Le Sun and Qihan Li. The miRNAs of Herpes Simplex Virus (HSV)*[J]. Virologica Sinica, 2012, 27(6): 333-338. doi: 10.1007/s12250-012-3266-5
Citation: Le Sun, Qihan Li. The miRNAs of Herpes Simplex Virus (HSV)* .VIROLOGICA SINICA, 2012, 27(6) : 333-338.  http://dx.doi.org/10.1007/s12250-012-3266-5

The miRNAs of Herpes Simplex Virus (HSV)

cstr: 32224.14.s12250-012-3266-5
  • 通讯作者: Qihan Li, imbcams.lq@gmail.com
  • 收稿日期: 2012-06-28
    录用日期: 2012-10-24
  • Herpes simplex virus (HSV) is a group of common human pathogens with two serotypes HSV-1 and HSV-2. The prevalence of HSV is worldwide. It primarily infects humans through epithelial cells, when it introduces a latent infection into the nervous system. During viral latency, only a region known as the latency-associated transcript (LAT) is expressed. The discovery of HSV miRNAs helps to draw a larger picture of the infection and pathogenesis of the virus. This review summarizes miRNAs found in HSV-1 and HSV-2 so far. The functional studies of miRNAs in HSV to date indicate that they play a stage-specific role coordinated with viral proteins to maintain the virus life cycle.

The miRNAs of Herpes Simplex Virus (HSV)*

  • Corresponding author: Qihan Li, imbcams.lq@gmail.com
  • Received Date: 28 June 2012
    Accepted Date: 24 October 2012

    Fund Project: the National Natural Sciences Foundation of China 30700028Youth Science Research Foundation of PUMC 2012X23the National Natural Sciences Foundation of China 30670094

  • Herpes simplex virus (HSV) is a group of common human pathogens with two serotypes HSV-1 and HSV-2. The prevalence of HSV is worldwide. It primarily infects humans through epithelial cells, when it introduces a latent infection into the nervous system. During viral latency, only a region known as the latency-associated transcript (LAT) is expressed. The discovery of HSV miRNAs helps to draw a larger picture of the infection and pathogenesis of the virus. This review summarizes miRNAs found in HSV-1 and HSV-2 so far. The functional studies of miRNAs in HSV to date indicate that they play a stage-specific role coordinated with viral proteins to maintain the virus life cycle.

  • 加载中
    1. Bartel D P. 2004. Micrornas: Genomics, biogenesis, mechanism, and function. Cell, 116(2): 281-297.
        doi: 10.1016/S0092-8674(04)00045-5

    2. Bunzli D, Wietlisbach V, Barazzoni F, et al. 2004. Seroepidemiology of herpes simplex virus type 1 and 2 in western and southern switzerland in adults aged 25-74 in 1992-93: A population-based study. BMC Infect Dis, 4: 10.
        doi: 10.1186/1471-2334-4-10

    3. Cai W, Schaffer P A. 1992. Herpes simplex virus type 1 icp0 regulates expression of immediate-early, early, and late genes in productively infected cells. J Virol, 66(5): 2904-2915.

    4. Cai W, Astor T L, Liptak L M, et al. 1993. The herpes simplex virus type 1 regulatory protein icp0 enhances virus replication during acute infection and reactivation from latency. J Virol, 67(12): 7501-7512.

    5. Cho W C. 2007. Oncomirs: The discovery and progress of micrornas in cancers. Mol Cancer, 6: 60.
        doi: 10.1186/1476-4598-6-60

    6. Chou J, Roizman B. 1986. The terminal a sequence of the herpes simplex virus genome contains the promoter of a gene located in the repeat sequences of the l component. J Virol, 57(2): 629-637.

    7. Cui C, Griffiths A, Li G, et al. 2006. Prediction and identification of herpes simplex virus 1-encoded micrornas. J Virol, 80(11): 5499-5508.
        doi: 10.1128/JVI.00200-06

    8. Duan F, Liao J, Huang Q, et al. 2012. Hsv-1 mir-h6 inhibits hsv-1 replication and il-6 expression in human corneal epithelial cells in vitro. Clin Dev Immunol, doi:10.1155/ 2012/192791

    9. Everett R D. 1987. A detailed mutational analysis of vmw110, a trans-acting transcriptional activator encoded by herpes simplex virus type 1. EMBO J, 6(7): 2069-2076.

