{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T17:22:06Z","timestamp":1791220926480,"version":"4.1.0"},"reference-count":35,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2010,5,25]],"date-time":"2010-05-25T00:00:00Z","timestamp":1274745600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2010,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Polyomavirus infection occurring during childhood is followed by a lifelong latency in immunocompetent subjects. The major site of polyomavirus persistence are the uroepithelial cells which leads to oral transmission. It has recently been hypothesized that tonsils could be a possible reservoir. The role of tonsil, adenoid, and peripheral blood mononuclear cells (PBMCs) as possible sites of JCV, BKV, and SV40 latency in young healthy children was assessed. Two hundred fifteen fresh specimens, including 57 tonsil, 80 adenoid, and 78 PBMC samples from 80 immunocompetent children (mean age 4.8 years) were analyzed to determine the viral load by quantitative real\u2010time PCR. The human herpes virus 6 (HHV\u20106) was tested as a lymphotropic reference virus. Polyomavirus was detected in 5\/80 (6.2%) children while HHV\u20106 infection affected 27\/80 children (33.7%) (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.001). SV40 was detected in one adenoid sample, while footprints of BKV were found in one adenoid and three tonsil samples. JCV was never found in all samples. Polyomavirus sequences were not detected in the 78 blood samples. One adenoid and two tonsils from three children (1.4%) were positive for both polyomavirus and HHV\u20106. Infections were characterized by low replication rates ranging typically from 1\u2009\u00d7\u200910e<jats:sup>2<\/jats:sup>\/5.5\u2009\u00d7\u200910e<jats:sup>4<\/jats:sup> to 6.8\u2009\u00d7\u200910e<jats:sup>3<\/jats:sup>\/8.5\u2009\u00d7\u200910e<jats:sup>4<\/jats:sup> viral copies\/number of cells. In conclusion, tonsils and adenoids of children could effectively harbor BKV and SV40, although only very few cells proved to be infected. Nevertheless, the low prevalence of polyomavirus, in comparison with the lymphotropic HHV\u20106, suggests that these tissues are unlikely to be the preferred site of polyomavirus latency, at least in younger children. J. Med. Virol. 82:1236\u20131240, 2010. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jmv.21786","type":"journal-article","created":{"date-parts":[[2010,5,26]],"date-time":"2010-05-26T14:50:16Z","timestamp":1274885416000},"page":"1236-1240","source":"Crossref","is-referenced-by-count":34,"title":["JCV\/BKV and SV40 viral load in lymphoid tissues of young immunocompetent children from an area of North\u2010East 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