Human Herpesvirus Latency

Herpesviruses are among the most successful human pathogens. In healthy individuals, primary infection is most often inapparent. After primary infection, the virus becomes latent in ganglia or blood mononuclear cells. Three major subfamilies of herpesviruses have been identified based on similar gro...

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Bibliographic Details
Published in:Brain pathology (Zurich, Switzerland) Switzerland), 2001-10, Vol.11 (4), p.465-474
Main Authors: Cohrs, Randall J., Gilden, Donald H.
Format: Article
Language:English
Subjects:
Acquired immune deficiency syndrome
Adaptations
Alphaherpesvirinae - genetics
Alphaherpesvirinae - pathogenicity
Alphaherpesvirus
Animals
Blood
Bone marrow
DNA, Viral - genetics
Dorsal root ganglia
Epstein-Barr virus
Ganglia
Ganglia, Sensory - pathology
Ganglia, Sensory - physiopathology
Ganglia, Sensory - virology
Gene Expression Regulation, Viral - physiology
genomics
Herpes simplex virus 1
Herpesviridae - genetics
Herpesviridae - pathogenicity
Herpesviridae Infections - genetics
Herpesviridae Infections - physiopathology
Human cytomegalovirus
Human herpesvirus
Humans
Latent infection
Leukocytes (mononuclear)
Lymphocytes B
Neurological complications
Osteoprogenitor cells
Pathogens
Reviews
SYMPOSIUM: Herpesvirus Infections of the Nervous System
Transplants
Varicella-zoster virus
Virus Latency - genetics
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Summary:Herpesviruses are among the most successful human pathogens. In healthy individuals, primary infection is most often inapparent. After primary infection, the virus becomes latent in ganglia or blood mononuclear cells. Three major subfamilies of herpesviruses have been identified based on similar growth characteristics, genomic structure, and tissue predilection. Each herpesvirus has evolved its own unique ecological niche within the host that allows the maintenance of latency over the life of the individual (e.g. the adaptation to specific cell types in establishing latent infection and the mechanisms, including expression of different sets of genes, by which the virus remains latent). Neurotropic alpha‐herpesviruses become latent in dorsal root ganglia and reactivate to produce epidermal ulceration, either localized (herpes simplex types 1 and 2) or spread over several dermatomes (varicalla‐zoster virus). Human cytomegalovirus, the prototype beta‐herpesvirus, establishes latency in bone marrow‐derived myeloid progenitor cells. Reactivation of latent virus is especially serious in transplant recipients and AIDS patients. Lymphotropic gammaher‐pesviruses (Epstein‐Barr virus) reside latent in resting B cells and reactivate to produce various neurologic complications. This review highlights the alphaherpesvirus, specifically herpes simplex virus type 1 and varicella‐zoster virus, and describes the characteristics of latent infection.
ISSN:1015-6305
1750-3639
DOI:10.1111/j.1750-3639.2001.tb00415.x