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49 - HHV-6A, 6B, and 7: persistence in the population: epidemiology and transmission

from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7

Published online by Cambridge University Press:  24 December 2009

Vincent C. Emery
Affiliation:
Department of Virology, Royal Free and University College Medical School of UCL, London, UK
Duncan A. Clark
Affiliation:
Department of Virology, Royal Free and University College Medical School of UCL, London, UK
Ann Arvin
Affiliation:
Stanford University, California
Gabriella Campadelli-Fiume
Affiliation:
Università degli Studi, Bologna, Italy
Edward Mocarski
Affiliation:
Emory University, Atlanta
Patrick S. Moore
Affiliation:
University of Pittsburgh
Bernard Roizman
Affiliation:
University of Chicago
Richard Whitley
Affiliation:
University of Alabama, Birmingham
Koichi Yamanishi
Affiliation:
University of Osaka, Japan
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Summary

Introduction

In common with all human herpesviruses, HHV-6 and HHV-7 establish lifelong infection following initial exposure and seroconversion. True latency as exemplified by HSV-1 and VZV, in which the genome is maintained in a transcriptionally restricted state, has not been conclusively shown for HHV-6 or HHV-7. However, the betaherpesviruses may persist in individuals via low grade replication which is continuously suppressed by a functional immune response. In this chapter we will summarize the current understanding of the epidemiology and persistence of HHV-6 and HHV-7 in the human host and its relevance to transmission. In addition, we will highlight a novel form of persistence for HHV-6 which involves integration into host chromosomal DNA.

Persistence of HHV-6 and HHV-7 in individuals

In the case of both HHV-6 and HHV-7, PCR analysis of peripheral blood mononuclear cells (PBMC) shows that a sensitive nested assay and an adequate quantity of input DNA (at least equivalent to approximately 150000 mononuclear cells or 1μg DNA) can detect viral DNA in healthy immunocompetent individuals suggestive of low levels of latent/persisting virus in peripheral blood (Jarrett et al., 1990; Clark et al., 1996; Kidd et al., 1996). In contrast, viral loads are maintained at high levels in saliva of seropositive individuals, particularly in the case of HHV-7 (Kidd et al., 1996; Fujiwara et al., 2000; see Fig. 49.1).

Type
Chapter
Information
Human Herpesviruses
Biology, Therapy, and Immunoprophylaxis
, pp. 875 - 882
Publisher: Cambridge University Press
Print publication year: 2007

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