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MeSH Review

Herpesvirus 2, Human

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Disease relevance of Herpesvirus 2, Human

  • It has been established that HSV-1 and HSV-2 infectivity may be neutralized in vitro with antisera directed specifically against each of the four major glycoproteins of the virus (gA/gB, gC, gD and gE) and antisera against glycoprotein gD, of either HSV-1 or HSV-2, are capable of neutralizing both HSV-1 and HSV-2 infectivity in vitro and in vivo [1].
  • Among the HPV DNA-positive women, HSV-2 seropositivity was associated with increased risks of squamous-cell carcinoma (OR = 2.19, 95% CI = 1.41 to 3.40) and adeno- or adenosquamous-cell carcinoma (OR = 3.37, 95% CI = 1.47 to 7.74) after adjustment for potential confounders [2].
  • A hypothesis is proposed which states that multiple sclerosis (MS) is caused by herpes simplex virus type 2 (HSV-2) in persons lacking herpes simplex virus type 1(HSV-1) immunity [3].
  • OBJECTIVE: To evaluate the safety and immunogenicity of a recombinant glycoprotein vaccine for herpes simplex virus type 2 (HSV-2), which contains glycoproteins gD2 and gB2 combined with the novel MF59 adjuvant emulsion, in HSV-2-seronegative persons [4].
  • We review herpesvirus infections of the nervous system and illustrate the expanding spectrum of disease by including examples of a 75-year-old male on steroid treatment for chronic lung disease with fatal HSV-2 meningitis and an 81-year-old male with myasthenia gravis, long-term azathioprine use, and an EBV-associated primary CNS lymphoma [5].

Psychiatry related information on Herpesvirus 2, Human

  • Although heroin and cocaine use, during drug injection, and rates of infection with parenterally transmitted infectious agents appear to be lower among these youth, sexual risk behaviors and chlamydial and HSV-2 infection are widespread [6].

High impact information on Herpesvirus 2, Human

  • HSV-2 antibody was assessed with an immunodot assay specific for glycoprotein gG-2 of HSV-2 [7].
  • The recognition of HSV-2 by TLR9 was mediated through an endocytic pathway that was inhibited by chloroquine or bafilomycin A1 [8].
  • Next, we identified that IFN-alpha secretion by pDCs required the expression of the adaptor molecule MyD88, suggesting the involvement of a Toll-like receptor (TLR) in HSV-2 recognition [8].
  • Further, we demonstrated that purified HSV-2 DNA can trigger IFN-alpha secretion from pDCs and that inhibitory CpG oligonucleotide treatment diminished HSV-induced IFN-alpha secretion by pDCs in a dose-dependent manner [8].
  • Here, we examined the cell types responsible for the initiation of protective Th1 immunity to HSV-2 [9].

Chemical compound and disease context of Herpesvirus 2, Human

  • We also report that solubilized gC-2, the genetically related glycoprotein specified by HSV-2, binds to iC3-Sepharose. mAb specific for gC-1 or gC-2 and mutant viral strains were used to identify the C3-binding glycoproteins [10].
  • Daily samples of genital secretions were obtained from 27 HSV-2 seropositive women; a subset of subjects obtained samples while receiving oral acyclovir 400 mg PO twice a day [11].
  • Hybrids were exposed to bromodeoxyuridine (BrdUrd) as a means of selection for cells that had lost HSV-2 TK activity [12].
  • Breakthrough reactivations that occurred while patients were receiving famciclovir were infrequent, short, and often asymptomatic, HSV-2 isolates from these reactivations were susceptible to penciclovir in vitro [13].
  • Resistance to 2'NDG by HSV-2 ts6 can be overcome in the presence of combinations of 2'NDG and phosphonoacetic acid, indicating drug synergism within the viral DNA polymerase locus [14].

