[1] Yousaf M Z, Qasim M, Zia S, et al. Rabies molecular virology, diagnosis, prevention and treatment[J]. Virology Journal, 2012, 9(1):1-5.
[2] 焦洋, 黄平, 唐青,等. 狂犬病病毒糖蛋白的性质及其应用[J]. 慢性病学杂志, 2013,8:600-604.
[3] Gaudin Y, Tuffereau C, Benmansour A, et al. Fatty acylation of rabies virus proteins[J]. Virology, 1991,184(1):441-444.
[4] Dietzschold B, Wiktor T J, Wunner W H, et al. Chemical and immunological analysis of the rabies soluble glycoprotein[J]. Virology, 1983, 124(2):330-337.
[5] Kuzmina N, Kuzmin I V, Ellison J A, et al. Conservation of binding epitopes for monoclonal antibodies on the rabies virus glycoprotein[J]. Journal of Antivirals &Antiretrovirals, 2013, 5(2):37-43.
[6] Galelli A, Baloul L, Lafon M. Abortive rabies virus central nervous infection is controlled by T lymphocyte local recruitment and induction of apoptosis[J]. Engineering Optimization, 2000, 6(5):359-372.
[7] Sato S, Ohara S, Tsutsui K, et al. Effects of G-gene deletion and replacement on rabies virus vector gene expression[J]. PLoS One, 2015, 10(5):e0128020.
[8] Hu R, Zhang S, Fooks A R, et al. Prevention of rabies virus infection in dogs by a recombinant canine adenovirus type-2 encoding the rabies virus glycoprotein[J]. Microbes & Infection, 2006, 8(4):1090-1097.
[9] Huang Y, Chen Z, Huang J, et al. Parainfluenza virus 5 expressing the G protein of rabies virus protects mice after rabies virus infection[J]. Journal of Virology, 2015, 89(6):3427-3429.
[10] Wojczyk B S, Takahashi N, Levy M T, et al. N-glycosylation at one rabies virus glycoprotein sequon influences N-glycan processing at a distant sequon on the same molecule[J]. Glycobiology, 2005, 15(6):655-666.
[11] Lafon M. Rabies virus receptors[J]. Journal of Neurovirology, 2005, 11(1):82-87.
[12] Thoulouze M I, Lafage M, Schachner M, et al. The neural cell adhesion molecule is a receptor for rabies virus[J]. Journal of Virology, 1998, 72(9):7181-7190.
[13] Kashyap A, Anand K, Kashyap S. Rabies and other lyssavirus diseases[J]. Lancet, 2004, 363(9424):1906-1907.
[14] Morimoto K, Foley H D, Mcgettigan J P, et al. Reinvestigation of the role of the rabies virus glycoprotein in viral pathogenesis using a reverse genetics approach[J]. Journal of Neurovirology, 2000, 6(5):373-381.
[15] Sarmento L, Li X Q, Howerth E, et al. Glycoprotein-mediated induction of apoptosis limits the spread of attenuated rabies viruses in the central nervous system of mice[J].Journal of Neurovirology,2006,11(6):571-581.
[16] Ghanem A, Conzelmann K K. G gene-deficient single-round rabies viruses for neuronal circuit analysis[J]. Virus Research,2015,216:41-54.
[17] Wen Y, Wang H, Wu H, et al. Rabies virus expressing dendritic cell-activating molecules enhances the innate and adaptive immune response to vaccination[J].Journal of Virology,2011, 85(4):1634-1644.
[18] Etessami R, Conzelmann K K, Fadai-Ghotbi B, et al. Spread and pathogenic characteristics of a G-deficient rabies virus recombinant:An in vitro and in vivo study[J]. Journal of General Virology, 2000, 81(3):2147-2153.
[19] Juntrakul S, Ruangvejvorachai P, Shuangshoti S, et al. Mechanisms of escape phenomenon of spinal cord and brainstem in human rabies[J]. Bmc Infectious Diseases, 2005, 5(1):1-9.
[20] Yang Y, Huang Y, Gnanadurai C W, et al. The inability of wild-type rabies virus to activate dendritic cells is dependent on the glycoprotein and correlates with its low level of the de novo-synthesized leader RNA[J]. Journal of Virology, 2015, 89(4):2157-2169.
[21] Li X Q, Sarmento L, Fu Z F. Degeneration of neuronal processes after infection with pathogenic, but not attenuated, rabies viruses[J]. Journal of Virology, 2005, 79(15):10063-10068.
[22] Feng G, Mellor R H, Bernstein M, et al. Imaging neuronal subsets in transgenic mice expressing multiple spectral variants of GFP[J]. Neuron, 2000, 28(1):41-51.
[23] Scott C A, Rossiter J P, Andrew R D, et al. Structural abnormalities in neurons are sufficient to explain the clinical disease and fatal outcome of experimental rabies in yellow fluorescent protein-expressing transgenic mice[J]. Journal of Virology, 2008, 82(1):513-521.
[24] Dun A R, Rickman C, Duncan R R. The t-SNARE complex:A close up[J]. Cellular & Molecular Neurobiology, 2010, 30(8):1321-1326.
[25] Reading S A, Dimmock N J. Neutralization of animal virus infectivity by antibody[J]. Archives of Virology, 2007, 152(6):1047-1059.
[26] Hotta K, Bazartseren B, Kaku Y, et al. Effect of cellular cholesterol depletion on rabies virus infection[J]. Virus Research, 2008, 139(1):85-90.
[27] Bigler W J, Hoff G L, Smith J S, et al. Persistence of rabies antibody in free-ranging raccoons[J]. Journal of Infectious Diseases, 1983, 148(3):610.
[28] WHO expert committee on rabies[J]. World Health Organization Technical Report, 1992, 824:1-84.
[29] Aubert M F. Practical significance of rabies antibodies in cats and dogs[J]. Revue Scientifique Et Technique, 1992, 11(3):735-760.
[30] Briggs D J, Schweitzer K. Importation of dogs and cats to rabies-free areas of the world[J]. Veterinary Clinics of North America Small Animal Practice, 2001, 31(3):573-583.
[31] Welch R J, Anderson B L, Litwin C M. An evaluation of two commercially available ELISAs and one in-house reference laboratory ELISA for the determination of human anti-rabies virus antibodies[J]. Journal of Medical Microbiology, 2009, 58(6):806-810. |