The safety and efficacy of the JXA1-R vaccine, an attenuated strain of highly pathogenic porcine reproductive and respiratory syndrome virus (HP-PRRSV), were examined using an intramuscular challenge model in piglets. The JXA1-R vaccine was obtained by passing HP-PRRSV JXA1 through Marc-145 cells (82nd passage). Genomic sequence comparisons showed that strain JXA1-R and its parental strain, JXA1, differ by 47 amino acids, and most of these differences are scattered throughout the PRRSV genome. Four-week-old PRRSV-free piglets were inoculated intramuscularly with JXA1-R vaccine (10 3.0 , 10 4.0 , 10 5.0 , 10 6.0 , and 10 7.0 50% tissue culture infective doses [TCID 50 ]/ml for groups 1 to 5, respectively) and then challenged intramuscularly with the 5th passage virus of JXA1 virus (JXA1-F5, 3 ml ؋ 10 4.5 TCID 50 /ml) 28 days after inoculation. The humoral immune response, swine growth, clinical signs, and differential organ lesions were monitored. The results showed that all vaccinated piglets had a perceptible humoral immune response to vaccination after day 7, which then promptly increased, almost reaching the maximum sample/positive (S/P) ratio value at 28 days postimmunization.
Viremia detection indicated that the viral replication levels of the challenge virus in the immunized groups (immunization doses >104.0 /ml) were significantly lower than that of the virus-challenged unvaccinated control group. Piglets in groups 2 to 5 were effectively protected against lethal HP-PRRSV infection and did not show any obvious changes in body temperature or clinical signs of disease at any point during the experiment. However, two of five piglets in group 1 showed mild pathological lesions and transitory high fever. These results suggest that JXA1-R (TCID 50 /ml >10 4.0 ) is sufficiently attenuated and can provide effective protection against the lethal wild-type HP-PRRSV. P orcine reproductive and respiratory syndrome (PRRS) was first discovered in the United States in 1987 (1, 2). It is characterized by reproductive failure in pregnant sows and respiratory disorder in growing swine. PRRS has spread through most of the world's swine-producing regions and has caused substantial economic losses to the swine industry worldwide.PRRS virus (PRRSV) is the causative agent of PRRS. It is a single-stranded, positive-sense RNA virus belonging to the family Arteriviridae, order Nidovirales (3, 4). The viral genome is approximately 15 kb in size and contains 10 open reading frames (ORFs), designated ORF1a, ORF1b, ORF2a, ORF2b, ORF3, ORF4, ORF5a, ORF5, ORF6, and ORF7 (5-8). Among these ORFs, ORF1a encodes 9 nonstructural proteins (NSPs), including NSP1␣, NSP1, and NSP2 to NSP8; ORF1b encodes NSP9 to NSP12. ORF1a and ORF1b encode the viral nonstructural proteins, which are involved in viral replication and transcription. ORF2a, ORF2b, and ORFs 3 to 7 encode the viral structural proteins GP2, E, GP3, GP4, GP5a, GP5, M, and N, respectively (5-8). The ORF5a protein is a novel structural protein in PRRSV, which is encoded by an alternate...