摘要 痘病毒(Poxvirus)是病毒颗粒最大的一类 DNA 病毒,结构复杂;感染人和动物后常引起局部或全身化脓性皮肤损害,给畜牧业带来严重的经济损失同时也威胁着人类健康。痘病毒可通过多种策略调控宿主基因的转录进而影响其免疫应答。基因芯片通过对宿主细胞在病毒感染前后基因表达谱的检测,为病毒的致病机制及病毒感染对宿主的调控机制的研究提供了便利手段。本文综述了有关基因芯片在痘病毒研究中的应用。
Abstract:Poxvirus is the largest DNA virus, containing complicated structure. It can cause local or systemic purulent damage to skin after infection of humans or animals. Furthermore, it brings about serious economic loss to livestock and threatens human health. Poxvirus could regulate and controlle host cell gene transcription by a variety of strategies, which in turn affect the host immune response. Gene microarray provides a convenient mean for studying the pathogenic mechanism of virus and regulatory mechanism of the host by detection of the host cell gene expression profile before or after the poxvirus infection. This paper reviews the related application of gene microarray on the poxvirus research.
[1] Cyrklaff M, Risco C, Fernandez JJ, et al. Cryo-electron tomography of vaccinia virus[J]. Proc Natl Acad Sci U S A, 2005, 102(8): 2772-2777. doi:10.1073/pnas.0409825102. [2] Hobi S, Mueller RS, Hill M, et al. Neurogenic inflammation and colliquative lymphadenitis with persistent orthopox virus DNA detection in a human case of cowpox virus infection transmitted by a domestic cat[J]. Br J Dermatol, 2015, 173(2): 535-539. doi:10.1111/bjd.13700. [3] Haller SL, Peng C, Mcfadden G, et al. Poxviruses and the evolution of host range and virulence[J]. Infect Genet Evol, 2014, 21: 15-40. doi:10.1016/j.meegid.2013.10.014. [4] Joseph RH, Haddad FA, Matthews AL, et al. Erythema multiforme after orf virus infection: a report of two cases and literature review[J]. Epidemiol Infect, 2015, 143(2): 385-390. doi:10.1017/S0950268814000879. [5] Veraldi S, Nazzaro G, Vaira F, et al. Presentation of orf (ecthyma contagiosum) after sheep slaughtering for religious feasts[J]. Infection, 2014, 42(4): 767-769. doi:10.1007/s15010-014-0591-7. [6] Thurman RJ, Fitch RW. Images in clinical medicine. Contagious ecthyma[J]. N Engl J Med, 2015, 372(8): e12. doi:10.1056/NEJMicm1304779. [7] Orbuch DE, Kim RH, Cohen DE. Ecthyma: a potential mimicker of zoonotic infections in a returning traveler[J]. Int J Infect Dis, 2014, 29: 178-180. doi:10.1016/j.ijid.2014.08.014. [8] Kilic SS, Puel A, Casanova JL. Orf infection in a patient with Stat1 gain-of-function[J]. J Clin Immunol, 2015, 35(1):80-83. doi:10.1007/s10875-014-0111-7. [9] Johnston JB, Mcfadden G. Poxvirus immunomodulatory strategies: current perspectives[J]. J Virol, 2003, 77(11): 6093-6100. doi:10.1128/JVI.77.11.6093-6100.2003 [10] Schena M, Shalon D, Davis RW, et al. Quantitative monitoring of gene expression patterns with a complementary DNA microarray[J]. Science, 1995, 270(5235): 467-470. DOI. [11] Jebar AH, Errington-Mais F, Vile RG, et al. Progress in clinical oncolytic virus-based therapy for hepatocellular carcinoma[J]. J Gen Virol, 2015, 96(7): 1533-1550. doi:10.1099/vir.0.000098. [12] Ya Z, Hailemichael Y, Overwijk W, et al. Mouse model for pre-clinical study of human cancer immunotherapy[J]. Curr Protoc Immunol, 2015, 108: 20-21. doi:10.1002/0471142735.im2001s108. [13] Rosales R, Rosales C. Immune therapy for human papillomaviruses-related cancers[J]. World J Clin Oncol, 2014, 5(5): 1002-1019. doi:10.5306/wjco.v5.i5.1002. [14] Knitlova J, Hajkova V, Voska L, et al. Development of eczema vaccinatum in atopic mouse models and efficacy of MVA vaccination against lethal poxviral infection[J]. PLoS One, 2014, 9(12): e114374. doi:10.1371/journal.pone.0114374. [15] Swadling L, Capone S, Antrobus RD, et al. A human vaccine strategy based on chimpanzee adenoviral and MVA vectors that primes, boosts, and sustains functional HCV-specific T cell memory[J]. Sci Transl Med, 2014, 6(261): 153r-261r. doi:10.1126/scitranslmed.3009185. [16] Thiele F, Tao S, Zhang Y, et al. Modified vaccinia virus Ankara-infected dendritic cells present CD4 + T-cell epitopes by endogenous major histocompatibility complex class II presentation pathways[J]. J Virol, 2015, 89(5): 2698-2709. doi:10.1128/JVI.03244-14. [17] Royo S, Sainz BJ, Hernandez-Jimenez E, et al. Differential induction of apoptosis, interferon signaling, and