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

Abstract

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.

The Synergic Role of Emerging and Endemic Swine Virus in the Porcine Respiratory Disease Complex: Pathological and Biomolecular Analysis

“…TTSuV (Anelloviridae, Anellovirus) is a non-enveloped virus first reported in 1999, with a circular, small, single-stranded, negative-sense DNA genome [15][16][17]. TTSuV transmits horizontally via a fecal-oral route, vertically and sexually, as demonstrated by the presence of TTSuV in boars' semen [18][19][20]. Mixed transmission routes promote worldwide spreading of TTSuV [19,21,22].…”

“…TTSuV transmits horizontally via a fecal-oral route, vertically and sexually, as demonstrated by the presence of TTSuV in boars' semen [18][19][20]. Mixed transmission routes promote worldwide spreading of TTSuV [19,21,22]. Although TTSuV causes lung lesions in pigs affected by PRDC, macroscopic and microscopic lesions caused by this virus are still underinvestigated [23][24][25][26][27].…”

Detection of torque teno sus virus infection in Indian pigs

“…However, there is a report that inoculation of gnotobiotic pigs with TTSuV1-containing tissue homogenate caused mild interstitial pneumonia, transient thymic atrophy, membranous glomerulonephropathy, and modest lymphocytic-to-histiocytic liver infiltrates [7]. In addition, there are studies in gnotobiotic pigs, which indicated that swine TTVs, TTSuV1 in particular, can act as a primary or coinfecting pathogen in pathological conditions such as porcine dermatitis and nephropathy syndrome [7,8] and post-weaning multisystemic wasting syndrome [8,9]. Further, there is a report that the rate of detection of TTSuVs in pigs with clinical signs of the coinfecting pathogens is roughly double than that of clinically healthy pigs [10].…”

“…Further, there is a report that the rate of detection of TTSuVs in pigs with clinical signs of the coinfecting pathogens is roughly double than that of clinically healthy pigs [10]. In addition, recent studies have reported a high rate of coinfection between TTSuVs and porcine circovirus (PCV)-associated disease including in PCV3 infection [9,11,12]. In India, there are few studies on the presence and distribution of TTVs in the human population [13][14][15]; nevertheless, the rate of TTV detection has been found to be significantly higher (92.8%) for Available at www.veterinaryworld.org/Vol.12/September-2019/17.pdf non-A-E hepatitis group [16].…”