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Open Access Highly Accessed Research article

Comparative genomic analyses of Mycoplasma hyopneumoniae pathogenic 168 strain and its high-passaged attenuated strain

Wei Liu1, Shaobo Xiao1, Mao Li1, Shaohua Guo1, Sha Li1, Rui Luo1, Zhixin Feng2, Bin Li2, Zhemin Zhou3, Guoqing Shao2, Huanchun Chen1 and Liurong Fang1*

Author affiliations

1 Division of Animal Infectious Diseases, State Key Laboratory of Agricultural Microbiology, College of Veterinary Medicine, Huazhong Agricultural University, Wuhan, 430070, People’s Republic of China

2 Institute of Veterinary Medicine, Jiangsu Academy of Agricultural Sciences, Nanjing, 210014, People’s Republic of China

3 Environmental Research Institute, University College Cork, Cork, Ireland

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Citation and License

BMC Genomics 2013, 14:80  doi:10.1186/1471-2164-14-80

Published: 5 February 2013

Abstract

Background

Mycoplasma hyopneumoniae is the causative agent of porcine enzootic pneumonia (EP), a mild, chronic pneumonia of swine. Despite presenting with low direct mortality, EP is responsible for major economic losses in the pig industry. To identify the virulence-associated determinants of M. hyopneumoniae, we determined the whole genome sequence of M. hyopneumoniae strain 168 and its attenuated high-passage strain 168-L and carried out comparative genomic analyses.

Results

We performed the first comprehensive analysis of M. hyopneumoniae strain 168 and its attenuated strain and made a preliminary survey of coding sequences (CDSs) that may be related to virulence. The 168-L genome has a highly similar gene content and order to that of 168, but is 4,483 bp smaller because there are 60 insertions and 43 deletions in 168-L. Besides these indels, 227 single nucleotide variations (SNVs) were identified. We further investigated the variants that affected CDSs, and compared them to reported virulence determinants. Notably, almost all of the reported virulence determinants are included in these variants affected CDSs. In addition to variations previously described in mycoplasma adhesins (P97, P102, P146, P159, P216, and LppT), cell envelope proteins (P95), cell surface antigens (P36), secreted proteins and chaperone protein (DnaK), mutations in genes related to metabolism and growth may also contribute to the attenuated virulence in 168-L. Furthermore, many mutations were located in the previously described repeat motif, which may be of primary importance for virulence.

Conclusions

We studied the virulence attenuation mechanism of M. hyopneumoniae by comparative genomic analysis of virulent strain 168 and its attenuated high-passage strain 168-L. Our findings provide a preliminary survey of CDSs that may be related to virulence. While these include reported virulence-related genes, other novel virulence determinants were also detected. This new information will form the foundation of future investigations into the pathogenesis of M. hyopneumoniae and facilitate the design of new vaccines.

Keywords:
Mycoplasma hyopneumoniae; Genetic variation; Virulence attenuation; Sequence analysis; Repetitive sequences; Virulence factors