    10. Everett R D. 2000. Icp0, a regulator of herpes simplex virus during lytic and latent infection. Bioessays, 22(8): 761-770.
        doi: 10.1002/1521-1878(200008)22:8<>1.0.CO;2-0

    11. Goujon M, McWilliam H, Li W, et al. 2010. A new bioinformatics analysis tools framework at EMBL-EBI. Nucleic Acids Res, 38 Suppl: W695-W699.

    12. Honess R W, Roizman B. 1974. Regulation of herpesvirus macromolecular synthesis. I. Cascade regulation of the synthesis of three groups of viral proteins. J Virol, 14(1): 8-19.

    13. Hukkanen V, Paavilainen H, Mattila R K. 2010. Host responses to herpes simplex virus and herpes simplex virus vectors. Future Virol, 5(4): 493-512.
        doi: 10.2217/fvl.10.35

    14. Javier R T, Stevens J G, Dissette V B, et al. 1988. A herpes simplex virus transcript abundant in latently infected neurons is dispensable for establishment of the latent state. Virology, 166(1): 254-257.
        doi: 10.1016/0042-6822(88)90169-9

    15. Jawa R S, Anillo S, Huntoon K, et al. 2011. Analytic review: Interleukin-6 in surgery, trauma, and critical care: Part i: Basic science. J Intensive Care Med, 26(1): 3-12.
        doi: 10.1177/0885066610395678

    16. Jurak I, Kramer M F, Mellor J C, et al. 2010. Numerous conserved and divergent micrornas expressed by herpes simplex viruses 1 and 2. J Virol, 84(9): 4659-4672.
        doi: 10.1128/JVI.02725-09

    17. Kramer M F, Jurak I, Pesola J M, et al. 2011. Herpes simplex virus 1 micrornas expressed abundantly during latent infection are not essential for latency in mouse trigeminal ganglia. Virology, 417(2): 239-247.
        doi: 10.1016/j.virol.2011.06.027

    18. Lagunoff M, Roizman B. 1995. The regulation of synthesis and properties of the protein product of open reading frame p of the herpes simplex virus 1 genome. J Virol, 69(6): 3615-3623.

    19. Larkin M A, Blackshields G, Brown N P, et al. 2007. Clustal W and Clustal X version 2.0. Bioinformatics, 23(21): 2947-2948.
        doi: 10.1093/bioinformatics/btm404

    20. Lin Z, Flemington E K. 2011. Mirnas in the pathogenesis of oncogenic human viruses. Cancer Lett, 305(2): 186-199.
        doi: 10.1016/j.canlet.2010.08.018

    21. Lu L F, Liston A. 2009. Microrna in the immune system, microrna as an immune system. Immunology, 127(3): 291-298.
        doi: 10.1111/imm.2009.127.issue-3

    22. Mador N, Goldenberg D, Cohen O, et al. 1998. Herpes simplex virus type 1 latency-associated transcripts suppress viral replication and reduce immediate-early gene mrna levels in a neuronal cell line. J Virol, 72(6): 5067-5075.

    23. Manni I, Artuso S, Careccia S, et al. 2009. The microrna mir-92 increases proliferation of myeloid cells and by targeting p63 modulates the abundance of its isoforms. FASEB J, 23(11): 3957-3966.
        doi: 10.1096/fj.09-131847

    24. Mavromara-Nazos P, Silver S, Hubenthal-Voss J, et al. 1986. Regulation of herpes simplex virus 1 genes: Alpha gene sequence requirements for transient induction of indicator genes regulated by beta or late (gamma 2) promoters. Virology, 149(2): 152-164.
        doi: 10.1016/0042-6822(86)90117-0

    25. Munson D J, Burch A D. 2012. A novel mirna produced during lytic hsv-1 infection is important for efficient replication in tissue culture. Arch Virol, 157(9):1677-1688.
        doi: 10.1007/s00705-012-1345-4

