Although North American and European serotypes of porcine reproductive and respiratory syndrome virus (PRRSV) are recognized, only the genome of the European Lelystad strain (LV) has been sequenced completely. Here, the genome of the pathogenic North American PRRSV isolate 16244B has been sequenced and compared with LV. The genomic organization of 16244B was the same as LV but with only 63n4 % nucleotide identity. The 189 nucleotide 5h non-coding region (NCR) of 16244B was distinct from the LV NCR, with good conservation (83 %) only over a 43 base region immediately upstream of open reading frame (ORF) 1a. Major differences were found in the region encoding the non-structural part of the ORF1a polyprotein, which shared only 47 % amino acid identity over 2503 residues of the six non-structural proteins (Nsps) encoded. Nsp2, thought to have a species-specific function, showed the greatest divergence, sharing only 32 % amino acid identity with LV and containing 120 additional amino acids in the central region. Nsps encoded by the 5h-proximal and central regions of ORF1b had from 66 to 75 % amino acid identity ; however, the carboxy-terminal protein CP4 was distinct (42 % identity). The ORF1a-1b frameshift region of 16244B had 98 % nucleotide identity with LV. Consistent with previous reports for North American isolates, the six structural proteins encoded were 58 to 79 % identical to LV proteins. The 3h NCR (150 nucleotides) was 76 % identical between isolates. These genomic differences confirm the presence of distinct North American and European PRRSV genotypes.

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Previous work in our laboratory demonstrated that passive transfer of porcine reproductive and respiratory syndrome virus (PRRSV)-neutralizing antibodies (NA) protected pregnant sows against reproductive failure and conferred sterilizing immunity in sows and offspring. We report here on the dose requirement for protection by passive transfer with NA in young weaned pigs. The presence of a 1:8 titer of PRRSV-NA in serum consistently protected pigs against viremia. Nevertheless, their lungs, tonsils, buffy coat cells, and peripheral lymph nodes contained replicating PRRSV similar to the infected control group. Likewise, these animals excreted infectious virus to sentinels similar to the infectivity control animals. In an attempt to reach complete protective immunity equivalent to that previously observed in sows, the pigs were transferred with a higher titer of PRRSV-NA (1:32), and even then apparent sterilizing immunity was attained in only 50% of the animals. In conclusion, the presence of anti-PRRSV-NA in serum with a titer of 1:8 is enough to block viremia but not peripheral tissue seeding and transmission to contact animals. While a relatively low level of NA in blood is capable of conferring sterilizing immunity against PRRSV in sows, the amount of NA necessary to obtain full protection of a young weaned pig would be significantly higher, suggesting that differences exist in the PRRSV pathogenesis between both age groups. In addition, the titer of NA could be a helpful parameter of protection in the assessment of PRRSV vaccines.

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