Biological context of Herpesvirus 2, Human

  • Isoenzyme and karyotyping data obtained from 33 BrdUrd-resistant sublines were consistent with the hypothesis that the HSV-2 TK gene is associated with chromosome No. 18 in the HB-2-3 cell line [12].
  • Apoptosis induced by HSV-2 was not inhibited by cycloheximide and only partially by an UV-treatment which completely abrogated infectivity [15].
  • These findings indicate that the recovery of HSV-2 from the model of latency in IMR-32 cells is enhanced by HMBA treatment, which induces a significant decrease of total genomic DNA methylation level, and is inhibited by cyclosporin A treatment [16].
  • By day 7 PI, HSV-2 glycoprotein B transcript expression was no longer detectable in vaginal tissue from the IFN-alpha1 transgene-treated group (0/8) compared with levels expressed in plasmid vector-treated controls (4/6 mice surveyed were positive) [17].
  • HSV-2 also increases CE synthesis and 3-hydroxy- 3-methylglutaryl-CoA reductase activity but concomitantly reduces CE hydrolysis and cholesterol efflux [18].

Anatomical context of Herpesvirus 2, Human

  • HSV-2 infection marginally increases the level of TNF-alpha mRNA and protein in resting macrophages, whereas a strong increase is observed in IFN-gamma-activated cells infected with the virus [19].
  • With a panel of 60 overlapping peptides covering the entire sequence of the VP16 protein, a major Ag for HSV-2, we generated a panel of class II MHC tetramers loaded with peptide pools that were used to stain peripheral lymphocytes of an HSV-2 infected individual [20].
  • Hence, we have for the first time been able to identify a potential function of the secreted portion of HSV-2 glycoprotein G. We propose that the proinflammatory gG-2p20 peptide identified could contribute to a reduced function and viability of NK cells during HSV-2 infection due to its ability to recruit and activate phagocytic cells [21].
  • A reduction in virus isolations from lumbosacral ganglia was noted during both acute and latent infection with HSV-2 (WT-186) in the acyclovir-treated groups [22].
  • The antigens recognized by many HSV-specific CD4 T cells localizing to genital HSV-2 lesions are unknown [23].

Gene context of Herpesvirus 2, Human

  • SP was shown to weakly interfere with the HSV-2 replication [24].
  • In conclusion, the present results indicate that SP and NK1R signaling contributes to the innate resistance against HSV-2 infection in mice [24].
  • Furthermore, normal HSV-2-specific IgG responses were generated in the LT beta-deficient mice following intravaginal HSV-2 infection even in the absence of the spleen [25].
  • Furthermore, we showed that IL-15 is important for CpG oligodeoxynucleotide (ODN)-induced innate protection against genital HSV-2 infection [26].
  • Lastly, a treatment of RAW264.7 cells with mrIL-15 induced the production of tumor necrosis factor alpha and beta interferon (IFN-beta), but not IFN-alpha, and significantly protected them against HSV-2 infection in vitro [26].