    26. Nakahara K, Carthew R W. 2004. Expanding roles for mirnas and sirnas in cell regulation. Curr Opin Cell Biol, 16(2): 127-133.
        doi: 10.1016/j.ceb.2004.02.006

    27. Nicoll M P, Proenca J T, Efstathiou S. 2012. The molecular basis of herpes simplex virus latency. FEMS Microbiol Rev, 36(3): 684-705.
        doi: 10.1111/j.1574-6976.2011.00320.x

    28. Paludan S R. 2001. Requirements for the induction of interleukin-6 by herpes simplex virus-infected leukocytes. J Virol, 75(17): 8008-8015.
        doi: 10.1128/JVI.75.17.8008-8015.2001

    29. Pellett P E, Roizman B. 2007. The family herpesviridae: A brief introduction. In: Fields' Virology, 5th Ed. Philadelphia: Lippincott Williams & Wilkins. Knipe D M, Howley P M, Griffin D E, et al. ed. pp2479-2499.

    30. Randall G, Lagunoff M, Roizman B. 1997. The product of orf o located within the domain of herpes simplex virus 1 genome transcribed during latent infection binds to and inhibits in vitro binding of infected cell protein 4 to its cognate DNA site. Proc Natl Acad Sci U S A, 94(19): 10379-10384.
        doi: 10.1073/pnas.94.19.10379

    31. Randall G, Lagunoff M, Roizman B. 2000. Herpes simplex virus 1 open reading frames o and p are not necessary for establishment of latent infection in mice. J Virol, 74(19): 9019-9027.
        doi: 10.1128/JVI.74.19.9019-9027.2000

    32. Roizman B, Knipe D M, Whitley R J. 2007. Herpes simplex viruses, In: Fields virology, 5th ed. Knipe D M, Howley P, Griffin D E, et al, ed. Philadelphia: Lippincott Williams & Wilkins, pp2501-2601.

    33. Sawtell N M, Poon D K, Tansky C S, et al. 1998. The latent herpes simplex virus type 1 genome copy number in individual neurons is virus strain specific and correlates with reactivation. J Virol, 72(7): 5343-5350.

    34. Steiner I, Spivack J G, Lirette R P, et al. 1989. Herpes simplex virus type 1 latency-associated transcripts are evidently not essential for latent infection. EMBO J, 8(2): 505-511.

    35. Stern-Ginossar N, Elefant N, Zimmermann A, et al. 2007. Host immune system gene targeting by a viral mirna. Science, 317(5836): 376-381.
        doi: 10.1126/science.1140956

    36. Stevens J G, Wagner E K, Devi-Rao G B, et al. 1987. Rna complementary to a herpesvirus alpha gene mrna is prominent in latently infected neurons. Science, 235(4792): 1056-1059.
        doi: 10.1126/science.2434993

    37. Tang S, Patel A, Krause P R. 2009. Novel less-abundant viral micrornas encoded by herpes simplex virus 2 latency-associated transcript and their roles in regulating icp34.5 and icp0 mrnas. J Virol, 83(3): 1433-1442.
        doi: 10.1128/JVI.01723-08

    38. Tang S, Bertke A S, Patel A, et al. 2011. Herpes simplex virus 2 microrna mir-h6 is a novel latency-associated transcript-associated microrna, but reduction of its expression does not influence the establishment of viral latency or the recurrence phenotype. J Virol, 85(9): 4501-4509.
        doi: 10.1128/JVI.01997-10

    39. Tang S, Bertke A S, Patel A, et al. 2008. An acutely and latently expressed herpes simplex virus 2 viral microrna inhibits expression of icp34.5, a viral neurovirulence factor. Proc Natl Acad Sci U S A, 105(31): 10931-10936.
        doi: 10.1073/pnas.0801845105

    40. Toma H S, Murina A T, Areaux R G, et al. 2008. Ocular hsv-1 latency, reactivation and recurrent disease. Semin Ophthalmol, 23(4): 249-273.
        doi: 10.1080/08820530802111085

    41. Umbach J L, Nagel M A, Cohrs R J, et al. 2009. Analysis of human alphaherpesvirus microrna expression in latently infected human trigeminal ganglia. J Virol, 83(20): 10677-10683.
        doi: 10.1128/JVI.01185-09

    42. Umbach J L, Kramer M F, Jurak I, et al. 2008. Micrornas expressed by herpes simplex virus 1 during latent infection regulate viral mrnas. Nature, 454(7205): 780-783.

