Genetic characterization of porcine circovirus type 2 in piglets from PMWS-affected and -negative farms in Thailand

Postweaning multisystemic wasting syndrome (PMWS) is a major disease of swine, caused by porcine circovirus type 2 (PCV2). The major clinical signs of PMWS are wasting, paleness of the skin, enlargement of the lymph nodes, respiratory distress, and occasional diarrhea as well as icterus [1,2]. PCV2 has a significant impact on the pig industry worldwide [3]. PCV2 is a small non-enveloped DNA virus which contains a single-stranded circular genome of 1.7 kb [4,5]. The PCV2 genome has three major open reading frames (ORFs), which encode replication-associated proteins (ORF1) [6], viral capsid protein (ORF2) [7], and apoptotic protein (ORF3) [8]. The ORF2 is an essential determinant for the genetic typing of PCV2 isolates, since the capsid gene has more variability than the other ORFs [9]. Phylogenetic analysis demonstrated two major subtypes of PCV2, which are PCV2a (Group2) and PCV2b (Group 1). Each subtype was classified into different clusters, 1A to 1C for the subtype PCV2b, and 2A to 2E for the subtype PCV2a [9]. Furthermore, a third subtype (PCV2c), found only in the Danish pigs, was described [10]. A novel subtype, PCV2d, which is dominant in Chinese pigs, was recently reported [11]. A number of studies suggested that PCV2b is more virulent than PCV2a and predominant in PMWS-affected herds [12,13]. However, an experimental inoculation of pigs with PCV2a and PCV2b demonstrated no divergence in the virulence of both subtypes [14]. Thus, no association of the PCV2 subtype designations, the disease status, or the geographical distribution appears to be evident.Since PMWS was first observed in Canada in 1991 [1], the prevalence of PCV2 and the occurrence of PMWS have been worldwide reported [15-25]. The first case of PMWS in 7 to 9 week-old pigs was described in Thailand in 1998 [26]; however, a retrospective study suggested that the PCV2 infection had been previously detected in 1993 [21]. Although the infection has been widespread in Thailand since 1998, genetic inf