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Parvovirus B19 quiescence during the course of human immunodeficiency virus infection in persons with hemophilia
Author(s) -
Goedert James J.,
Erdman Dean D.,
Konkle Barbara A.,
Török Thomas J.,
Lederman Michael M.,
Kleinert Dorothy,
Mandalaki Titica,
Kessler Craig M.,
Anderson Larry J.,
Luban Naomi L. C.
Publication year - 1997
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/(sici)1096-8652(199712)56:4<248::aid-ajh9>3.0.co;2-x
Subject(s) - seroconversion , parvovirus , viremia , immunology , antibody , medicine , immune system , virology , virus , viral disease , coagulopathy , immunoglobulin m , immunoglobulin g , lymphocyte
To detect and characterize parvovirus B19 infection during the course of progressive immune deficiency from human immunodeficiency virus (HIV), ten subjects enrolled in the Multicenter Hemophilia Cohort Study were followed for 6.4 to 15 years from HIV seroconversion through extreme immune deficiency. Four to five sera or plasma samples from each subject, collected at predetermined CD4 + lymphocyte levels, were tested for immunoglobulin G (IgG) and M (IgM) B19 antibodies and DNA. All 42 samples were positive for B19 IgG antibodies, and three were weakly positive for IgM antibodies. Only one sample, collected coincident with HIV seroconversion, was unequivocally positive for B19 DNA. No persistent hematologic adverse effects of B19 infection were observed. Thus, although B19 IgG antibodies are highly prevalent among HIV‐infected persons with hemophilia or related disorders, B19 viremia and its hematologic consequences were not detected, even with severe depletion of CD4 + lymphocytes. If primary B19 infection occurs after immune deficiency, however, the consequences may be more adverse. Am. J. Hematol. 56:248–251, 1997. © 1997 Wiley‐Liss, Inc.