Analytical, diagnostic and therapeutic context of Herpesvirus 2, Human


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  2. Herpes simplex virus-2 as a human papillomavirus cofactor in the etiology of invasive cervical cancer. Smith, J.S., Herrero, R., Bosetti, C., Muñoz, N., Bosch, F.X., Eluf-Neto, J., Castellsagué, X., Meijer, C.J., Van den Brule, A.J., Franceschi, S., Ashley, R. J. Natl. Cancer Inst. (2002) [Pubmed]
  3. Herpes simplex virus types 1 and 2 and multiple sclerosis. Martin, J.R. Lancet (1981) [Pubmed]
  4. A recombinant glycoprotein vaccine for herpes simplex virus type 2: safety and immunogenicity [corrected]. Langenberg, A.G., Burke, R.L., Adair, S.F., Sekulovich, R., Tigges, M., Dekker, C.L., Corey, L. Ann. Intern. Med. (1995) [Pubmed]
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  6. Sex, drugs, and infections among youth. Parenterally and sexually transmitted diseases in a high-risk neighborhood. Friedman, S.R., Curtis, R., Jose, B., Neaigus, A., Zenilman, J., Culpepper-Morgan, J., Borg, L., Kreek, J., Paone, D., Des Jarlais, D.C. Sexually transmitted diseases. (1997) [Pubmed]
  7. Herpes simplex virus type 2 in the United States, 1976 to 1994. Fleming, D.T., McQuillan, G.M., Johnson, R.E., Nahmias, A.J., Aral, S.O., Lee, F.K., St Louis, M.E. N. Engl. J. Med. (1997) [Pubmed]
  8. Toll-like receptor 9-mediated recognition of Herpes simplex virus-2 by plasmacytoid dendritic cells. Lund, J., Sato, A., Akira, S., Medzhitov, R., Iwasaki, A. J. Exp. Med. (2003) [Pubmed]
  9. Vaginal submucosal dendritic cells, but not Langerhans cells, induce protective Th1 responses to herpes simplex virus-2. Zhao, X., Deak, E., Soderberg, K., Linehan, M., Spezzano, D., Zhu, J., Knipe, D.M., Iwasaki, A. J. Exp. Med. (2003) [Pubmed]
  10. Herpes simplex virus glycoproteins gC-1 and gC-2 bind to the third component of complement and provide protection against complement-mediated neutralization of viral infectivity. McNearney, T.A., Odell, C., Holers, V.M., Spear, P.G., Atkinson, J.P. J. Exp. Med. (1987) [Pubmed]
  11. Frequent genital herpes simplex virus 2 shedding in immunocompetent women. Effect of acyclovir treatment. Wald, A., Corey, L., Cone, R., Hobson, A., Davis, G., Zeh, J. J. Clin. Invest. (1997) [Pubmed]
  12. Association of herpes simplex thymidine kinase gene with chromosome No. 18 in transformed human cells. McKinlay, M.A., Wilson, D.E., Harrison, B., Povey, S. J. Natl. Cancer Inst. (1980) [Pubmed]
  13. Famciclovir for the suppression of symptomatic and asymptomatic herpes simplex virus reactivation in HIV-infected persons. A double-blind, placebo-controlled trial. Schacker, T., Hu, H.L., Koelle, D.M., Zeh, J., Saltzman, R., Boon, R., Shaughnessy, M., Barnum, G., Corey, L. Ann. Intern. Med. (1998) [Pubmed]
  14. Resistance of herpes simplex virus to 9-[[2-hydroxy-1-(hydroxymethyl)ethoxy]methyl]guanine: physical mapping of drug synergism within the viral DNA polymerase locus. Crumpacker, C.S., Kowalsky, P.N., Oliver, S.A., Schnipper, L.E., Field, A.K. Proc. Natl. Acad. Sci. U.S.A. (1984) [Pubmed]
  15. Herpes simplex virus 2 causes apoptotic infection in monocytoid cells. Mastino, A., Sciortino, M.T., Medici, M.A., Perri, D., Ammendolia, M.G., Grelli, S., Amici, C., Pernice, A., Guglielmino, S. Cell Death Differ. (1997) [Pubmed]
  16. Effect of hexamethylene bisacetamide and cyclosporin A on recovery of herpes simplex virus type 2 from the in vitro model of latency in a human neuroblastoma cell line. Kondo, Y., Yura, Y., Iga, H., Yanagawa, T., Yoshida, H., Furumoto, N., Sato, M. Cancer Res. (1990) [Pubmed]
