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Epstein‐Barr virus and HIV play no direct role in persistent generalized lymphadenopathy syndrome
Author(s) -
BOYLE M. J.,
SCULLEY T. B.,
COOPER D. A.,
TURNER J. J.,
PENNY R.,
SEWELL W. A.
Publication year - 1992
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1992.tb03002.x
Subject(s) - polyclonal antibodies , epstein–barr virus , virus , biology , immunology , virology , lymph node , polymerase chain reaction , lymphatic system , generalized lymphadenopathy , viral disease , epstein–barr virus infection , t cell , lymphoma , gene , antibody , immune system , genetics
SUMMARY Persistent generalized lymphadenopathy (PGL) and polyclonal B cell activation are features of infection with HIV. Epstein‐Barr virus (EBV) and HIV are known to activate B cells in vitro , but whether they are important B cell activators in patients infected with HIV is less clear. In this study, lymph node tissue was obtained from 10 patients with PGL and assessed for evidence of EBV and HIV gene sequences. DNA was extracted and specific viral gene sequences identified using the polymerase chain reaction (PCR). EBV sequences were difficult to detect in the PGL tissue, with a signal intensity similar to that of other benign and malignant lymphoid conditions not associated with EBV. HIV sequences were also rare in the PGL tissue, consistent with HIV infection of the small number of peripheral blood cells and nodal T cells likely to be present in such a sample. These findings suggest that the polyclonal B cell activation typical of HIV is not driven by direct EBV or HIV infection of B cells.

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