Update on Herpes Virus Infections of the Nervous System
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INFECTION (J BERGER, SECTION EDITOR)
Update on Herpes Virus Infections of the Nervous System Israel Steiner & Felix Benninger
# Springer Science+Business Media New York 2013
Abstract Herpes simplex viruses types 1 and 2 (HSV-1 and HSV-2) are human neurotropic viruses that establish latent infection in dorsal root ganglia (DRG) for the entire life of the host. From the DRG they can reactivate to cause human morbidity and mortality. Although they vary, in part, in the clinical disorders they cause, and in their molecular structure, they share several features that govern the biology of their infection of the human nervous system. HSV-1 is the causative agent of encephalitis, corneal blindness, and several peripheral nervous system disorders; HSV-2 is responsible for meningoencephalitis in neonates and meningitis in adults. The biology of their ability to establish latency, maintain it for the entire life of the host, reactivate, and cause primary and recurrent disease is being studied in animal models and in humans. This review covers recent advances in understanding the biology and pathogenesis of HSV-related disease.
but also in birds, fish, and others. Eight human herpesviruses (HHVs) are known: herpes simplex virus (HSV) 1 and 2, varicella zoster virus (or HHV-3), Epstein–Barr virus (or HHV-4), cytomegalovirus (or HHV-5), HHV-6, and HHV-7, and HHV-8 [1], also known as Kaposi sarcoma associated herpesvirus. Here, we focus on the two neurotropic herpes simplex viruses HSV-1 and HSV-2, not trying to provide a comprehensive overview, but rather covering newest developments related to pathophysiology, clinical disorders, and treatment.
Structure, Primary Infection, Latency, and Reactivation Structure
“An inefficient virus kills its host. A clever virus stays with it” by the British scientist James Lovelock is a charming description of the one common characteristic feature of all herpes viruses: their ability to become latent and establish a lifelong infection. The Herpesviridae family is comprised of about 130 large double-stranded DNA viruses found in mammals,
HSV-1 and HSV-2 are closely related, with nearly 70 % genomic homology [2–4]. The genome is a double-stranded DNA molecule located within an icosapentahedral capsid consisting of 162 capsomers. An amorphous material called the tegument that is enclosed by an envelope consisting of polyamines, lipids, and glycoproteins. Of the 12 or more viral envelope proteins, four glycoproteins (gD, gB, gH, and gL) seem to be of importance for cell entry. After cell surface attachment, binding to gD receptor occurs, activating the membrane fusion machinery. HSV-2 is usually the cause of genital herpes, whereas HSV-1 is typically transmitted during childhood via the orolabial mucocutaneous surfaces and primarily causes herpes labialis [5•].
This article is part of the Topical Collection on Infection
Primary Infection
I. Steiner (*) : F. Benninger Department of Neurology, Rabin Medical Center, Beilinson Campus, 49100 Petach Tikva, Israel e-mail: [email protected]
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