Epstein-Barr Virus Infects B and Non-B Lymphocytes in HIV-1–Infected Children and Adolescents

Epstein-Barr virus (EBV) is a widespread, persistent herpesvirus that can transform B cells and that is associated with malignant lymphomas. EBV dynamics and specific immunity in human immunodeficiency virus (HIV)–1–infected children are unknown. We found that, in 74% of EBV-seropositive, HIV-1–infe...

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Published inThe Journal of infectious diseases Vol. 194; no. 9; pp. 1323 - 1330
Main Authors Bekker, Vincent, Scherpbier, Henriëtte, Beld, Marcel, Piriou, Erwan, Breda, Alex van, Lange, Joep, Leth, Frank van, Jurriaans, Suzanne, Alders, Sophie, Dillen, Pauline Wertheim-van, Baarle, Debbie van, Kuijpers, Taco
Format Journal Article
LanguageEnglish
Published Chicago, IL The University of Chicago Press 01.11.2006
University of Chicago Press
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Summary:Epstein-Barr virus (EBV) is a widespread, persistent herpesvirus that can transform B cells and that is associated with malignant lymphomas. EBV dynamics and specific immunity in human immunodeficiency virus (HIV)–1–infected children are unknown. We found that, in 74% of EBV-seropositive, HIV-1–infected children, EBV DNA loads at the start of highly active antiretroviral therapy (HAART) were comparable with those in acutely EBV-infected, HIV-negative children. EBV DNA load remained elevated in most HIV-1–infected children for months to years of follow-up. Frequencies of interferon-γ–producing EBV-specific CD8+ T cells were comparable with those in healthy control children, and antibodies to EBV nuclear antigen were detected in 73% of EBV-seropositive children. Detectable EBV DNA load was not correlated with HIV-1 RNA level or with CD4+ T cell count increase after the start of HAART. Because of its resemblance to chronic active EBV, we studied the cellular tropism of EBV in these patients. EBV DNA was found not only in the CD19+ B cell fraction but also—at stable levels—in the CD4+ and CD8+ T cell fractions. Although the reason for the aberrant T cell tropism of EBV remains unclear, these data may provide an explanation for the differential EBV dynamics in the presence of normal serological findings
Bibliography:ark:/67375/HXZ-WVQF5Z8B-2
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ISSN:0022-1899
1537-6613
DOI:10.1086/508197