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Strong interaction between human herpesvirus 6 and peripheral blood monocytes/macrophages during acute infection
Author(s) -
Kondo Kazuhiro,
Kondo Toshio,
Shimada Kazuya,
Amo Kiyoko,
Miyagawa Hiromi,
Yamanishi Koichi
Publication year - 2002
Publication title -
journal of medical virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 121
eISSN - 1096-9071
pISSN - 0146-6615
DOI - 10.1002/jmv.10082
Subject(s) - virology , biology , viremia , tropism , peripheral blood mononuclear cell , virus , chemokine , tissue tropism , cc chemokine receptors , chemokine receptor , population , ccl13 , viral replication , human herpesvirus 6 , immunology , herpesviridae , viral disease , inflammation , in vitro , medicine , biochemistry , environmental health
Abstract Human herpesvirus 6 (HHV‐6) encodes a viral chemokine and chemokine receptors that may modify the functions of monocytes/macrophages (MO/Mϕ) during productive HHV‐6 infection. The interactions between HHV‐6 and MO/Mϕ during acute infection, however, remain poorly understood. In this study, we investigated the tropism of HHV‐6 in peripheral blood mononuclear cells (PBMCs) during acute infection. We detected 637 ± 273 copies of viral DNA in 10 4 MO/Mϕ. in contrast, in 10 4 CD4+ T cells, which have been reported to be viral carriers during the acute infection of HHV‐6, we found only 115 ± 42 copies of viral DNA. Consistent with these data, virus was isolated from MO/Mϕ an order of magnitude more frequently than from CD4+ T cells. Viral mRNA U79/80, which indicates viral replication, was detectable in the MO/Mϕ. In addition, the mRNAs that encode viral chemokine receptors U12 and U51, which may modify the function of MO/Mϕ, were expressed in the cells. Therefore, productively infected MO/Mϕ may be the dominant cell population that is responsible for HHV‐6 viremia during acute HHV‐6 infection. The strong interaction of HHV‐6 with MO/Mϕ may be partly responsible for the pathogenesis of this virus. J. Med Virol. 67:364–369, 2002. © 2002 Wiley‐Liss, Inc.