phagocytosis in macrophages infected with a panel of attenuated and nonattenuated poxviruses[J]. J Virol, 2014, 88(10): 5511-5523. doi:10.1128/JVI.00468-14. [18] Reinboth J, Ascierto ML, Chen NG, et al. Correlates between host and viral transcriptional program associated with different oncolytic vaccinia virus isolates[J]. Hum Gene Ther Methods, 2012, 23(5): 285-296. doi:10.1089/hgtb.2012.057. [19] Bourquain D, Dabrowski PW, Nitsche A. Comparison of host cell gene expression in cowpox, monkeypox or vaccinia virus-infected cells reveals virus-specific regulation of immune response genes[J]. Virol J, 2013, 10: 61. doi:10.1186/1743-422X-10-61. [20] Gomez CE, Perdiguero B, Garcia-Arriaza J, et al. Clinical applications of attenuated MVA poxvirus strain[J]. Expert Rev Vaccines, 2013, 12(12): 1395-1416. doi:10.1586/14760584.2013.845531. [21] Guerra S, Lopez-Fernandez LA, Pascual-Montano A, et al. Host response to the attenuated poxvirus vector NYVAC: upregulation of apoptotic genes and NF-kappaB-responsive genes in infected HeLa cells[J]. J Virol, 2006, 80(2): 985-998. doi:10.1128/JVI.80.2.985-998.2006. [22] Guerra S, Najera JL, Gonzalez JM, et al. Distinct gene expression profiling after infection of immature human monocyte-derived dendritic cells by the attenuated poxvirus vectors MVA and NYVAC[J]. J Virol, 2007, 81(16): 8707-8721. doi:10.1128/JVI.00444-07. [23] Guerra S, Gonzalez JM, Climent N, et al. Selective induction of host genes by MVA-B, a candidate vaccine against HIV/AIDS[J]. J Virol, 2010, 84(16): 8141-8152. doi:10.1128/JVI.00749-10. [24] Delaloye J, Filali-Mouhim A, Cameron MJ, et al. Interleukin-1- and type I interferon-dependent enhanced immunogenicity of an NYVAC-HIV-1 Env-Gag-Pol-Nef vaccine vector with dual deletions of type I and type II interferon-binding proteins[J]. J Virol, 2015, 89(7): 3819-3832. doi:10.1128/JVI.03061-14. [25] Rubins KH, Hensley LE, Jahrling PB, et al. The host response to smallpox: analysis of the gene expression program in peripheral blood cells in a nonhuman primate model[J]. Proc Natl Acad Sci U S A, 2004, 101(42): 15190-15195. doi:10.1073/pnas.0405759101. [26] Rubins KH, Hensley LE, Bell GW, et al. Comparative analysis of viral gene expression programs during poxvirus infection: a transcriptional map of the vaccinia and monkeypox genomes[J]. PLoS One, 2008, 3(7): e2628. doi:10.1371/journal.pone.0002628. [27] Bin L, Howell MD, Kim BE, et al. Inhibition of S100A11 gene expression impairs keratinocyte response against vaccinia virus through downregulation of the IL-10 receptor 2 chain[J]. J Allergy Clin Immunol, 2009, 124(2): 270-277. doi:10.1016/j.jaci.2009.05.002. [28] Bartee E, Mohamed MR, Lopez MC, et al. The addition of tumor necrosis factor plus beta interferon induces a novel synergistic antiviral state against poxviruses in primary human fibroblasts[J]. J Virol, 2009, 83(2): 498-511. doi:10.1128/JVI.01376-08. [29] Messaoudi I, Asquith M, Engelmann F, et al. Moderate alcohol consumption enhances vaccine-induced responses in rhesus macaques[J]. Vaccine, 2013, 32(1): 54-61. doi:10.1016/j.vaccine.2013.10.076. [30] Weber O, Siegling A, Friebe A, et al. Inactivated parapoxvirus ovis (Orf virus) has antiviral activity against hepatitis B virus and herpes simplex virus[J]. J Gen Virol, 2003, 84(Pt 7): 1843-1852. doi:10.1099/vir.0.19138-0. [31] Friebe A, Friederichs S, Scholz K, et al. Characterization of immunostimulatory components of orf virus (parapoxvirus ovis)[J]. J Gen Virol, 2011, 92(Pt 7): 1571-1584. doi:10.1099/vir.0.028894-0. [32] Diel DG, Delhon G, Luo S, et al. A novel inhibitor of the NF-{kappa}B signaling pathway encoded by the parapoxvirus orf virus[J]. J Virol, 2010, 84(8): 3962-3973. doi:10.1128/JVI.02291-09. [33] Offerman K, Deffur A, Carulei O, et al. Six host-range restricted poxviruses from three genera induce distinct gene expression profiles in an in vivo mouse model[J]. BMC Genomics, 2015, 16: 510. doi:10.1186/s12864-015-1659-1. [34] Yates NL, Liao HX, Fong Y, et al. Vaccine-induced Env V1-V2 IgG3 correlates with lower HIV-1 infection risk and declines soon after vaccination[J]. Sci Transl Med, 2014, 6(228): 228r-239r. doi:10.1126/scitranslmed.3007730.