Aim: To study prevalence of Karolinska Institutet (KI) and Washington University (WU) polyomavirus (PyV) in 100 tonsils, 100 adenoids, 146 throat swab and 15 middle ear fluid samples collected from 146 patients (120 children and 26 adults), to analyze the sequence of noncoding control region (NCCR) and complete WUPyV genomes. Materials & methods: Viruses were detected by quantitative real-time PCR. The NCCRs and WUPyV genomes were sequenced and analyzed. Results: The frequency of WUPyV and KIPyV DNA was 27 and 11% in adenoids, 4 and 3% in tonsils, 4.1 and 1.4% in throat swab samples, respectively. The WUPyV DNA was detected in one middle ear fluid sample as well. The WUPyV NCCRs showed mutations which may alter the putative transcription factor binding sites. Phylogenetic analysis revealed three clades of WUPyV. Conclusion: Tonsils and adenoids might be site of virus replication and/or persistence, and WUPyV may invade into the middle ear.

In blood, the hydrogen peroxide concentration is regulated by catalase. Decreased activity of catalase may lead to increased hydrogen peroxide concentration, which may contribute to the manifestation of age-related disease. The aim of this study is to examine association of decreased blood catalase activity and catalase exon mutations in patients (n = 617) with diabetes (n = 380), microcytic anemia (n = 58), beta-thalassemia (n = 43) and presbycusis (n = 136) and in controls (n = 295). Overall, 51 patients (8.3%) had less than half of normal blood catalase activity. Their genomic DNA was used for mutation screening of all exons and exon/intron boundaries with polymerase chain reaction-single-strand conformation polymorphism (PCR-SSCP) and PCR-heteroduplex analyses, and mutations were verified with nucleotide sequencing. Seven patients (type 2 diabetes (n = 3), gestational diabetes (n = 1), microcytic anemia (n = 2)) had four novel catalase exon mutations namely, c.106_107insC, p.G36Afs*5(n = 3, Hungarian type G1), c.379C>T, p.R127Y (n = 2, Hungarian type H1), c.390T>C, p.R129L, (n = 1, Hungarian type H2) and c.431A>T, p.N143V (n = 1, Hungarian type H3). In patients with decreased blood catalase, the incidence of acatalasemia mutations was significantly high (P < 0.0002) in microcytic anemia, type 2 and gestational diabetes. The four novel mutations were probably responsible for low blood catalase activity in 7/51 patients. In the remainder of the cases, other polymorphisms and epigenetic/regulatory factors may be involved.