The molecular genetics of herpes simplex virus latency and pathogenesis: A puzzle with many pieces still missing

References

• Becker Y, Gilden D H, Shtram Y, Asher Y, Tabor E, Wellish M, Devlin M, Snipper D, Hadar J, Gordon Y. Herpes simplex virus type I thymidine kinase gene activity controls virus latency and neurovirulence in mice. Latent Herpesviruses Infections in Veterinary Medicine, G Wittman, R M Gaskell, H J Rziha. Martinus Nijhoff Publishers, Boston 1984; 3–19
   Google Scholar
• Becker Y, Hadar J, Tabor E, Ben-Hur T, Raibstein I, Rosen A, Darai G. A sequence in Hpal-P fragment of herpes simplex virus-1 DNA determines intraperitoneal virulence in mice. Virology 1986; 149: 255–259
   PubMed Web of Science ®Google Scholar
• Ben-Hur T, Hadar J, Shtram Y, Gilden D H, Becker Y. Neurovirulence of herpes simplex virus type I depends on age in mice and thymidine kinase expression. Arch Virol 1983; 78: 303–308
   Google Scholar
• Ben-Hur T, Asher Y, Tabor E, Darai G, Becker Y. HSV-1 virulence for mice by the intracerebral route is encoded by the BamHI-L DNA fragment containing the cell fusion gene. Arch Virol 1987; 96: 117–122
   Google Scholar
• Ben-Hur T, Rosenthal J, Itzik A, Weidenfeld J. Rescue of HSV-1 neurovirulence is associated with induction of brain interleukin-1 expression, prostaglandin synthesis and neuroendocrine responses. J NeuroVirol 1996; 2279–288
   Google Scholar
• Birmanns B, Reibstein I, Steiner I. Characterization of an in vivo reactivation model of herpes simplex virus from mice trigeminal ganglia. J Gen Virol 1993; 74: 2487–2491
   Google Scholar
• Block T M, Spivack J G, Steiner I, Deshmane S, McIntosh M T, Lirette R P, Fraser N W. A herpes simplex virus type 1 latency-associated transcript mutant reactivates with normal kinetics from latent infection. J Virol 1990; 64: 3417–3426
   PubMed Web of Science ®Google Scholar
• Block T M, Deshmane S, Masonis J, Maggioncalda J, Valyi-Nagi T, Fraser N W. An HSV LAT null mutant reactivates slowly from latent infection and makes small plaques on CV-1 monolayers. Virology 1993; 192: 618–630
   PubMed Web of Science ®Google Scholar
• Centifanto-Fitzgerald Y M, Yamaguchi T, Kaufman H E, Tognon M, Roizman B. Ocular disease pattern induced by herpes simplex is genetically determined by a specific region of viral DNA. J Exp Med 1982; 155: 475–489
   PubMed Web of Science ®Google Scholar
• Chou J, Kern E R, Whitley R J, Roizman B. Mapping of herpes simplex virus-1 neurovirulence to 134.5, a gene nonessential for growth in culture. Science 1990; 250: 1262–1266
   PubMed Web of Science ®Google Scholar
• Day S P, Lausch R N, Oakes J E. Evidence that thee gene for herpes simplex virus type 1 DNA polymerase accounts for the capacity of an intertypic recombinant to spread from eye to central nervous system. Virology 1988; 163: 166–173
   PubMed Web of Science ®Google Scholar
• Deatly A M, Spivack J G, Lavi E, Fraser N W. 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 USA 1987; 84: 3204–3208
   PubMed Web of Science ®Google Scholar
• Debroy C, Pederson N, Person S. Nucleotide sequence of a herpes simplex virus type 1 gene that causes cell fusion. Virology 1985; 145: 36–48
   PubMed Web of Science ®Google Scholar
• Devi-Rao G B, Bloom D C, Stevens J G, Wagner E K. Herpes simplex virus type 1 DNA replication and gene expression during explant-induced reactivation of latently infected murine sensory ganglia. J Virol 1994; 68: 1271–1282
   Google Scholar
• Dix R D, McKendall R R, Baringer J R. Comparative neurovirulence of herpes simplex virus type 1 strain after peripheral or intracerebral inoculation of BALB/c mice. Infect Immun 1983; 40: 103–112
   PubMed Web of Science ®Google Scholar
• Field H J, Coen D M. Pathogenicity of herpes simplex virus mutants containing drug resistance mutations in the viral DNA polymerase gene. J Virol 1986; 60: 286–289
   PubMedGoogle Scholar
• Field H J, Wildy P. The pathogenicity of thymidine kinase-deficient mutants of herpes simplex virus in mice. J Hyg (Camb) 1978; 81: 267–277
