Bioinformatics analysis of rabbit haemorrhagic disease virus genome

Virology Journal

Ji-xing Liu¹  Wen-qiang Jiao¹  Liang Zhang¹  Bao-yu Li¹  Xiao-ting Tian¹ 

[1] State Key Laboratory of Veterinary Etiological Biology, Key Laboratory of Grazing Animal Diseases of Ministry of Agriculture, Key Laboratory of Animal Virology of Ministry of Agriculture, State Key Laboratory of Veterinary Etiological Biology, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Xujia ping 1, Yanchang bu, Lanzhou, Gansu, Post Code 730046, China

关键词: Expression;    Evolution;    Codon usage;    Rabbit haemorrhagic disease virus (RHDV);   

Others  :  1155736
DOI  :  10.1186/1743-422X-8-494

 received in 2011-09-14, accepted in 2011-11-01,  发布年份 2011

【 摘 要 】

Background

Rabbit haemorrhagic disease virus (RHDV), as the pathogeny of Rabbit haemorrhagic disease, can cause a highly infectious and often fatal disease only affecting wild and domestic rabbits. Recent researches revealed that it, as one number of the Caliciviridae, has some specialties in its genome, its reproduction and so on.

Results

In this report, we firstly analyzed its genome and two open reading frameworks (ORFs) from this aspect of codon usage bias. Our researches indicated that mutation pressure rather than natural is the most important determinant in RHDV with high codon bias, and the codon usage bias is nearly contrary between ORF1 and ORF2, which is maybe one of factors regulating the expression of VP60 (encoding by ORF1) and VP10 (encoding by ORF2). Furthermore, negative selective constraints on the RHDV whole genome implied that VP10 played an important role in RHDV lifecycle.

Conclusions

We conjectured that VP10 might be beneficial for the replication, release or both of virus by inducing infected cell apoptosis initiate by RHDV. According to the results of the principal component analysis for ORF2 of RSCU, we firstly separated 30 RHDV into two genotypes, and the ENC values indicated ORF1 and ORF2 were independent among the evolution of RHDV.

