Book contents
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Foreword
- Preface
- Introduction
- Part I Scientific basis of pediatric HIV care
- Part II General issues in the care of pediatric HIV patients
- Part III Antiretroviral therapy
- Part IV Clinical manifestations of HIV infection in children
- Part V Infectious problems in pediatric HIV disease
- 37 Serious infections caused by typical bacteria
- 38 Tuberculosis
- 39 Disseminated Mycobacterium avium complex infection
- 40 Fungal infections
- 41 Herpesvirus infections
- 42 Pneumocystis carinii pneumonia (PCP)
- Part VI Medical, social, and legal issues
- Appendices
- Index
- Plate section
- References
41 - Herpesvirus infections
from Part V - Infectious problems in pediatric HIV disease
Published online by Cambridge University Press: 03 February 2010
- Frontmatter
- Contents
- List of contributors
- List of abbreviations
- Foreword
- Preface
- Introduction
- Part I Scientific basis of pediatric HIV care
- Part II General issues in the care of pediatric HIV patients
- Part III Antiretroviral therapy
- Part IV Clinical manifestations of HIV infection in children
- Part V Infectious problems in pediatric HIV disease
- 37 Serious infections caused by typical bacteria
- 38 Tuberculosis
- 39 Disseminated Mycobacterium avium complex infection
- 40 Fungal infections
- 41 Herpesvirus infections
- 42 Pneumocystis carinii pneumonia (PCP)
- Part VI Medical, social, and legal issues
- Appendices
- Index
- Plate section
- References
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.
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- Information
- Textbook of Pediatric HIV Care , pp. 604 - 619Publisher: Cambridge University PressPrint publication year: 2005