   PubMedGoogle Scholar
• Fraser N W, Block T M, Spivack J G. The latency-associated transcripts of herpes simplex virus: RNA in search of function. [Review]. Virology 1992; 191: 1–8
   PubMed Web of Science ®Google Scholar
• Gruskin E A, Rich A. B-DNA to Z-DNA structural transitions in the SV40 enhancer: stabilization of Z-DNA in negatively supercoiled DNA minicircles. Biochemistry 1993; 32: 2167–2176
   Google Scholar
• Guo Z S, DePamphilis M L. Specific transcription factors stimulate simian virus 40 and polyomavirus origins of DNA replication. Mol Cell Biol 1992; 12: 2514–2524
   PubMedGoogle Scholar
• Hay K A, Gaydos A, Tenser R B. The role of herpes simplex diymidine kinase expression in neurovirulence and latency in newborn vs. adult mice. J Neuroimmunol 1995; 61: 41–52
   Google Scholar
• Ho D Y, Mocarski E S. Herpes simplex virus latent RNA (LAT) is not required for latent infection in the mouse. Proc Natl Acad Sci USA 1989; 86: 7596–7600
   PubMed Web of Science ®Google Scholar
• Izumi K M, McKelvey A M, Devi-Rao G, Wagner E K, Stevens J G. Molecular and biological characterization of a type 1 herpes simplex virus (HSV-1) specifically deleted for expression of the latency-associated transcript (LAT). Microb Pathog 1989; 7: 121–134
   Google Scholar
• Izumi K M, Stevens J G. Molecular and biological characterization of a herpes simplex virus type 1 (HSV-1) neuroinvasiveness gene. J Exp Med 1990; 172: 487–496
   PubMed Web of Science ®Google Scholar
• Javier R T, Thompson R L, Stevens J G. Genetic and biological analyses of a herpes simplex virus intertypic recombinant reduced specifically for neurovirulence. J Virol 1987; 61: 1978–1984
   Google Scholar
• Javier R T, Izumi K M, Stevens J G. Localization of a herpes simplex virus neurovirulence gene dissociated from high-titer virus replication in the brain. J Virol 1988a; 62: 1381–1387
   Google Scholar
• Javier R T, Stevens J G, Dissette V B, Wagner E K. A herpes simplex virus transcript abundant in latently infected neurons is dispensable for establishment of the latent state. Virology 1988b; 166: 254–257
   PubMed Web of Science ®Google Scholar
• Kilwinski J, Baack M, Heiland S, Knippers R. Transcription factor Octl binds to the AT-rich segment of the simian virus 40 replication origin. J Virol 1995; 69: 575–578
   PubMedGoogle Scholar
• Lieb D A, Bogard C L, Kosz-Vnenchak M, Hicks K A, Coen D M, Knipe D M, Schaffer P A. A deletion mutant of the latency-associated transcript of herpes simplex virus type 1 reactivates from the latent state with reduced frequency. J Virol 1989; 63: 2893–2900
   Google Scholar
• Lillycrop K A, Estridge J K, Latchman D S. The octamer binding protein Oct-2 inhibits transactivation of the herpes simplex virus immediate-early genes by die virion protein Vmw65. Virology 1993; 196: 888–891
   PubMedGoogle Scholar
• MacLean A R, Ul-Fareed M, Robertson L, Harland J, Brown S M. Herpes simplex virus type 1 deletion variants 1714 and 1716 pinpoint neurovirulence-related sequences in Glasgow strain 17+ between immediate early gene 1 and the ‘a’ sequence. J Gen Virol 1991; 72: 631–639
   PubMed Web of Science ®Google Scholar
• Maggioncalda J, Mehta A, Fraser N W, Block T M. Analysis of a herpes simplex virus type 1 LAT mutant with a deletion between the putative promoter and the 5′ end of the 2.0-kilobase transcript. J Virol 1994; 68: 7816–7824
   PubMedGoogle Scholar
• Maggioncalda J, Mehta A, Bagasra O, Fraser N W, Block T M. A Herpes simplex virus type 1 mutant with a deletion immediately upstream of the LAT locus establishes latency and reactivates from latently infected mice with normal kinetics. J Neuro Virol 1996; 2268–278
   Google Scholar
• Mehta A, Maggioncalda J, Bagasra O, Thikkavarapu S, Saikumari P, Valyi-Nagy T, Fraser N W, Block T M. In situ DNA PCR and RNA hybridization detection of herpes simplex virus sequences in trigeminal ganglia of latently infected mice. Virology 1995; 206: 633–640
   Web of Science ®Google Scholar
