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Viruses 2013, 5(5), 1208-1218; doi:10.3390/v5051208

The Role of the CoREST/REST Repressor Complex in Herpes Simplex Virus 1 Productive Infection and in Latency

Marjorie B. Kovler Viral Oncology Laboratories, The University of Chicago, 910 East 58th Street, Chicago, IL 60637, USA
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Received: 11 March 2013 / Revised: 21 April 2013 / Accepted: 23 April 2013 / Published: 29 April 2013
(This article belongs to the Special Issue Chromatin Control of Viral Infection)
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Abstract

REST is a key component of the HDAC1 or 2, CoREST, LSD1, REST (HCLR) repressor complex. The primary function of the HCLR complex is to silence neuronal genes in non-neuronal cells. HCLR plays a role in regulating the expression of viral genes in productive infections as a donor of LDS1 for expression of α genes and as a repressor of genes expressed later in infection. In sensory neurons the HCLR complex is involved in the silencing of viral genome in the course of establishment of latency. The thesis of this article is that (a) sensory neurons evolved a mechanism to respond to the presence and suppress the transmission of infectious agents from the periphery to the CNS and (b) HSV evolved subservience to the HCLR with at least two objectives: to maintain a level of replication consistent with maximal person-to-person spread and to enable it to take advantage of neuronal innate immune responses to survive and be available for reactivation shielded from adaptive immune responses of the host.
Keywords: HCLR; herpes viruses; productive infection; latency HCLR; herpes viruses; productive infection; latency
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).

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Zhou, G.; Du, T.; Roizman, B. The Role of the CoREST/REST Repressor Complex in Herpes Simplex Virus 1 Productive Infection and in Latency. Viruses 2013, 5, 1208-1218.

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