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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, June 01, 2009: Journal of Virology, June 2009, p. 6039-6047, Vol. 83, No. 12
JNK and p38 Mitogen-Activated Protein Kinase Pathways Contribute to Porcine Circovirus Type 2 Infection
Li Wei, Zhongwu Zhu, Jing Wang, and Jue Liu
Infection with a wide variety of viruses often perturbs host cell signaling pathways including the Jun NH2-terminal kinase/stress-activated kinase (JNK/SAPK) and the p38 mitogen-activated protein kinase (p38/MAPK), which are important components of cellular signal transduction pathways. The present study demonstrated for the first time that porcine circovirus type 2 (PCV2), which is the primary causative agent of an emerging swine disease, postweaning multisystemic wasting syndrome, can activate JNK1/2 and p38 MAPK pathways in PCV2-infected PK15 cells. However, PCV2 at an early stage of infection, as well as UV-irradiated PCV2, failed to activate these two MAPK families, which demonstrated that PCV2 replication was necessary for their activation. We further found that PCV2 activated the phosphorylation of JNK1/2 and p38 MAPK downstream targets c-Jun and ATF-2 with virus replication in the cultured cells. The roles of these kinases in PCV2 infection were further evaluated using specific inhibitors: the JNK inhibitor 1 for JNK1/2 and SB202190 for p38. Inhibition of JNK1/2 and p38 kinases by these specific inhibitors did result in significant reduction of PCV2 viral mRNA transcription and protein synthesis, viral progeny release, and blockage of PCV2-induced apoptotic caspase-3 activation in the infected cells. Taken together, these data suggest that JNK/SAPK and p38 MAPK pathways play important roles in the PCV2 replication and contribute to virus-mediated changes in host cells.

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