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Porcine reproductive and respiratory syndrome virus: origin hypothesis.

Plagemann PG - Emerging Infect. Dis. (2003)

Bottom Line: Porcine reproductive and respiratory syndrome is a serious swine disease that appeared suddenly in the midwestern United States and central Europe approximately 14 years ago; the disease has now spread worldwide.My hypothesis, which explains the origin and evolution of the two distinct PRRSV genotypes, is that a mutant of a closely related arterivirus of mice (lactate dehydrogenase-elevating virus) infected wild boars in central Europe.These wild boars functioned as intermediate hosts and spread the virus to North Carolina in imported, infected European wild boars in 1912; the virus then evolved independently on the two continents in the prevalent wild hog populations for approximately 70 years until independently entering the domestic pig population.

View Article: PubMed Central - PubMed

Affiliation: University of Minnesota, Minneapolis, Minnesota 55455, USA. plage001@umn.edu

ABSTRACT
Porcine reproductive and respiratory syndrome is a serious swine disease that appeared suddenly in the midwestern United States and central Europe approximately 14 years ago; the disease has now spread worldwide. In North America and Europe, the syndrome is caused by two genotypes of porcine reproductive and respiratory syndrome virus (PRRSV), an arterivirus whose genomes diverge by approximately 40%. My hypothesis, which explains the origin and evolution of the two distinct PRRSV genotypes, is that a mutant of a closely related arterivirus of mice (lactate dehydrogenase-elevating virus) infected wild boars in central Europe. These wild boars functioned as intermediate hosts and spread the virus to North Carolina in imported, infected European wild boars in 1912; the virus then evolved independently on the two continents in the prevalent wild hog populations for approximately 70 years until independently entering the domestic pig population.

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Related in: MedlinePlus

Nucleotide alignment of a segment of open reading frame (ORF) 1b of lactate dehydrogenase-elevating virus–P, porcine reproductive and respiratory syndrome virus VR-2332, and porcine reproductive and respiratory syndrome virus–Lelystad virus beginning at nucleotides 1169, 1165, and 1165, respectively. *Indicates identical nucleotides. Degenerate primer sets for polymerase chain reaction were previously made to the underlined segments (41).
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Figure 4: Nucleotide alignment of a segment of open reading frame (ORF) 1b of lactate dehydrogenase-elevating virus–P, porcine reproductive and respiratory syndrome virus VR-2332, and porcine reproductive and respiratory syndrome virus–Lelystad virus beginning at nucleotides 1169, 1165, and 1165, respectively. *Indicates identical nucleotides. Degenerate primer sets for polymerase chain reaction were previously made to the underlined segments (41).

Mentions: An approach that is more suitable to detect LDV-PRRSV intermediates is reverse transcription–polymerase chain reaction (RT-PCR) with primers to highly conserved genomic sequences, for example, in a segment of the RNA polymerase domain upstream of the nidovirus characteristic SDD protein sequence (Figure 4). This nucleotide segment exhibits 53% identity between LDV, Lelystad virus, and VR-2332 (118/224 nucleotides; amino acid identity of the encoded protein segment is even higher, 75%). This segment contains short segments with complete nucleotide identity (Figure 4, stars); in addition, 25, 30, and 31 nucleotides are identical for LDV and VR-2332, LDV and Lelystad virus, and Lelystad virus and VR-2332, respectively, indicating again the close, but distinct, relationship between LDV and both Lelystad virus and VR-2332. My laboratory has previously used degenerate primer sets of this region designed on the bases of LDV, equine arteritis virus, and Lelystad virus sequence information (Figure 4) that detected not only the genomes of these three viruses but also those of VR-2332 and simian hemorrhagic fever virus, for which no sequence information was available at the time (41). The additional advantages of the RT-PCR approach are that this method can be readily applied to both serum and tissue samples and that the sequence of the PCR-amplified segment allows conclusions about the relatedness of the detected virus to existing viruses and the synthesis of specific gene probes for this virus. Also, degenerate primer sets can be designed to detect specific LDV-PRRSV intermediates. The same approach can be used to examine other species for the presence of arteriviruses.


