Effect of SO 2 on the Pathogenesis of Viral Upper Respiratory Infection in Mice

Abstract

Summary

The mouse-adapted strain of PR₈ influenza virus was inoculated intranas-ally into unanesthetized DS mice which had been continually exposed to 0.03-0.1 ppm of SO₂ for 4 weeks. Histopathological changes in nasal tissues showed that inflammatory response was more rapid and more severe, and regeneration was initiated sooner, in these mice than in virus-inoculated controls. The HI titer also developed more rapidly and reached higher levels in mice exposed to SO₂ plus virus than in mice receiving virus alone, and antibody to the virus appeared earlier in the exposed mice.

Animals which were exposed to SO₂ and were not given the virus showed a sixfold increase in the number of goblet cells in nasal respiratory epithelial cells, though the olfactory epithelial cells were apparently unaffected.

The results suggest that increased severity of influenza infection after continued exposure to low levels of SO₂ resulted from a progressive alteration of the nasal mucous membranes by SO₂ which then allowed rapid destructive proliferation of subsequently introduced virus. This destruction of nasal tissues would eliminate a major defensive barrier against lower tract disease.