Herpesvirus infections

doi:10.1017/CBO9780511544798.044

41 - Herpesvirus infections

from Part V - Infectious problems in pediatric HIV disease

Published online by Cambridge University Press: 03 February 2010

Richard M. Rutstein and

Stuart E. Starr

Edited by

Steven L. Zeichner and

Jennifer S. Read

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Richard M. Rutstein: Affiliation:
Division of General Pediatrics, Children's Hospital of Philadelphia, Philadelphia, PA
Stuart E. Starr: Affiliation:
Division of Allergy, Immunologic and Infectious Diseases, Children's Hospital of Philadelphia, Philadelphia, PA
Steven L. Zeichner: Affiliation:
National Cancer Institute, Bethesda, Maryland
Jennifer S. Read: Affiliation:
National Cancer Institute, Bethesda, Maryland

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Summary

Introduction

The eight known herpesviruses share a common structure consisting of double-stranded DNA, surrounded by a protein capsid and then a lipid and glycoprotein envelope. Herpesviruses infect humans worldwide, but prevalence varies among populations.

For most herpesviruses, primary infection usually occurs during childhood or early adult years. Beyond the neonatal period, infection rarely results in serious illness in the immunocompetent host. Herpesvirus infections are usually controlled by elements of the cellular immune system (see Chapters 1 and 3); patients significantly compromised by HIV infection can develop serious, sometimes life-threatening herpesvirus infections. In the normal host, after primary infection, herpesviruses establish life-long, latent infection, in which virus is sequestered in a non-replicative state, with the potential for recurrent or chronic disease after reactivation. The sites of latent infection for herpes simplex virus (HSV) and varicella-zoster virus (VZV) are believed to be sensory ganglia. For cytomegalovirus (CMV), Epstein—Barr virus (EBV) and human herpesvirus 6 (HHV-6), lymphocytes represent the reservoir of latent infection. With EBV, the target cell appears to be B lymphocytes, for HHV-6, T lymphocytes. The site of latency for CMV appears to be bone marrow-derived monocytes and monocyte precursors. A complex interplay exists between herpesviruses and HIV [1]. In some in vitro systems, infection with CMV, or HSV may increase susceptibility of cells to infection with HIV. In cells chronically infected with HIV, CMV or HSV infections appear capable of upregulating expression of HIV, with enhanced viral replication.

Type: Chapter
Information: Textbook of Pediatric HIV Care , pp. 604 - 619

DOI: https://doi.org/10.1017/CBO9780511544798.044 [Opens in a new window]

Publisher: Cambridge University Press

Print publication year: 2005

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