【 授权许可】

   
2011 Tian et al; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

【 参考文献 】

• [1]Karlin S, Mrazek J: What drives codon choices in human genes? J Mol Biol 1996, 262(4):459-472.
• [2]Sharp PM, Tuohy TM, Mosurski KR: Codon usage in yeast: cluster analysis clearly differentiates highly and lowly expressed genes. Nucleic Acids Res 1986, 14(13):5125-5143.
• [3]Lesnik T, Solomovici J, Deana A, Ehrlich R, Reiss C: Ribosome traffic in E-coli and regulation of gene expression. Journal of Theoretical Biology 2000, 202(2):175-185.
• [4]Shackelton LA, Parrish CR, Holmes EC: Evolutionary basis of codon usage and nucleotide composition bias in vertebrate DNA viruses. J Mol Evol 2006, 62(5):551-563.
• [5]Mooers AO, Holmes EC: The evolution of base composition and phylogenetic inference. Trends Ecol Evol 2000, 15(9):365-369.
• [6]Jenkins GM, Holmes EC: The extent of codon usage bias in human RNA viruses and its evolutionary origin. Virus Res 2003, 92(1):1-7.
• [7]Zhou J, Liu WJ, Peng SW, Sun XY, Frazer I: Papillomavirus capsid protein expression level depends on the match between codon usage and tRNA availability. J Virol 1999, 73(6):4972-4982.
• [8]Zhao KN, Liu WJ, Frazer IH: Codon usage bias and A+T content variation in human papillomavirus genomes. Virus Res 2003, 98(2):95-104.
• [9]Karlin S, Blaisdell BE, Schachtel GA: Contrasts in codon usage of latent versus productive genes of Epstein-Barr virus: data and hypotheses. J Virol 1990, 64(9):4264-4273.
• [10]Sewatanon J, Srichatrapimuk S, Auewarakul P: Compositional bias and size of genomes of human DNA viruses. Intervirology 2007, 50(2):123-132.
• [11]Van Hemert FJ, Berkhout B, Lukashov VV: Host-related nucleotide composition and codon usage as driving forces in the recent evolution of the Astroviridae. Virology 2007, 361(2):447-454.
• [12]Wirblich C, Thiel HJ, Meyers G: Genetic map of the calicivirus rabbit hemorrhagic disease virus as deduced from in vitro translation studies. J Virol 1996, 70(11):7974-7983.
• [13]Wirblich C, Sibilia M, Boniotti MB, Rossi C, Thiel HJ, Meyers G: 3C-like protease of rabbit hemorrhagic disease virus: identification of cleavage sites in the ORF1 polyprotein and analysis of cleavage specificity. J Virol 1995, 69(11):7159-7168.
• [14]Meyers G, Wirblich C, Thiel HJ, Thumfart JO: Rabbit hemorrhagic disease virus: genome organization and polyprotein processing of a calicivirus studied after transient expression of cDNA constructs. Virology 2000, 276(2):349-363.
• [15]Meyers G: Translation of the minor capsid protein of a calicivirus is initiated by a novel termination-dependent reinitiation mechanism. J Biol Chem 2003, 278(36):34051-34060.
• [16]Comeron JM, Aguade M: An evaluation of measures of synonymous codon usage bias. J Mol Evol 1998, 47:268-274.
• [17]Wright F: The "effective number of codons" used in a gene. Gene 1990, 87:23-29.
• [18]Lu H, Zhao WM, Zheng Y, Wang H, Qi M, Yu XP: Analysis of Synonymous Codon Usage Bias in Chlamydia. Acta Biochim Biophys Sin 2005, 37:1-10.
• [19]Nei M, Gojobori T: Simple methods for estimating the numbers of synonymous and nonsynonymous nucleotide substitutions. Molecular Biology and Evolution 1986, 3:418-426.
• [20]Tamura K, Dudley J, Nei M, Kumar S: MEGA4: Molecular Evolutionary Genetics Analysis (MEGA) software version 4.0. Molecular Biology and Evolution 2007, 24:1596-1599.
• [21]Mardia KV, Kent JT, Bibby JM: Multivariate analysis. NewYork. Academic press; 1979.
• [22]Ewens WJ, Grant GR: Statistical Methods in Bioinformatics. NewYork. Springer; 2001.
• [23]Egger D, Wolk B, Gosert R, Bianchi L, Blum HE, Moradpour D, Bienz K: Expression of Hepatitis C virus proteins induced distinct membrane alterations including a candidate viral replication complex. J Virol 2002, 76(12):5974-5984.
• [24]Espert L, Codogno P, Biard-Piechaczyk K: Involvement of autophagy in viral infections: antiviral function and subversion by viruses. J Mol Med 2007, 85:811-823.
• [25]Jackson WT, Giddings TH, Taylor MP, Mulinyawe S, Rabinovitch M, Ropito R, Kirkegaard K: Subversion of cellular autophagosomal machinery by RNA viruses. PLoS Biol 2005, 3(5):e156.
• [26]Lee YR, Lei HY, Liu MT, Wang JR, Chen SH, Jiang-Shieh YF, Lin YS, Yeh TM, Liu CC, Liu HS: Autophagic machinery activated by dengue virus enhances virus replication. Virology 2008, 374:240-248.
• [27]Pedersen KW, van der Meer Y, Roos N, Snijder EJ: Open reading frame 1aencoded subunits of the arterivirus replicase induce endoplasmic reticulum derived double-membrane vesicles which carry the viral replication complex. J Virol 1999, 73(3):2016-2026.
• [28]Wileman T: Aggresomes and autophagy generate sites for virus replication. Science 2006, 312:875-878.
• [29]Wong J, Zhang J, Xiaoning S, Gao G, Mao I, McManus BM, Luo H: Autophagosome supports Coxsackievirus B3 replication in host cells. J Virol 2008, 82(18):9143-9153.