Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Introduction: definition and classification of the human herpesviruses
- Part II Basic virology and viral gene effects on host cell functions: alphaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: betaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: gammaherpesviruses
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
- Part III Pathogenesis, clinical disease, host response, and epidemiology: VZU
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HCMV
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
- 46 HHV-6A, 6B, and 7: pathogenesis, host response, and clinical disease
- 47 HHV-6A, 6B, and 7: molecular basis of latency and reactivation
- 48 HHV-6A, 6B, and 7: immunobiology and host response
- 49 HHV-6A, 6B, and 7: persistence in the population: epidemiology and transmission
- Part III Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
- Part IV Non-human primate herpesviruses
- Part V Subversion of adaptive immunity
- Part VI Antiviral therapy
- Part VII Vaccines and immunothgerapy
- Part VIII Herpes as therapeutic agents
- Index
- Plate section
- References
47 - HHV-6A, 6B, and 7: molecular basis of latency and reactivation
from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
Published online by Cambridge University Press: 24 December 2009
Book contents
- Frontmatter
- Contents
- List of contributors
- Preface
- Part I Introduction: definition and classification of the human herpesviruses
- Part II Basic virology and viral gene effects on host cell functions: alphaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: betaherpesviruses
- Part II Basic virology and viral gene effects on host cell functions: gammaherpesviruses
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HSV-1 and HSV-2
- Part III Pathogenesis, clinical disease, host response, and epidemiology: VZU
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HCMV
- Part III Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
- 46 HHV-6A, 6B, and 7: pathogenesis, host response, and clinical disease
- 47 HHV-6A, 6B, and 7: molecular basis of latency and reactivation
- 48 HHV-6A, 6B, and 7: immunobiology and host response
- 49 HHV-6A, 6B, and 7: persistence in the population: epidemiology and transmission
- Part III Pathogenesis, clinical disease, host response, and epidemiology: gammaherpesviruses
- Part IV Non-human primate herpesviruses
- Part V Subversion of adaptive immunity
- Part VI Antiviral therapy
- Part VII Vaccines and immunothgerapy
- Part VIII Herpes as therapeutic agents
- Index
- Plate section
- References
Summary
Introduction
The human β-herpesvirus subfamily consists of human cytomegalovirus (HCMV), human herpesvirus 6 (HHV-6), and human herpesvirus 7 (HHV-7). HHV-6 and HHV-7 belong to the Roseolovirus genus of the β-herpesviruses, and the HHV-6 species are divided into two variants: HHV-6A and HHV-6B. These viruses establish a lifelong infection of their host, reactivate frequently, and reactivated viruses are shed into the saliva (Jordan, 1983; Krueger et al., 1990). Some evidence suggests that the molecular mechanisms of viral latency and reactivation are shared among these viruses. HHV-6B is reactivated from latency after coinfection with HHV-7 (Katsafanas et al., 1996), and HCMV disease is frequently associated with concurrent HHV-6 and HHV-7 reactivation in transplant patients (Lautenschlager et al., 2000; Mendez et al., 2001)
The sites of these viruses during latency are not completely defined. For HHV-6B, viral DNA is detected predominantly in the peripheral blood monocytes/macrophages of seropositive healthy adults (Kondo et al., 1991). Furthermore, primary cultured macrophages support latent HHV-6B infection, and viral reactivation is induced in them by treatment with 12-0-tetradecanoylphorbol-13-acetate (TPA) (Kondo et al., 1991). HHV-6B also establishes latency in myeloid cell lines (Yasukawa et al., 1999), and that HHV-6B is detectable in CD34 (+) peripheral blood progenitor cells (Luppi et al., 1999). Therefore, HHV-6B appears to establish latency in hematopoietic progenitor cells.
HHV-6A is detectable in the peripheral blood of seropositive adults (Drobyski et al., 1993); however, a cell population that might harbor latent HHV-6A has not been identified.
- Type
- Chapter
- Information
- Human HerpesvirusesBiology, Therapy, and Immunoprophylaxis, pp. 843 - 849Publisher: Cambridge University PressPrint publication year: 2007
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