{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T17:44:24Z","timestamp":1791308664639,"version":"4.3.1"},"reference-count":35,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2008,8,7]],"date-time":"2008-08-07T00:00:00Z","timestamp":1218067200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2008,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Progressive multifocal leukoencephalopathy (PML) is a fatal demyelinating disease of the white matter affecting immunocompromised patients that results from the cytolytic destruction of glial cells by the human neurotropic JC virus (JCV). According to one model, during the course of immunosuppression, JCV departs from its latent state in the kidney and after entering the brain, productively infects and destroys oligodendrocytes. The goal of this study was to test the hypothesis that JCV may reside in a latent state in a specific region of the brains of immunocompetent (non\u2010PML) individuals without any neurological conditions.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Gene amplification was performed together with immunohistochemistry to examine the presence of JCV DNA sequences and expression of its genome in five distinct regions of the brain from seven immunocompetent non\u2010PML individuals.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Although no viral proteins were expressed in any of these cases, fragments of the viral DNA were present in various regions of normal brain. Laser\u2010capture microdissection showed the presence of JCV DNA in oligodendrocytes and astrocytes, but not in neurons.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>The detection of fragments of viral DNA in non\u2010PML brain suggests that JCV has full access to all regions of the brain in immunocompetent individuals. Thus, should the immune system become impaired, the passing and\/or the resident virus may gain the opportunity to express its genome and initiate its lytic cycle in oligodendrocytes. The brain as a site of JCV latency is a possibility. Ann Neurol 2008; 64:379\u2013387<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.21443","type":"journal-article","created":{"date-parts":[[2008,8,7]],"date-time":"2008-08-07T12:53:18Z","timestamp":1218113598000},"page":"379-387","source":"Crossref","is-referenced-by-count":112,"title":["Detection of JC virus DNA fragments but not proteins in normal brain tissue"],"prefix":"10.1002","volume":"64","author":[{"given":"Georgina","family":"Perez\u2010Liz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luis","family":"Del Valle","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Antonio","family":"Gentilella","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sidney","family":"Croul","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kamel","family":"Khalili","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2008,11,4]]},"reference":[{"key":"e_1_2_5_2_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/127.4.467"},{"key":"e_1_2_5_3_2","first-page":"99","article-title":"The epidemiology of human polyomaviruses","volume":"105","author":"Walker DL","year":"1983","journal-title":"Prog Clin Biol Res"},{"key":"e_1_2_5_4_2","doi-asserted-by":"publisher","DOI":"10.1007\/0-387-32957-9_7"},{"key":"e_1_2_5_5_2","doi-asserted-by":"crossref","first-page":"274","DOI":"10.1007\/0-387-32957-9_20","article-title":"The polyomavirus, JCV, and its involvement in human disease","volume":"577","author":"Khalili K","year":"2006","journal-title":"Adv Ex Med Biol"},{"issue":"2","key":"e_1_2_5_6_2","first-page":"S98","article-title":"Progressive multifocal leukoencephalopathy: JC virus induced demyelination in the immune compromised host","volume":"6","author":"Hou J","year":"2000","journal-title":"J Neurovirol"},{"key":"e_1_2_5_7_2","doi-asserted-by":"publisher","DOI":"10.1055\/s-2008-1040837"},{"issue":"1","key":"e_1_2_5_8_2","doi-asserted-by":"crossref","first-page":"38","DOI":"10.1080\/13550280390195261","article-title":"Progressive multifocal leukoencephalopathy in acquired immuno\u2010deficiency syndrome: explaining the high incidence and disproportionate frequency of the illness relative to other immunosuppressive conditions","volume":"9","author":"Berger JR","year":"2003","journal-title":"J Neurovirol"},{"key":"e_1_2_5_9_2","doi-asserted-by":"publisher","DOI":"10.1007\/s11910-007-0072-9"},{"key":"e_1_2_5_10_2","doi-asserted-by":"publisher","DOI":"10.2741\/1830"},{"key":"e_1_2_5_11_2","doi-asserted-by":"publisher","DOI":"10.1128\/JVI.51.2.458-469.1984"},{"key":"e_1_2_5_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.virol.2004.03.025"},{"key":"e_1_2_5_13_2","doi-asserted-by":"publisher","DOI":"10.1002\/jcp.20266"},{"key":"e_1_2_5_14_2","doi-asserted-by":"publisher","DOI":"10.3109\/01913129309027796"},{"key":"e_1_2_5_15_2","first-page":"17","article-title":"Anatomo\u2010pathological features of JCV infection in patients with acquired immunodeficiency syndrome (AIDS). 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