No abstract

Although defensins are known to inhibit the replication of human influenza A virus (IAV) in vitro, their in vivo expression during IAV infection is not known. Here we investigated mRNA and protein expression of several beta-defensins in the airways of IAV infected mice. Expression of murine beta-defensin (MBD)-3 and -4 was enhanced (3 to 5-fold, p<0.01) in infected lungs, trachea and sinonasal mucosa. MBD-3 and -4 expressions were correlated with the time course of acute IAV infection suggesting their induction by IAV infection. Infected mice also showed increased levels of surfactant protein-D especially in the sinonasal mucosa. MBD-3 and -4 were localized to the conducting airway epithelial cells but not the alveolar tissue. We conclude that IAV infection upregulated the expression of inducible beta-defensins in both the upper and lower airways. These novel findings suggest that beta-defensins might contribute to innate and adaptive immune responses targeted against IAV infection.

In the current study, the prevalence of HPV DNA in tonsillar tissue of patients without RRP is 2%, whereas the incidence of this disease is 2 to 4 cases per 100,000 (0.004%). These findings are significantly different (P = .005 within a 95% confidence interval) suggesting that host factors in addition to infection play a role in pathogenesis of RRP. The molecular methods described in this study are well suited for detection of HPV in tonsillar tissue.

Recent investigations have shown that guinea pigs are important for the study of influenza A virus (IAV) transmission. However, very little is known about IAV replication and histopathology in the guinea pig respiratory tract. Here, we describe viral growth kinetics, target cells and histopathology in the nasosinus, trachea and lungs of IAV-infected guinea pigs. We found that guinea pigs infected with either A/Puerto Rico/8/34 (H1N1) or A/Hong Kong/8/68 (H3N2) developed a predominantly upper airway infection with high nasal viral titres. IAV grew to moderate titres in the lungs but induced marked inflammatory responses, resulting in severe bronchopneumonia and alveolitis. Although non-lethal at the high dose of 2¾10 6 p.f.u., infections with these IAV strains were associated with reduced weight gain. IAV infection in guinea pigs is characterized by extensive viral replication in the ciliated nasal epithelial cells followed by heavy nasal mucus secretion.