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This study describes the genetic and antigenic characterization of a newly emerging porcine circovirus type 2b (PCV2b) mutant first isolated in cases of vaccine failure in Korea. The full genome of the PCV2b isolates (SNUVR130689 and SNUVR140004) is 1,767 base pairs (bp) in length. The size of ORF1 is 945 bp, encoding a protein of 314 amino acids (aa), and the size of ORF2 is 705 bp, encoding a protein of 234 aa, which is 1 aa longer than that of the common PCV2 (233 aa). Korean PCV2b mutant strains had higher levels of nucleotide sequence identity to other PCV2b mutant strains (99.7-99.8 %) than to reference PCV2a (94.5-95.0 %) and PCV2b (95.5-96.1 %) strains. There was no difference in antigenic reactivity among PCV2a, PCV2b and PCV2b mutant strains to the polyclonal and monoclonal PCV2a antibodies. PCV2b mutant strains have distinct genetic characteristics but similar antigenic reactivity when compared to common PCV2a and 2b strains.

The objective of the present study was to compare the efficacy of two commercial type 1 porcine reproductive and respiratory syndrome virus (PRRSV) modified live vaccines against heterologous type 1 and type 2 PRRSV challenge in growing pigs. Vaccination with a type 1 PRRSV vaccine reduced the level of viremia after type 1 PRRSV challenge but did not reduce the level of viremia after the type 2 PRRSV challenge in pigs. Increased levels of interleukin-10 (IL-10) stimulated by type 2 PRRSV coincided with the low numbers of type 2 PRRSV-specific interferon gamma-secreting cells (IFN-␥-SC) in vaccinated pigs after type 2 PRRSV challenge, whereas low levels of IL-10 stimulated by type 1 PRRSV coincided with high numbers of type 1 PRRSV-specific IFN-␥-SC in vaccinated pigs after type 1 PRRSV challenge. Additionally, vaccination with the type 1 PRRSV vaccine effectively reduced the lung lesions and type 1 PRRSV nucleic acids in type 1 PRRSV-challenged pigs but did not reduce lung lesions and type 2 PRRSV nucleic acids in type 2 PRRSV-challenged pigs. There were no significant differences between two commercial type 1 PRRSV vaccines against type 1 and type 2 PRRSV challenge based on virological results, immunological responses, and pathological outcomes. This study demonstrates that vaccinating pigs with the type 1 PRRSV vaccine provides partial protection against respiratory disease with heterologous type 1 PRRSV challenge but no protection with heterologous type 2 PRRSV challenge. P orcine reproductive and respiratory syndrome (PRRS), caused by PRRS virus (PRRSV), is one of the most economically devastating diseases facing pig production worldwide. The infection of growing pigs with PRRSV causes severe respiratory diseases, leading to impaired growth in postweaned and growing pigs (1). The virus can also give rise to reproductive failure in sows (1). PRRSV is a small, positive-sense, enveloped, single-stranded RNA virus belonging to the family Arteriviridae in the order Nidovirales (2). PRRSV is classified into type 1 (European) and type 2 (North American) genotypes based on the 3=-terminal structural genes or the entire genome (3, 4). Type 1 PRRSV is further divided into three subtypes: a pan-European subtype 1 and East European subtypes 2 and 3, with nucleocapsid protein sizes of 128, 125, and 124 amino acids, respectively (5).In South Korea, type 2 PRRSV was first isolated in 1994 (6). Until 2005, only type 2 PRRSV was detected in Korean swine herds (7,8 Since the first introduction of type 1 PRRSV vaccines, crossprotection is a major clinical issue because of the coexistence of the type 1 and type 2 PRRSVs in swine herds. Previous crossprotection studies have provided inconsistent results (11, 12). The Porcilis PRRS vaccine (MSD Animal Health) provides no protection against heterologous type 2 PRRSV challenge (11), whereas the Amervac PRRS vaccine (Hipra) provides partial protection against heterologous type 2 PRRSV challenge (12). However, a comparison of two commercial type 1 PRRSV-based modified live vaccines a...

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The objective of the present study was to determine the effects of the commercially available type 2 Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)-based modified live vaccine against type 1 and type 2 PRRSV challenge in pregnant sows. Half of the sows in the study were vaccinated with a type 2 PRRSV-based vaccine 4 weeks prior to artificial insemination while the other half remained non-vaccinated. Sows were then challenged intranasally with type 1 or type 2 PRRSV at 93 days of gestation. The sows which received the type 2 PRRSV-based vaccine followed by type 2 PRRSV challenge had significantly higher neutralizing antibody titers against type 2 PRRSV than they did against type 1 PRRSV. These same sows had higher frequencies of IFN-γ-secreting cells when stimulated with type 2 PRRSV compared to those stimulated with type 1 PRRSV. Subsequent virological evaluation demonstrated that the type 2 PRRSV-based vaccine reduced the type 2 PRRSV load but not the type 1 PRRSV load present in the blood of the sows. Additionally, vaccination of pregnant sows with the type 2 PRRSV-based vaccine effectively reduced the level of type 2 PRRSV nucleic acids observed in fetal tissues from type 2 PRRSV-challenged sows but did not reduce the level of type 1 PRRSV nucleic acid observed in fetal tissues from type 1 PRRSV-challenged sows. This study demonstrates that the vaccination of pregnant sows with the type 2 PRRSV-based vaccine protects against type 2 PRRSV challenge but does not protect against type 1 PRRSV challenge.

The objective of the present study was to compare the effects of the modified live porcine reproductive and respiratory syndrome virus (PRRSV) vaccine (Ingelvac PRRS MLV; Boehringer Ingelheim Animal Health, St. Joseph, MO) on European and North American PRRSV shedding in the semen of experimentally infected boars. The boars were randomly divided into six groups. Vaccinated boars shed the North American PRRSV at the rate of 10 0.1 to 10 1.0 viral genome copies per ml and 3.63 to 10 1.1 50% tissue culture infective doses (TCID 50 )/ml, respectively, in semen, whereas nonvaccinated boars shed the North American PRRSV at the rate of 10 0.2 to 10 4.7 viral genome copies per ml and 1.14 to 10 3.07 TCID 50 /ml, respectively, in semen. Vaccinated boars shed the European PRRSV at the rate of 10 0.1 to 10 4.57 viral genome copies per ml and 1.66 to 10 3.10 TCID 50 /ml, respectively, in semen, whereas nonvaccinated boars shed the European PRRSV at the rate of 10 0.3 to 10 5.14 viral genome copies per ml and 1.69 to 10 3.17 TCID 50 /ml, respectively, in semen. The number of genomic copies of the European PRRSV in semen samples was not significantly different between vaccinated and nonvaccinated challenged European PRRSV boars. The present study demonstrated that boar vaccination using commercial modified live PRRSV vaccine was able to decrease subsequent shedding of North American PRRSV in semen after challenge but was unable to decrease shedding of European PRRSV in semen after challenge.

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