Alphaherpesvirus Latency: Its Role in Disease and Survival of the Virus in Nature

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Herpesviruses have been identified that infect nearly all groups of vertebrates. This chapter focuses on the latency of α-herpesviruses. Several mammalian viruses belong to this group: equine herpes virus 1( EHV-l ), pseudorabies virus (PRV), bovine herpes virus 1 (BHV-1), herpes simplex virus type 1 (HSV-1), herpes simplex virus type 2 (HSV-2), and varicella zoster virus (VZV). Although most latency studies have been performed using HSV-1, significant contributions have been made using the animal viruses, and thus studies related to BHV-1 are included in this chapter. In general, it is believed that sensory neurons within ganglia are the primary site of latency. In latently infected sensory neurons, the only abundant viral gene product that is transcribed is LAT (latency-associated transcript; HSV-1 or HSV-2) or LRT (latencyrelated transcript; BHV-1). Consequently, it has been hypothesized that LAT or LRT regulates some aspect of latency. Although VZV is a member of the α-herpesvirus family, it appears that its program of latency is unique with respect to HSV and BHV-1. VZV is present in many sensory ganglia throughout the body and the central nervous system.

References (267)

  • E. Hanon et al.

    Bovine herpesvirus 1–induced apoptosis occurs at the G0/G1 phase of the cell cycle

    Virology

    (1997)
  • K.A. Heichman et al.

    Rules to replicate by

    Cell

    (1994)
  • J.M. Hill et al.

    Herpes simplex virus latent phase transcription facilitates in vivo reactivation

    Virology

    (1990)
  • M. Ackerman et al.

    DNA of bovine herpesvirus type 1 in the trigeminal ganglia of latently infected calves

    Am. J. Vet. Res.

    (1982)
  • J.S. Arthur et al.

    Intranuclear foci containing low abundance herpes simplex virus latency-associated transcripts visualized by nonisotopic in situ hybridization

    J. Gen. Virol.

    (1993)
  • J.S. Arthur et al.

    Disruption of the 5′ and 3′ splice sites flanking the major latency-associated transcripts of herpes simplex virus type 1: Evidence for alternative splicing in lytic and latent infection

    J. Gen. Virol.

    (1998)
  • J.R. Baringer et al.

    Recovery of herpes simplex virus from human trigeminal ganglions

    New Engl. J. Med.

    (1973)
  • F.O. Bastian et al.

    Herpesvirus hominis: Isolation from human trigeminal ganglion

    Science

    (1972)
  • A.H. Batchelor et al.

    Regulation and cell-type-specific activity of a promoter located upstream of the latency-associated transcript of herpes simplex virus type 1

    J. Virol.

    (1990)
  • A.H. Batchelor et al.

    Localization of cis-acting sequence requirements in the promoter of the latency-associated transcript of herpes simplex virus type 1 required for cell-type-specific activity

    J. Virol.

    (1992)
  • A.H. Batchelor et al.

    Binding and repression of the latency-associated promoter of herpes simplex virus by the immediate early 175K protein

    J. Gen. Virol.

    (1994)
  • T.M. Becker et al.

    Seroprevalence of and risk factors for antibodies to herpes simplex viruses, hepatitis B, and hepatitis C among southwestern Hispanic and non-Hispanic white women

    Sex Transm. Dis.

    (1996)
  • T.M. Block et al.

    The latency associated transcripts (LAT) of herpes simplex virus: Still no end in sight

    J. Neurovirol.

    (1997)
  • T.M. Block et al.

    A herpes simplex virus type 1 latency-associated transcript mutant reactivates with normal kinetics from latent infection

    J. Virol.

    (1990)
  • D.C. Bloom et al.

    Molecular analysis of herpes simplex virus type 1 during epinephrine-induced reactivation of latently infected rabbits in vivo

    J. Virol.

    (1994)
  • D.C. Bloom et al.

    A 348 base pair region in the latency-associated transcript facilitates herpes simplex virus type 1 reactivation

    J. Virol.

    (1996)
  • R.A. Bohenzky et al.

    Identification of a promoter mapping within the reiterated sequences that flank the herpes simplex virus type 1 UL region

    J. Virol.

    (1993)
  • R.A. Bohenzky et al.

    Two overlapping transcription units which extend across the L-S junction of herpes simplex virus type 1

    J. Virol.

    (1995)
  • D.M. Bortner et al.

    Overexpression of cyclin A in the mammary glands of transgenic mice results in the induction of nuclear abnormalities and increased apoptosis

    Cell Growth Different.

    (1995)
  • A.C. Bratanich et al.

    Localization of cis-acting sequences in the latency-related promoter of bovine herpesvirus 1 which are regulated by neuronal cell type factors and immediate-early genes

    J. Virol.

    (1992)
  • R. Bruni et al.