Porcine reproductive and respiratory syndrome virus: origin hypothesis.

Plagemann PG - Emerging Infect. Dis. (2003)

Nucleotide alignment of a segment of open reading frame (ORF) 1b of lactate dehydrogenase-elevating virus–P, porcine reproductive and respiratory syndrome virus VR-2332, and porcine reproductive and respiratory syndrome virus–Lelystad virus beginning at nucleotides 1169, 1165, and 1165, respectively. *Indicates identical nucleotides. Degenerate primer sets for polymerase chain reaction were previously made to the underlined segments (41).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3020618&req=5

Figure 4: Nucleotide alignment of a segment of open reading frame (ORF) 1b of lactate dehydrogenase-elevating virus–P, porcine reproductive and respiratory syndrome virus VR-2332, and porcine reproductive and respiratory syndrome virus–Lelystad virus beginning at nucleotides 1169, 1165, and 1165, respectively. *Indicates identical nucleotides. Degenerate primer sets for polymerase chain reaction were previously made to the underlined segments (41).
Mentions: An approach that is more suitable to detect LDV-PRRSV intermediates is reverse transcription–polymerase chain reaction (RT-PCR) with primers to highly conserved genomic sequences, for example, in a segment of the RNA polymerase domain upstream of the nidovirus characteristic SDD protein sequence (Figure 4). This nucleotide segment exhibits 53% identity between LDV, Lelystad virus, and VR-2332 (118/224 nucleotides; amino acid identity of the encoded protein segment is even higher, 75%). This segment contains short segments with complete nucleotide identity (Figure 4, stars); in addition, 25, 30, and 31 nucleotides are identical for LDV and VR-2332, LDV and Lelystad virus, and Lelystad virus and VR-2332, respectively, indicating again the close, but distinct, relationship between LDV and both Lelystad virus and VR-2332. My laboratory has previously used degenerate primer sets of this region designed on the bases of LDV, equine arteritis virus, and Lelystad virus sequence information (Figure 4) that detected not only the genomes of these three viruses but also those of VR-2332 and simian hemorrhagic fever virus, for which no sequence information was available at the time (41). The additional advantages of the RT-PCR approach are that this method can be readily applied to both serum and tissue samples and that the sequence of the PCR-amplified segment allows conclusions about the relatedness of the detected virus to existing viruses and the synthesis of specific gene probes for this virus. Also, degenerate primer sets can be designed to detect specific LDV-PRRSV intermediates. The same approach can be used to examine other species for the presence of arteriviruses.

Bottom Line: Porcine reproductive and respiratory syndrome is a serious swine disease that appeared suddenly in the midwestern United States and central Europe approximately 14 years ago; the disease has now spread worldwide.My hypothesis, which explains the origin and evolution of the two distinct PRRSV genotypes, is that a mutant of a closely related arterivirus of mice (lactate dehydrogenase-elevating virus) infected wild boars in central Europe.These wild boars functioned as intermediate hosts and spread the virus to North Carolina in imported, infected European wild boars in 1912; the virus then evolved independently on the two continents in the prevalent wild hog populations for approximately 70 years until independently entering the domestic pig population.

View Article: PubMed Central - PubMed

Affiliation: University of Minnesota, Minneapolis, Minnesota 55455, USA. plage001@umn.edu

ABSTRACT
Porcine reproductive and respiratory syndrome is a serious swine disease that appeared suddenly in the midwestern United States and central Europe approximately 14 years ago; the disease has now spread worldwide. In North America and Europe, the syndrome is caused by two genotypes of porcine reproductive and respiratory syndrome virus (PRRSV), an arterivirus whose genomes diverge by approximately 40%. My hypothesis, which explains the origin and evolution of the two distinct PRRSV genotypes, is that a mutant of a closely related arterivirus of mice (lactate dehydrogenase-elevating virus) infected wild boars in central Europe. These wild boars functioned as intermediate hosts and spread the virus to North Carolina in imported, infected European wild boars in 1912; the virus then evolved independently on the two continents in the prevalent wild hog populations for approximately 70 years until independently entering the domestic pig population.

Show MeSH
Related in: MedlinePlus