  17. The application of a plasmid DNA encoding IFN-alpha 1 postinfection enhances cumulative survival of herpes simplex virus type 2 vaginally infected mice. Härle, P., Noisakran, S., Carr, D.J. J. Immunol. (2001) [Pubmed]
  18. Altered cholesterol trafficking in herpesvirus-infected arterial cells. Evidence for viral protein kinase-mediated cholesterol accumulation. Hsu, H.Y., Nicholson, A.C., Pomerantz, K.B., Kaner, R.J., Hajjar, D.P. J. Biol. Chem. (1995) [Pubmed]
  19. Expression of TNF-alpha by herpes simplex virus-infected macrophages is regulated by a dual mechanism: transcriptional regulation by NF-kappa B and activating transcription factor 2/Jun and translational regulation through the AU-rich region of the 3' untranslated region. Paludan, S.R., Ellermann-Eriksen, S., Kruys, V., Mogensen, S.C. J. Immunol. (2001) [Pubmed]
  20. Tetramer-guided epitope mapping: rapid identification and characterization of immunodominant CD4+ T cell epitopes from complex antigens. Novak, E.J., Liu, A.W., Gebe, J.A., Falk, B.A., Nepom, G.T., Koelle, D.M., Kwok, W.W. J. Immunol. (2001) [Pubmed]
  21. A proinflammatory peptide from herpes simplex virus type 2 glycoprotein G affects neutrophil, monocyte, and NK cell functions. Bellner, L., Thorén, F., Nygren, E., Liljeqvist, J.A., Karlsson, A., Eriksson, K. J. Immunol. (2005) [Pubmed]
  22. Effect of acyclovir on genital infection with herpes simplex virus types 1 and 2 in the guinea pig. Landry, M.L., Lucia, H.L., Hsiung, G.D., Pronovost, A.D., Dann, P.R., August, M.J., Mayo, D.R. Am. J. Med. (1982) [Pubmed]
  23. Recognition of herpes simplex virus type 2 tegument proteins by CD4 T cells infiltrating human genital herpes lesions. Koelle, D.M., Frank, J.M., Johnson, M.L., Kwok, W.W. J. Virol. (1998) [Pubmed]
  24. Neurokinin 1 receptor signaling affects the local innate immune defense against genital herpes virus infection. Svensson, A., Kaim, J., Mallard, C., Olsson, A., Brodin, E., Hökfelt, T., Eriksson, K. J. Immunol. (2005) [Pubmed]
  25. MAdCAM-1 expressing sacral lymph node in the lymphotoxin beta-deficient mouse provides a site for immune generation following vaginal herpes simplex virus-2 infection. Soderberg, K.A., Linehan, M.M., Ruddle, N.H., Iwasaki, A. J. Immunol. (2004) [Pubmed]
  26. NK and NKT cell-independent contribution of interleukin-15 to innate protection against mucosal viral infection. Gill, N., Rosenthal, K.L., Ashkar, A.A. J. Virol. (2005) [Pubmed]
  27. Recombinant glycoprotein vaccine for the prevention of genital HSV-2 infection: two randomized controlled trials. Chiron HSV Vaccine Study Group. Corey, L., Langenberg, A.G., Ashley, R., Sekulovich, R.E., Izu, A.E., Douglas, J.M., Handsfield, H.H., Warren, T., Marr, L., Tyring, S., DiCarlo, R., Adimora, A.A., Leone, P., Dekker, C.L., Burke, R.L., Leong, W.P., Straus, S.E. JAMA (1999) [Pubmed]
  28. Rheumatoid factors react with Fab fragments of monoclonal antibodies to herpes simplex virus types 1 and 2 Fc gamma-binding proteins. Tsuchiya, N., Malone, C., Hutt-Fletcher, L.M., Williams, R.C. Arthritis Rheum. (1991) [Pubmed]
  29. Induction of murine p30 by superinfecting herpesviruses. Reed, C.L., Rapp, F. J. Virol. (1976) [Pubmed]
  30. Superior cytostatic activity of the ganciclovir elaidic acid ester due to the prolonged intracellular retention of ganciclovir anabolites in herpes simplex virus type 1 thymidine kinase gene-transfected tumor cells. Balzarini, J., Degrève, B., Andrei, G., Neyts, J., Sandvold, M., Myhren, F., de Clercq, E. Gene Ther. (1998) [Pubmed]
  31. Locations of herpes simplex virus type 2 glycoprotein B epitopes recognized by human serum immunoglobulin G antibodies. Goade, D.E., Bell, R., Yamada, T., Mertz, G.J., Jenison, S. J. Virol. (1996) [Pubmed]
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