    43. Umbach J L, Wang K, Tang S, et al. 2010. Identification of viral micrornas expressed in human sacral ganglia latently infected with herpes simplex virus 2. J Virol, 84(2): 1189-1192.
        doi: 10.1128/JVI.01712-09

    44. Veksler-Lublinsky I, Shemer-Avni Y, Kedem K, et al. 2010. Gene bi-targeting by viral and human mirnas. BMC Bioinformatics, 11: 249.
        doi: 10.1186/1471-2105-11-249

    45. Vyse A J, Gay N J, Slomka M J, et al. 2000. The burden of infection with hsv-1 and hsv-2 in england and wales: Implications for the changing epidemiology of genital herpes. Sex Transm Infect, 76(3): 183-187.
        doi: 10.1136/sti.76.3.183

    46. Wagner E K, Devi-Rao G, Feldman L T, et al. 1988. Physical characterization of the herpes simplex virus latency-associated transcript in neurons. J Virol, 62(4): 1194-1202.

    47. Wald A, Corey L. 2007. Persistence in the population: Epidemiology, transmission. In: Human herpesviruses: Biology, therapy, and immunoprophylaxis. Arvin A, Campadelli-Fiume G, Mocarski E, et al. , ed. Cambridge: Cambridge University Press, p656-672.

    48. Wang Y, Lee C G. 2009. Microrna and cancer--focus on apoptosis. J Cell Mol Med, 13(1): 12-23.

    49. Wienholds E, Koudijs M J, Van Eeden F J, et al. 2003. The microrna-producing enzyme dicer1 is essential for zebrafish development. Nat Genet, 35(3): 217-218.
        doi: 10.1038/ng1251

    50. Xu F, Schillinger J A, Sternberg M R, et al. 2002. Seroprevalence and coinfection with herpes simplex virus type 1 and type 2 in the united states, 1988-1994. J Infect Dis, 185(8): 1019-1024.
        doi: 10.1086/jid.2002.185.issue-8

    51. Xu F, Sternberg M R, Kottiri B J, et al. 2006. Trends in herpes simplex virus type 1 and type 2 seroprevalence in the united states. JAMA, 296(8): 964-973.
        doi: 10.1001/jama.296.8.964

    52. Zabolotny J M, Krummenacher C, Fraser N W. 1997. The herpes simplex virus type 1 2.0-kilobase latency-associated transcript is a stable intron which branches at a guanosine. J Virol, 71(6): 4199-4208.

  • 加载中

Tables(3)

Article Metrics

Article views(8180) PDF downloads(21) Cited by(0)

Related
Proportional views
    通讯作者: 陈斌, bchen63@163.com
    • 1. 

      沈阳化工大学材料科学与工程学院 沈阳 110142

    1. 本站搜索
    2. 百度学术搜索
    3. 万方数据库搜索
    4. CNKI搜索

    The miRNAs of Herpes Simplex Virus (HSV)*

      Corresponding author: Qihan Li, imbcams.lq@gmail.com
    • Department of Viral Immunology, Institute of Medical Biology, Chinese Academy of Medicine Science, Peking Union Medical College, Kunming 650118, China
    Fund Project:  the National Natural Sciences Foundation of China 30700028Youth Science Research Foundation of PUMC 2012X23the National Natural Sciences Foundation of China 30670094

    Abstract: Herpes simplex virus (HSV) is a group of common human pathogens with two serotypes HSV-1 and HSV-2. The prevalence of HSV is worldwide. It primarily infects humans through epithelial cells, when it introduces a latent infection into the nervous system. During viral latency, only a region known as the latency-associated transcript (LAT) is expressed. The discovery of HSV miRNAs helps to draw a larger picture of the infection and pathogenesis of the virus. This review summarizes miRNAs found in HSV-1 and HSV-2 so far. The functional studies of miRNAs in HSV to date indicate that they play a stage-specific role coordinated with viral proteins to maintain the virus life cycle.