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Vaccination
Management
Disease Information
A PMWS update (Jake Waddilove)
ABOUT PMWS & PDNS
National Pork Board PMWS Fact Sheet
About PDNS (Jake Waddilive)
CEI Emerging Disease Notices: PMWS / PDNS
Conference and meetings archive
Case Histories
Yorkshire Farm, UK - Mike Muirhead - Final Update, June 2002
Mike Muirhead's case history of a Yorkshire farm with PMWS and PDNS.
East Anglia Farm, UK - Philip Richardson
This paper charts the course and effects of the disease on a single herd as well as highlighting the economic impact.
Photographs
Clinical signs
Photos of the clinical signs that are seen generally in pigs with PMWS and PDNS. Includes skin lesions, enlarged lymph glands, wasting and dead pigs.
Post mortem (1)
Photos of the signs that are seen in post-mortem samples of pigs with PMWS and PDNS. Includes interstitial pneumonia, secondary bacterial infection, enlarged lymph nodes, oedema and intra cytoplasmic inclusions
Post mortem (2)
More Photos of the signs that are seen in post-mortem samples of pigs with PMWS and PDNS.


PMWS Research Archives

Published Monday, November 01, 2010: Journal of Virology, November 2010, p. 11440-11447, Vol. 84, No. 21
Cytotoxicity of ORF3 Proteins from a Nonpathogenic and a Pathogenic Porcine Circovirus
Mark Chaiyakul, Karolynn Hsu, Rkia Dardari, Frank Marshall, and Markus Czub
Porcine circovirus type 2 (PCV2) infection is associated with significant and serious swine diseases worldwide, while PCV1 appears to be a nonpathogenic virus. Previous studies demonstrated that the ORF3 protein of PCV2 (PCV2ORF3) was involved in PCV2 pathogenesis via its proapoptotic capability (J. Liu, I. Chen, Q. Du, H. Chua, and J. Kwang, J. Virol. 80:5065-5073, 2006). If PCV2ORF3-induced apoptosis is a determinant of virulence, PCV1ORF3 is hypothesized to lack this ability. The properties of PCV1 and PCV2 ORF3, expressed as fusion proteins to an enhanced green fluorescent protein (eGFP), were characterized with regard to their ability to cause cellular morphological changes, detachment, death, and apoptosis. PCV1ORF3 significantly induced more apoptotic cell death and was toxic to more different cell types than PCV2ORF3 was. PCV1ORF3-associated cell death was caspase dependent. PCV1ORF3 also induced poly(ADP-ribose) polymerase 1 (PARP) cleavage; however, whether PARP was involved in cell death requires further studies. Truncation of PCV1 and elongation of PCV2 ORF3 proteins revealed that the first 104 amino acids contain a domain capable of inducing cell death, whereas the C terminus of PCV1ORF3 contains a domain possibly responsible for enhancing cell death. These results suggest that the pathogenicity of PCV2 for pigs is either not determined or not solely determined by the ORF3 protein.

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