• Mitchell W J, Lirette R P, Fraser N W. Mapping of low abundance latency-associated RNA in the trigeminal ganglia of mice latently infected with herpes simplex virus type 1. J Gen Virol 1990; 71: 125–132
   PubMed Web of Science ®Google Scholar
• Nicosia M, Deshmane S L, Zabolotny J M, Valyi-Nagy T, Fraser N W. Herpes simplex virus type 1 latency-associated transcript (LAT) promoter deletion mutants can express a 2-kilobase transcript mapping to the LAT region. J Virol 1993; 67: 7276–7283
   PubMedGoogle Scholar
• Ramakrishnan R, Levine M, Fink D J. PCR-based analysis of herpes simplex virus type 1 latency in the rat trigeminal ganglion established with a ribonucleotide reductase-deficient mutant. J Virol 1994; 68: 7083–7091
   Google Scholar
• Rozenberg F, Lebon P. Analysis of herpes simplex virus type 1 glycoprotein D nucleotide sequence in human herpes simplex encephalitis. J Neuro Virol 1996; 2, (this issue)
   Google Scholar
• Sawtell N M, Thompson R L. Herpes simplex virus type 1 latency-associated transcription unit promotes anatomical site-dependent establishment and reactivation from latency. J Virol 1992; 66: 2157–2169
   Google Scholar
• Sprecher E, Becker Y. Herpes simplex virus type 1 pathogenicity in footpad and ear skin of mice depends on Langerhans cell density, mouse genetics, and virus strain. J Virol 1987; 61: 2515–2522
   Google Scholar
• Spivack J G, Fraser N W. Detection of herpes simplex virus type 1 transcripts during latent infection in mice [published erratum appears. J Virol Feb, 1988; 62(2)663
   Google Scholar
• J Virol 1987; 61: 3841–3847
   PubMed Web of Science ®Google Scholar
• Steiner I, Spivack J G, Lirette R P, Brown S M, MacLean A R, Subak-Sharpe J H, Fraser N W. Herpes simplex virus type 1 latency-associated transcripts are evidently not essential for latent infection. EMBO J 1989; 8: 505–511
   PubMed Web of Science ®Google Scholar
• Steiner I, Spivack J G, Deshmane S L, Ace C I, Preston C M, Fraser N W. A herpes simplex virus type 1 mutant containing a nontransinducing Vmw65 protein establishes latent infection in vivo in the absence of viral replication and reactivates efficiently from explanted trigeminal ganglia. J Virol 1990; 64: 1630–1638
   PubMed Web of Science ®Google Scholar
• Steiner I, Kennedy P G. Herpes simplex virus latent infection in the nervous system. J NeuroVirol 1995; 1: 19–29
   PubMed Web of Science ®Google Scholar
• Stevens J G, Wagner E K, Devi-Rao G B, Cook M L, Feldman L T. RNA complementary to a herpesvirus alpha gene mRNA is prominent in latently infected neurons. Science 1987; 235: 1056–1059
   PubMed Web of Science ®Google Scholar
• Stroop W G, Baringer J R. Persistent, slow and latent viral infections. Prog Med Virol 1982; 28: 1–43
   PubMedGoogle Scholar
• Stroop W G, Schaefer D C. Severity of experimentally reactivated herpetic eye disease is related to the neurovirulence of the latent virus. Invest Ophthalmol Vis Sci 1987; 28: 229–237
   PubMed Web of Science ®Google Scholar
• Thompson R L, Wagner E K, Stevens J G. Physical location of a herpes simplex virus type 1 function(s) specifically involved with a 10 million-fold increase in HSV neurovirulence. Virology 1983; 131: 180–192
   PubMedGoogle Scholar
• Trousdale M D, Steiner I, Spivack J G, Deshmane S L, Brown S M, MacLean A R, Subak-Sharpe J H, Fraser N W. In vivo and in vitro reactivation impairment of a herpes simplex virus type 1 latency-associated transcript variant in a rabbit eye model. J Virol 1991; 65: 6989–6993
   PubMedGoogle Scholar
• Wagner E K, Devi-Rao G, Feldman L T, Dobson A T, Zhang Y F, Flanagan W M, Stevens J G. Physical characterization of the herpes simplex virus latency-associated transcript in neurons. J Virol 1988; 62: 1194–1202
   PubMed Web of Science ®Google Scholar
• Wilcox C L, Smith R L, Freed C R, Johnson E, Jr. Nerve growth factor-dependence of herpes simplex virus latency in peripheral sympathetic and sensory neurons in vitro. J Neurosci 1990; 10: 1268–1275
   PubMed Web of Science ®Google Scholar