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2013 | 62 | 3 |

Tytuł artykułu

The influence of toll-like receptor stimulation on expression of EBV lytic genes

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Epstein-Barr virus (EBV) establishes latency in the resting memory B-cell compartment. It has been recently suggested that maintenance of chronic infection is dependent on periodic reactivation. Although the stimuli for EBV reactivation in vivo during natural infections are largely unknown, there is evidence indicating that heterologous infections could trigger herpesviruses reactivation. The purpose of this work was to identify the influence of Toll-like receptors stimulation on EBV replication in EBV latently infected Burkitt lymphoma cells (P3HR-1, Raji and Namalwa). The cells were stimulated with Pam3CSK4 (synthetic triacylated lipoprotein), PolyI:C (synthetic analog of dsRNA), LPS (lipopolysaccharide from E.coli), measles virus (MeV) and PMA (phorbol myristate acetate). Non-stimulated cells (NS) served as control. EBV expression was investigated at mRNA level for three viral lytic genes: BZLF1 (immediate early, ZEBRA), BALF2 (early, EA) and BcLF1 (late, VCA). Additionally, the effect of stimulation on NF-kBp65 and inflammatory cytokines (IL-1b, IL-6, IL-8, IL-10, IL-12p70, and TNF) was investigated. Stimulation of TLRs led to limited changes in EBV expression manifesting as increase of ZEBRA at mRNA level in cells treated with PolyI:C and Pam3CSK4. Stimulation with PolyI:C, Pam3CSK4 and LPS also lead to considerable increase of NF-kBp65, while increased levels of inflammatory cytokines were observed for IL-8, TNF and IL-6 in cells treated with PMA and MeV. In conclusion, the results of our experiments support the suggestion that TLRs stimulation with microbial ligands influences EBV virus replication.

Wydawca

-

Rocznik

Tom

62

Numer

3

Opis fizyczny

p.237-242,fig.,ref.

Twórcy

autor
  • Department of Virology, National Institute of Public Heath - National Institute of Hygiene, Chocimska 24, 00-791 Warsaw, Poland
autor
  • Department of Virology, National Institute of Public Heath - National Institute of Hygiene, Chocimska 24, 00-791 Warsaw, Poland
autor
  • Department of Virology, National Institute of Public Heath - National Institute of Hygiene, Chocimska 24, 00-791 Warsaw, Poland
  • Department of Virology, National Institute of Public Heath - National Institute of Hygiene, Chocimska 24, 00-791 Warsaw, Poland
autor
  • Department of Virology, National Institute of Public Heath - National Institute of Hygiene, Chocimska 24, 00-791 Warsaw, Poland

