Journal of Medical Virology 76:223–228 (2005) Detection of Human Herpesvirus 7 DNA in Peripheral Blood Reflects Mainly CD4 þ Cell Count in Patients Infected With HIV David Boutolleau, 1,2 * Olivia Bonduelle, 3 Ame ´ lie Sabard, 1 Laure Devers, 4 Henri Agut, 1 Agne ` s Gautheret-Dejean, 1,5 and the French ALT Study Group 1 Laboratoire de Virologie, UPRES EA 2387, Groupe Hospitalier Pitie ´-Salpe ˆtrie`re, Paris, France 2 Laboratoire de Bacte ´riologie-Virologie, Faculte ´ de Me´decine Paris Sud, CHU de Bice ˆtre, Le Kremlin-Bice ˆtre, France 3 Laboratoire d’Immunologie Cellulaire et Tissulaire, INSERM U543, Groupe Hospitalier Pitie ´-Salpe ˆtrie ` re, Paris, France 4 Site Transfusionnel, Groupe Hospitalier Pitie ´-Salpe ˆtrie`re, Paris, France 5 Laboratoire de Microbiologie, Faculte´des Sciences Pharmaceutiques et Biologiques, Paris, France The opportunistic behavior and the potential interactions of human herpesvirus 7 (HHV-7) with human immunodeficiency virus (HIV)-1 in HIV-1- infected patients were investigated in compar- ison with HHV-6, another human roseolovirus. Roseolovirus DNAs were detected and quantified in peripheral blood mononuclear cells (PBMCs) from 198 HIV-seronegative healthy blood donors, 38 HIV-1-infected patients classified as long-term non-progressors, and 99 HIV-1-infected patients classified as progressors. The rate of HHV-7 DNA detection was higher in healthy donors (78%) than in long-term non-progressors (47%; P ¼ 0.0003) or in progressors (52%; P < 0.0001). HHV- 7 cell load was higher in healthy donors (median: 212 EqCop/10 6 PBMCs) and in long-term non- progressors (median: 105 EqCop/10 6 PBMCs) than in progressors (median: 48 EqCop/10 6 PBMCs; P < 0.0001 and P ¼ 0.015, respectively). Among progressors, HHV-7 detection was correlated positively with the CD4 þ T-lymphocyte count (P ¼ 0.028). Neither HHV-7 detection rate nor cell load was correlated with the HIV-1 plasma load. As a whole, HHV-6 detection rate and cell load were lower than the HHV-7 counterparts, albeit exhibiting similar differences between healthy donors, long-term non-progressors, and progres- sors. In conclusion, HHV-7 infection does not appear to be stimulated by HIV-1 infection, nor interact with it. Rather, HHV-7 detection rate and cell load reflect CD4 þ T-lymphocyte count, with higher values in healthy donors and long-term non-progressors than in progressors. J. Med. Virol. 76:223 – 228, 2005. ß 2005 Wiley-Liss, Inc. KEY WORDS: HHV-7; HHV-6; HIV-1; opportu- nistic agent; interactions; CD4 þ T-lymphocytes INTRODUCTION Human herpesviruses 6 and 7 (HHV-6 and -7) are two T-lymphotropic viruses belonging to the Roseolovirus genus in the Betaherpesvirinae subfamily [Lawrence et al., 1990; Berneman et al., 1992]. They are highly prevalent in the human adult population [Levy et al., 1990a; Clark et al., 1993]. As with other herpesviruses, HHV-6 and -7 persist in the host throughout life after primary infection, and they may reactivate, resulting in clinical symptoms, particularly in immunocompromised individuals such as stem cell transplant recipients [Clark et al., 2003]. By contrast, in human immunode- ficiency virus (HIV)-infected patients, the behavior and the pathogenic role of both viruses remain quite unclear and controversial. As other members of the Herpesviridae family, HHV-6 and -7 may act as opportunistic viral agents because of the deficiency of immune control associated with HIV infec- tion. Some anecdotal cases of HHV-6-associated clinical symptoms have been reported in HIV-infected patients, such as central nervous system disorders [Knox and Carrigan, 1995], retinitis [Qavi et al., 1995], or immuno- logical damage [Iuliano et al., 1997]. In addition, data obtained from the analysis of autopsy specimens from small numbers of AIDS patients support the hypothesis of active and disseminated HHV-6 infection at a late stage of HIV infection [Corbellino et al., 1993; Knox and Carrigan, Grant sponsor: Association pour la Recherche sur le Cancer; Grant number: 4763. *Correspondence to: David Boutolleau, Laboratoire de Virolo- gie, UPRES EA 2387, Groupe Hospitalier Pitie ´-Salpe ˆtrie `re, 83 boulevard de l’Ho ˆpital, 75013 Paris, France. E-mail: david.boutolleau@psl.ap-hop-paris.fr Accepted 8 February 2005 DOI 10.1002/jmv.20345 Published online in Wiley InterScience (www.interscience.wiley.com) ß 2005 WILEY-LISS, INC.