Details

Autor(en) / Beteiligte

• Vargas‐Ruiz, Alejandro
• García‐Camacho, Lucia Angélica
• Ramírez‐Alvarez, Hugo
• Rangel‐Rodriguez, Ignacio Carlos
• Alonso‐Morales, Rogelio Alejandro
• Sánchez‐Betancourt, José Iván

Titel

Molecular characterization of the ORF2 of Torque teno sus virus 1a and Torque teno sus virus 1b detected in cases of postweaning multisystemic wasting syndrome in Mexico

Ist Teil von

• Transboundary and emerging diseases, 2018-12, Vol.65 (6), p.1806-1815

Ort / Verlag

Germany: Hindawi Limited

Erscheinungsjahr

2018

Quelle

Access via Wiley Online Library

Beschreibungen/Notizen

• Worldwide Torque teno sus virus (TTSuV, genus Iotatorquevirus) species have been regarded as possible agents associated with porcine circovirus‐associated disease. Iotatorquevirus species possess high genomic variability, suggesting that diverse genotypes are widely geographically distributed. In this study, we validated the genomic variability of Iotaroquevirus species in pigs with postweaned multisystemic wasting syndrome. Genomic DNA from nine TTSuV1a‐positive tissues and 15 TTSuV1b‐positive tissues was used to amplify the complete ORF2 of each species by nested PCR to perform a molecular characterization. It was found that Mexican TTSuV1a sequences belong to genotype B, sharing phylogenetic origin, high nucleic acid and amino acid sequence similarity and dominant epitope conformation with commercially linked countries, such as the United States, Canada and China, whereas the Mexican TTSuV1b sequences belong to genotype A, being more divergent among each other and displaying low nucleotide identity with worldwide genotype A sequences. In both Iotatorquevirus species, a PTPase‐like signature motif was identified in the predicted amino acid sequence, being more conserved for Mexican TTSuV1b sequences than for Mexican TTSuV1a sequences, in which several substitutions were observed. These changes may influence the conformation of dominant epitopes as different arrays were determined among TTSuV1a genotypes. ORF2 variability may account for pathogenic differences by modifying viral replication and immune response, as depicted for human TTV.