{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,26]],"date-time":"2023-10-26T14:10:43Z","timestamp":1698329443188},"reference-count":31,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2006,7,18]],"date-time":"2006-07-18T00:00:00Z","timestamp":1153180800000},"content-version":"vor","delay-in-days":3886,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Intl Journal of Cancer"],"published-print":{"date-parts":[[1995,11,27]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The present study was performed with the aim of better defining the possible role of Epstein\u2010Barr\u2010virus(EBV)\u2010infected cells in the pathogenesis of HIV\u2010related lymphadenopathy syndrome (LAS). In addition, since LAS has been considered as a pre\u2010lymphomatous lesion, we also wished to elucidate the possible contribution of EBV\u2010carrying cells present in LAS tissues to the development of HIV\u2010associated malignant lymphomas. To this end, we have characterized EBV\u2010infected cells in LAS lymph nodes in terms of EBV DNA prevalence, tissue distribution in relation to HlV\u2010carrying cells, virus sub\u2010type, expression of latent and replicative antigens, and presence of clonal EBV episomes. When compared with HIV\u2010unrelated lymphadenopathies (4\/10, 40%), LAS showed a higher prevalence of EBV DNA (14\/20, 70%). Comparable values of EBV prevalence were detected in LAS with follicular hyperplasia (12\/16, 75%) and with follicular involution (4\/4, 100%). All EBV<jats:sup>+<\/jats:sup> non\u2010neoplastic lymph nodes from HIV\u2010seronegative patients carried type\u20101 EBV, whereas LAS specimens showed almost equivalent distribution of the 2 EBV sub\u2010types. Of the 14 EBV\u2010carrying LAS, 4 (29%) were positive by Southern\u2010blot analysis for the <jats:italic>Bam<\/jats:italic>HI\u2010W region of the virus genome but negative for the presence of monoclonal EBV episomes. <jats:italic>In situ<\/jats:italic> hybridization revealed a remarkably higher load of EBV\u2010infected cells in LAS than in HIV\u2010unrelated lymphadenopathies. In LAS lymph nodes, EBV\u2010carrying cells were identified as isolated, cytologically normal elements, sometimes with immunoblastic morphology, usually scattered throughout the interfollicular areas. By contrast, the expression of HIV p24 was restricted to germinal center cells. All the EBV<jats:sup>+<\/jats:sup> LAS samples were negative for the expression of EBV\u2010encoded latent (LMP\u20101 and EBNA\u20102) and replicative proteins (BZLF\u20101, BHLF\u20101, EA\u2010D, EA\u2010R and VCA). In addition, amplification of the immunoglobulin heavy\u2010chain genes using 2 different polymerase\u2010chain\u2010reaction protocols showed evidence of B\u2010cell clonal expansion in 2\/20 (10%) LAS, one EBV<jats:sup>\u2212<\/jats:sup> case, and one sample with low numbers of EBV\u2010infected cells. These results suggest that: (i) EBV\u2010carrying cells are probably not involved in the development of LAS, either directly or indirectly; (ii) type\u20102\u2010EBV\u2010infected cells are present in LAS lymph nodes from the early phases of HIV infection; (iii) EBV\u2010carrying LAS per se probably does not constitute a lesion at high risk for subsequent development of EBV<jats:sup>+<\/jats:sup> lymphomas; (iv) it is unlikely that a high viral load or strong EBV\u2010mediated antigenic stimulation plays a contributory role in the development of EBV\u2010unrelated lymphomas of HIV\u2010seropositive individuals. \u00a9 1995 <jats:italic>Wiley\u2010Liss, Inc<\/jats:italic>.<\/jats:p>","DOI":"10.1002\/ijc.2910630509","type":"journal-article","created":{"date-parts":[[2007,2,20]],"date-time":"2007-02-20T01:11:26Z","timestamp":1171933886000},"page":"652-659","source":"Crossref","is-referenced-by-count":21,"title":["Characteristics of EBV\u2010infected cells in HIV\u2010related lymphadenopathy: Implications for the pathogenesis of EBV\u2010associated and EBV\u2010unrelated lymphomas of HIV\u2010seropositive individuals"],"prefix":"10.1002","volume":"63","author":[{"given":"Riccardo","family":"Dolcetti","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Annunziata","family":"Gloghini","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Salvatore","family":"De Vita","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Emanuela","family":"Vaccher","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Valli","family":"De Re","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Umberto","family":"Tirelli","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Antonino","family":"Carbone","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mauro","family":"Boiocchi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2006,7,18]]},"reference":[{"key":"e_1_2_1_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/0042-6822(85)90253-3"},{"key":"e_1_2_1_3_1","doi-asserted-by":"crossref","first-page":"855","DOI":"10.1182\/blood.V69.3.855.855","article-title":"Chromosome abnormalities in AIDS\u2010associated lymphadenopathy","volume":"69","author":"Alonso L. 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