    Open reading frame P — A herpes simplex virus gene repressed during productive infection encodes a protein that binds a splicing factor and reduces synthesis of viral proteins made from spliced mRNA

    Proc. Natl. Acad. Sci. U.S.A.

    (1996)
  • R.L. Burke et al.

    Detection and characterization of latent HSV RNA by in situ and Northern blot hybridization in guinea pigs

    Virology

    (1991)
  • W. Cai et al.

    A cellular function can enhance gene expression and plating efficiency of a mutant defective in the gene for ICP0, a transactivating protein of herpes simplex virus type 1

    J. Virol.

    (1991)
  • E.M. Cantin et al.

    Gamma interferon expression during acute and latent nervous system infection by herpes simplex virus type 1

    J. Virol.

    (1995)
  • M.J. Carrozza et al.

    Interaction of the viral activator protein ICP4 with TFIID through TAF250

    Mol. Cell. Biol.

    (1996)
  • J. Chelly et al.

    Dystrophin gene transcribed from different promoters in neuronal and glial cells

    Nature

    (1990)
  • S.-H. Chen et al.

    A viral function represses accumulation of transcripts from productive-cycle genes in mouse ganglia latently infected with herpes simplex virus

    J. Virol.

    (1997)
  • X. Chen et al.

    Two herpes simplex virus type 1 latency-active promoters differ in their contribution to latency-associated transcript expression during lytic and latent infection

    J. Virol.

    (1995)
  • J. Chou et al.

    The herpes simplex virus 1 gene for ICP34.5, which maps in inverted repeats, is conserved in several limited passage isolates but not in strain 17syn+

    J. Virol.

    (1990)
  • J. Chou et al.

    Mapping of herpes simplex virus-1 neurovirulence to gamma 34.5, a gene nonessential for growth in culture

    Science

    (1990)
  • J.B. Clements et al.

    Temporal regulation of herpes simplex virus type 1 transcription: Location of transcripts on the viral genome

    Cell

    (1977)
  • D.M. Coen et al.

    Thymidine kinase negative herpes simplex virus mutants establish latency in mouse trigeminal ganglia but do not reactivate

    Proc. Natl. Acad. Sci. U.S.A.

    (1989)
  • R.J. Cohrs et al.

    Varicella-zoster virus (VZV) transcription during latency in human ganglia: Detection of transcripts mapping to genes 21, 29, 62, and 63 in a cDNA library enriched for VZV RNA

    J. Virol.

    (1996)
  • L. Corey et al.

    Infections with herpes simplex viruses

    New Engl. J. Med.

    (1986)
  • K.D. Croen et al.

    Latent herpes simplex virus in human trigeminal ganglia. Detection of an immediate early “anti-sense” transcript by in situ hybridization

    New Engl. J. Med.

    (1987)
  • K.D. Croen et al.

    Patterns of gene expression and sites of latency in human nerve ganglia are different for varicella-zoster and herpes simplex viruses

    Proc. Natl. Acad. Sci. U.S.A.

    (1988)
  • K.D. Croen et al.

    Characterization of herpes simplex virus type 2 latency-associated transcription in human sacral ganglia and in cell culture

    J. Infect. Dis.

    (1991)
  • D.H. Davies et al.

    Role of cell-mediated immunity in the recovery of cattle from primary and recurrent infections with infectious bovine rhinotracheitis virus

    Infect. Immunol.

    (1973)
  • A.M. Deatly et al.

    RNA from an immediate early region of the type 1 herpes simplex virus genome is present in the trigeminal ganglia of latently infected mice

    Proc. Natl. Acad. Sci. U.S.A.

    (1987)
  • A.M. Deatly et al.

    Latent herpes simplex virus type 1 transcripts in peripheral and central nervous system tissues of mice map to similar regions of the viral genome

    J. Virol.

    (1988)
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      The LAT locus expresses multiple transcripts, six micro-RNAs, and two small non-coding RNAs (Peng, Vitvitskaia, Carpenter, Wechsler, & Jones, 2008; Umbach et al., 2008, 2009). LAT inhibits apoptosis and viral gene expression (Ahmed, Lock, Miller, & Fraser, 2002; Branco & Fraser, 2005; Inman, Lovato, Doster, & Jones, 2001; Inman, Perng, et al., 2001; Inman, Zhang, Geiser, & Jones, 2001; Perng et al., 2000; Thompson & Sawtell, 2001), which protects neurons from cell death and promotes establishment and maintenance of latency (Jones, 1998, 2003; Perng & Jones, 2010). Further support for LAT maintaining latency comes from a study demonstrating that shedding of a LAT null mutant dramatically declines following multiple rounds of heat stress-induced reactivation in a mouse model of latency (Thompson & Sawtell, 2011).

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