Bibliografia

  • Adler B., E. Schaadt, B. Kempkes, U. Zimber-Strobl, B. Baier and G.W. Bornkamm. 2002. Control of Epstein-Barr virus reactivation by activated CD40 and viral latent membrane protein 1. Proc. Natl. Acad. Sci. USA 99: 437–442.
  • Arcenas R. and R.H. Widen. 2002. Epstein-Barr virus reactivation aXer superinfection of the +BJAB-B1 and P3HR-1 cell lines with cytomegalovirus. BMC Microbiol. 23: 2–20.
  • Bergallo M., C. Costa, S. Baro, T. Musso, L. Balbo, C. Merlino and R. Cavallo. 2007. Multiplex-nested RT-PCR to evaluate latent and lytic Epstein Barr virus gene expression. J. Biotechnol. 128: 462–476.
  • Bernasconi M., C. Berger, J.A. Sigrist, A. Bonanomi, J. Sobek, F.K. Niggli and D. Nadal. 2006. Quantitative profiling of housekeeping and Epstein-Barr virus gene transcription in Burkitt lymphoma cell lines using an oligonucleotide microarray. Virol. J. 3: 43.
  • Coleman C.B., M.S. Nealy and S.A. Tibbetts. 2010. Immature and transitional B cells are latency reservoirs for a gammaherpesvirus. J. Virol. 84: 13045–13052.
  • Decausin G., V. Leclerc and T. Ooke. 1995. The lytic cycle of Epstein-Barr virus in non-producer Raji lline can be rescued by the expression of a 135 kDa protein encoded by BALF2 ORF deleted cells. J. Virol. 69: 7309–7314.
  • El-Guindy A., L. Heston and G. Miller. 2010. A subset of replication proteins enhances origin recognition and lytic replication by the Epstein-Barr virus ZEBRA protein. PLoS Pathog. 6: e1001054.
  • Finberg R.W. and E.A. Kurt-Jones. 2004. Viruses and Toll-like receptors. Microbes Infect. 6: 1356–1360.
  • Gargano L.M., J.C. Forrest and S.H. Speck. 2009. Signaling through Toll-like receptors induces murine gammaherpes virus 68 reactivation in vivo. J. Virol. 83: 1474–1482.
  • Gray D., M. Gray and T. Barr. 2007. Innate responses of B cells. Eur. J. Immunol. 37: 3304–3310.
  • Henault M., L.N. Lee, G.F. Evans and S.H. Zuckerman. 2005. The human Burkitt lymphoma cell line Namalwa represents a homogenous cell system characterized by high levels of Toll-like receptor 9 and activation by CpG oligonucleotides. J. Immunol. Methods. 300: 93–99.
  • Hopkins P.A. and S. Sriskandan. 2005. Mammalian Toll-like receptors: to immunity and beyond. Clin. Exp. Immunol. 140: 395–407.
  • Hummel M. and M.M. Abecassis. 2002. A model for reactivation of CMV from latency. J. Clin. Virol. 25: 123–36.
  • Iskra S., M. Kalla, H.J. Delecluse, W. Hammerschmidt and A. Moosmann. 2010. Toll-like receptor agonists synergistically increase proliferation and activation of B cells by Epstein-Barr virus. J. Virol. 84: 3612–3623.
  • Kenney SC. 2007. Reactivation and lytic replication of EBV, pp. 403–433. In: Arvin A., Campadelli-Fiume G., Mocarski E., Moore P.S., Roizman B., Whotley R. and K. Yamanishi (eds). Human Herpes viruses: Biology, Therapy, and Immunoprophylaxis. Cambridge University Press, Cambridge.
  • Kieff E. and A.B. Rickinson. 2007. Epstein-Barr virus and its replication, pp. 2603–2654. In: Knipe D.M., Howley P.M., D.E. Griffin, R.A. Lamb, A.M. Malcolm, B. Roizman and S.E. Straus (eds). Fields virology. Lippincott Williams and Wilkins, Philadelphia, PA.
  • Merat R., A. Amara, C. Lebbe, H. de The, P. Morel and A. Saib. 2002. HIV-1 infection of primary effusion lymphoma cell line triggers Kaposi’s sarcoma-associated herpesvirus (KSHV) reactivation. Int. J. Cancer 97: 791–795.
  • Moynagh P.N. 2005. TLR signalling and activation of IRFs: revisiting old friends from the NF-kappaB pathway. Trends Immunol. 26: 469–473.
  • Pasare C. and R. Medzhitov. 2004. Toll-like receptors: linking innate and adaptive immunity. Microbes Infect. 6: 1382–1387.
  • Rickinson A.B. and E. Kieff. 2007. Epstein-Barr virus, pp. 2655–2700. In: Knipe D.M., Howley P.M., D.E. Griffin, R.A. Lamb, A.M. Malcolm, B. Roizman and S.E. Straus (eds). Fields virology. Lippincott Williams and Wilkins, Philadelphia, PA.
  • Rowe M., Kelly G.L., Bell A.I. and A.B. Rickinson. 2009. Burkitt’s lymphoma: the Rosetta Stone deciphering Epstein-Barr virus biology. Semin. Cancer Biol. 19: 377–388.
  • Shimozuma Y., T. Ito, M. Inokuchi, M. Uchikoshi, M. Miyashit, H. Nozawa, T. Shimazaki, K. Hiroishi and M. Imawari. 2010. Reactivation of Epstein-Barr virus in B cells of patients with chronic hepatitis C. J. Med. Virol. 82: 2064–2072.
  • Siennicka J., A. Trzcińska, A. Częścik and M. Dunal. 2011. Toll-like receptors expression on Burkitt lymphoma cells (In Polish). Med. Dośw. Mikrobiol. 63: 349–354.
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  • Varthakavi V., P.J. Browning and P. Spearman. 1999. Human immunodeficiency virus replication in a primary effusion lymphoma cell line stimulates lytic-phase replication of Kaposi’s sarcoma-associated herpesvirus. J. Virol. 73: 10329–10338.
  • Vogl B.A., U. Fagin, L. Nerbas, P. Schlenke, P. Lamprech and W.J. Jabs. 2012. Longitudinal analysis of frequency and reactivity of Epstein-Barr virus-specific T lymphocytes and their association with intermittent viral reactivation. J. Med. Virol. 84: 119–131.

Typ dokumentu

Bibliografia

Identyfikatory

Identyfikator YADDA

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