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J Virol 2007 Feb;81(4):1872-8

HSV-2 Establishes Latent Infection In a Different Population of Ganglionic Neurons than HSV-1: Role of LAT.

Margolis TP, Imai Y, Yang L, Vallas V, Krause PR

Margolis TP (reprint author), Univ Calif San Francisco, FI Proctor Fdn, Med Sci Bldg,S-310,513 Parnassus Ave,Box 0412,95, San Francisco, CA 94143 USA Univ Calif San Francisco, FI Proctor Fdn, San Francisco, CA 94143 USA Univ Calif San Francisco, Dept Ophthalmol, San Francisco, CA 94143 USA US FDA, Ctr Biol Evaluat & Res, Bethesda, MD 20892 USA

Abstract

HSV-1 and HSV-2 cause very similar acute infections, but differ in their ability to reactivate from trigeminal and dorsal root ganglia. To investigate differences in patterns of viral infection, we co-labeled murine sensory ganglia for evidence of HSV infection and for the sensory neuron markers A5 or KH10. During acute infection, 7-10% of HSV-1 or HSV-2 antigen-positive neurons were A5-positive, and 13-16% were KH10-positive, suggesting that both viruses reach each type of neuron proportional to their representation in uninfected ganglia. In murine trigeminal ganglia harvested during HSV latency, 25% of HSV-1 LAT and 4% of HSV-2 LAT expressing neurons were A5-positive, while 12% of HSV-1 LAT and 42% of HSV-2 LAT-expressing neurons were KH10-positive. A similar difference was observed in murine dorsal root ganglia. These differences could not be attributed to differences in LAT expression levels in A5 vs. KH10-positive neurons. Thus, HSV-1 demonstrated a preference for establishment of latency in A5-positive neurons, while HSV-2 demonstrated a preference for establishment of latency in KH10-positive neurons. A chimeric HSV-2 mutant that expresses the HSV-1 LAT exhibited an HSV-1 phenotype, preferentially establishing latency in A5-positive neurons. These data imply that the HSV-1 and HSV-2 LAT regions influence the ability of virus to establish latency in different neuronal subtypes. Because this same chimeric virus has a characteristic HSV-1 reactivation phenotype, this further suggests that LAT-influenced establishment of latency in specific neuronal subtypes could be an important part of the mechanism by which LAT influences viral reactivation phenotypes.


Category: Journal Article
PubMed ID: #17151134
Includes FDA Authors from Scientific Area(s): Biologics
Entry Created: 2011-10-04 Entry Last Modified: 2012-08-29
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