxygen free radical;
  • superoxide


Acute lung injury is an important cause of death in humans infected with H5N1. It has been found that oxygen free radicals (OFRs) are elevated in lung tissue during influenza virus infections. In this study, we used a mouse model to explore the role of OFRs in acute lung injury caused by H5N1 viral infection.


Four- to six-week-old male specific pathogen-free BALB/c mice were inoculated intranasally with 105 50% tissue culture infective doses (TCID50) of highly pathogenic A/Chicken/Hebei/108/2002 (H5N1) viruses and were then given 1000 IU of lauric acid modified superoxide dismutase (LA-SOD) by intraperitoneal injection, starting 2 days post-infection and continuing for 6 days.


The extent of lung injury and the concentration of OFRs were higher, and the SOD activity was lower in H5N1 virus-infected mice than that in uninfected control mice on days 3, 6, and 7 post-inoculation. Weak amelioration of clinical signs, a minor decrease in the total mortality and the extent of lung injury, and the lower OFRs concentration were seen in the LA-SOD treatment group, but a reduction in lung virus titers was not observed in the LA-SOD treatment at all time points.


The LA-SOD treatment has a mild inhibitory effect on H5N1 influenza virus infection in mice. OFRs, therefore, might play an important role in the pathogenesis of acute lung injury induced by H5N1 virus.