Background: Porcine reproductive and respiratory syndrome (PRRS) is an economically important viral disease of pigs worldwide. India has reported the first outbreak of PRRS in the pig population of Mizoram state to the Office International des Epizooties on the 26 June 2013. Hypothesis/Objectives: The aim of the present study was to determine the genotype and origin of porcine reproductive and respiratory syndrome virus (PRRSV) from the first outbreak in the pig population of Mizoram state, India, in 2013. Animals and methods: A total of 880 affected pigs from the outbreak were clinically examined, 51 animals were necropsied and tested by reverse transcription polymerase chain reaction (RT-PCR) to detect PRRSV and 148 serum samples were tested to detect PRRSV-specific antibodies. The full open reading frame 5 (ORF5) gene sequences from 12 and ORF7 gene sequences from three clinical cases were sequenced and analysed for genomic characterization, respectively. Results: The outbreak was confirmed by the detection of PRRSV-specific antibodies in 109 out of 148 serum samples (74%) and also by RT-PCR in 46 out of 51 necropsy samples (90%). Notably, ORF5 and ORF7 genes of Indian strain shares the same nucleotide positions i.e. 13,698À14,300 and 14,799À15,170, respectively, with the highly pathogenic (HP) strain of China and were grouped together in a phylogenetic tree. Conclusions and clinical importance: Sequence and phylogenetic analysis of ORF5 and ORF7 confirmed that the Indian strain has a close link with the HP-PRRSV of China. The current study forms an essential step for better understanding of the epidemiology as well as the movement and spread of the disease in India.

Since its first outbreak in 2013, porcine reproductive and respiratory syndrome (PRRS) has established as an enzootic disease in pig population of Mizoram state, India. Our previous studies based on phylogenetic analysis of ORF5 and ORF7 gene sequences revealed close relationship of Indian PRRSV with the highly pathogenic variant of PRRSV (HP-PRRSV) of Chinese origin. Despite the control measures, second major outbreak of the disease was recorded in Aizawl district of Mizoram in 2015. The objective of the present study was to examine the origin of PRRSV isolates of 2015 outbreak, identification of deleted region in Nsp2 gene and determination of any genetic variation between 2013 and 2015 isolates of PRRSV. The outbreak was confirmed by the detection of PRRSVspecific antibodies in 57 out of 92 serum samples (61.96 %) and also by RT-PCR in 42 out of 42 necropsy samples (100 %). Nucleotide sequence analysis of Nsp2 coding region of Indian isolates and comparison with reference sequences revealed 90 nucleotides discontinuous deletion further establishes the closeness of Indian PRRSV to Chinese HP-PRRSV. Further, sequence and phylogenetic analysis of ORF5, ORF7 and Nsp2 genes of Indian PRRSV from both 2013 and 2015 revealed that the outbreaks were caused by two different strains of HP-PRRSV closely associated with the Chinese 10 HEB-3 isolate and 07QN isolates of Vietnam origin respectively. The present study confirms that the Indian PRRSV is a highly pathogenic variant of PRRSV and this study serves as the basis for developing practical and effective control measures against this disease.

Background: Limited studies are available on molecular epidemiology of classical swine fever virus (CSFV) in India and are restricted to domestic pigs. These studies show the presence of 1.1. genotype. Hypothesis/objectives: The aim of the present study was to subgenotype four CSFV isolates, two each from the outbreaks of CSF in wild (Sus scrofa) and domestic pigs of Mizoram state, India, in 2011. Animals and methods: CSFV isolates were subjected to nucleotide sequencing in E2 and NS5B genomic regions. Phylogenetic analysis of the isolates in both genomic regions was carried out with 39 Indian isolates (4 isolates from the present study of Mizoram state and 35 isolates from the other states of India) and 57 reference sequences retrieved from the GenBank database. Two of the 39 isolates from India were collected from wild boar and were subgenotyped as 2.1. Out of 37 isolates from domestic pigs, only two were subgenotyped as 2.1. Results: The analysis revealed the emergence of 2.1. subgenotype of CSFV in both wild and domestic pigs in India. Conclusions and clinical importance:The isolates from domestic pigs of Mizoram state (CSF/MZ/KOL/73 and CSF/MZ/ AIZ/115) were grouped in genotype 1 and subgenotype 1.1., thus confirming that the source of CSF outbreaks in domesticated pigs in Mizoram was not from wild pigs. The current study forms an essential step for better understanding of the epidemiology of 2.1 subgroup as well as the movement and spread of the disease in India.

This study reports for the first time a natural outbreak of highly pathogenic porcine reproductive and respiratory syndrome (HP‐PRRS) caused by HP‐PRRS virus (HP‐PRRSV) in wild pigs characterized by sudden onset of depression, anorexia, respiratory distress, and high fever. The disease has caused severe haemorrhagic pneumonia, haemorrhagic lymphadenitis, enlarged spleen with areas of infarction, and petechial haemorrhages on the myocardium and on the surface of kidneys. HP‐PRRSV was detected in representative tissue samples by reverse transcription‐PCR, and the field strain was isolated in the MA104 cell line. The phylogenetic analyses based on the whole genome sequences and nucleotide sequences of open reading frame 5 (ORF5) gene showed close grouping with the subtype IV of lineage 8/8.7 of PRRSV II, which represents the HP‐PRRSV strains that predominate in the pig population of China since 2010. The amino acid sequence analysis of the ORF5 gene revealed the replacement of leucine (L) at position 39 to isoleucine (I) in the primary neutralizing epitope. Among the four potential N glycosylation sites, the N34 was mutated and found to be restricted to only three N glycosylation sites. The present findings have indicated that HP‐PRRSV can cause fatal outbreaks and may emerge as a major threat to the wild pig population.

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