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Major Expansions of Select CD8+Subsets in Acute Epstein‐Barr Virus Infection: Comparison with Chronic Human Immunodeficiency Virus Disease
Author(s) -
Jonathan E. Lynne,
Ingrid Schmid,
Jose L. Matud,
Karim F. Hirji,
Scott C. Buessow,
Deborah M. Shlian,
Janis V. Giorgi
Publication year - 1998
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/517400
Subject(s) - cd38 , virus , cd8 , immunology , virology , epstein–barr virus , biology , cytotoxic t cell , hiv antigens , antigen , lymphocyte , chronic infection , viral replication , viral disease , immune system , in vitro , stem cell , biochemistry , genetics , cd34
CD8+ lymphocyte phenotypes were characterized during acute Epstein-Barr virus (EBV) infection, and a comparison was made to previous studies of human immunodeficiency virus (HIV). This was of interest because CD8+ cells contribute to immunologic control of both infections, but the usual outcome of EBV infection is benign, whereas untreated HIV infection is fatal. During acute EBV infection, CD8+ cells expressed elevated levels of the activation antigens CD38 and HLA-DR, similar to that during chronic HIV infection. Within 16 weeks, when EBV latency is established, CD8+ cell activation had resolved. In contrast, activation persists in HIV infection. Expression of CD38 and HLA-DR on CD8+ cells could be a marker for ongoing viral replication in both infections. Other CD8+ cell alterations observed in this study of acute EBV infection included increases in both CD62L- and CD62L+ CD8+ cells and unique kinetics in the expansion of the CD57+CD8+ cell subset.

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