Human papilloma virus (HPV) is not implicated in the etiology of Warthin's tumor of the parotid gland.

CONCLUSION: The lack of human papilloma virus (HPV) sequences as well as potential HPV-activated cells such as cells that would be p16- and Ki-67 positive does not support a role of HPV in the pathogenesis of this lesion. OBJECTIVE: The exact etiopathogenesis of Warthin's tumor of the parotid gland is still unclear. The aim of the present study was to evaluate if HPV could play a role in the development of this parotid lesion. METHODS: Tissue samples from 40 Warthin's tumors of the parotid gland were investigated by PCR followed by in situ hybridization. The immunohistochemical expression of p16 and the dual immunostaining of p16 and Ki-67 were evaluated in all samples. RESULTS: Strong and diffuse p16 immunoreactivity was found in 7 of the 40 cases (17.5%). In situ hybridization showed a diffuse episomal signal in those samples. However, PCR could not reliably detect the presence of HPV genes. Furthermore, p16-expressing epithelial cells were mostly negative for the proliferation marker Ki-67.

Activation of STAT1 transcription factor precedes up-regulation of coxsackievirus-adenovirus receptor during viral myocarditis.

The coxsackievirus-adenovirus receptor (CAR) was originally described as a transmembrane protein involved in viral infection and was later found to be required for normal heart development. However, the role of CAR in virus-induced myocarditis has not been investigated so far. The purpose of this study was to assess myocardial CAR expression in response to cytokine-induced inflammatory reactions during the course of coxsackievirus-induced myocarditis. In Balb/c mice intraperitoneally infected with either 2x10(4) plaque-forming units (PFUs) of coxsackie B3 virus (CVB3) or 10(2) PFUs CVB3, CAR expression and tyrosine phosphorylation of signal transducer and activator of transcription 1 (STAT1), a known cytokine-inducible transcription factor involved in viral defense, were determined. Our results demonstrated that within the first 7 days after virus inoculation, when the viral replication and STAT1 activation in the heart tissue was most prominent, the expression of CAR did not surpass that of uninfected controls. However, the up-regulation of CAR was observed 9 weeks later, when enteroviral RNA was no longer detectable and activation of STAT1 had already ceased. In contrast to the STAT1 target genes Mig and Irf1, interferon gamma stimulation failed to up-regulate Car expression in isolated cardiomyocytes. In human endomyocardial biopsies, Car expression was found to be elevated in approximately one third of patients with dilated cardiomyopathy (9 of 30 patients) as compared with controls. Thus, activation of STAT1 clearly precedes the enhanced CAR expression observed during tissue reorganization, suggesting an essential role of STAT1 transcription factors in orchestrating the sequential actions involved in adaptive immune response.