Strong interaction between human herpesvirus 6 and peripheral blood monocytes/macrophages during acute infection
Version of Record online: 24 MAY 2002
Copyright © 2002 Wiley-Liss, Inc.
Journal of Medical Virology
Volume 67, Issue 3, pages 364–369, July 2002
How to Cite
Kondo, K., Kondo, T., Shimada, K., Amo, K., Miyagawa, H. and Yamanishi, K. (2002), Strong interaction between human herpesvirus 6 and peripheral blood monocytes/macrophages during acute infection. J. Med. Virol., 67: 364–369. doi: 10.1002/jmv.10082
- Issue online: 24 MAY 2002
- Version of Record online: 24 MAY 2002
- Manuscript Accepted: 4 JAN 2002
- Special Coordination Funds for Promoting Science and Technology
- Ministry of Education, Culture, Sports, Science and Technology, the Japanese Government
- virus carrier;
- chemokine receptor
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 104 MO/Mϕ. in contrast, in 104 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.