PMID- 23282224
OWN - NLM
STAT- MEDLINE
DCOM- 20130912
LR  - 20211021
IS  - 1743-422X (Electronic)
IS  - 1743-422X (Linking)
VI  - 10
DP  - 2013 Jan 3
TI  - Pathogenic characteristics of three genotype II porcine reproductive and 
      respiratory syndrome viruses isolated from China.
PG  - 7
LID - 10.1186/1743-422X-10-7 [doi]
AB  - BACKGROUND: We examined differences in pathogenicity in pigs from China that had 
      been experimentally infected with porcine reproductive and respiratory syndrome 
      virus (PRRSV). METHODS: We compared pathogenic characteristics of a field isolate 
      (GX-1/2008F), two PRRSV isolates (HN-1/2008, YN-1/2008) propagated in cells, and 
      GX-1/2008F that had been propagated in cells (GX-1/2008). The clinical courses, 
      along with humoral and cell-mediated responses, were monitored for 21 days 
      post-infection (DPI). Animals were sacrificed and tissue samples used for gross 
      pathological, histopathological and ultrastructure examination. RESULTS: At 2-3 
      DPI, animals infected with cell-propagated viruses exhibited signs of coughing, 
      anorexia and fever. However their rectal temperature did not exceed 40.5 degrees C. 
      Viremia was detectable as early as 3 DPI in animals infected with HN-1/2008 and 
      YN-1/2008. Animals inoculated with GX-1/2008F displayed clinical signs at 6 DPI; 
      the rectal temperature of two animals in this group exceeded 41.0 degrees C, with viremia 
      first detected at 7 DPI. Seroconversion for all challenged pigs, except those 
      infected with GX-1/2008, was seen as early as 7 DPI. All of these pigs had fully 
      seroconverted by 11 DPI. All animals challenged with GX-1/2008 remained 
      seronegative until the end of the experiment. Innate immunity was inhibited, with 
      levels of IFN-alpha and IL-1 not significantly different between control and infected 
      animals. The cytokines IFN-gamma and IL-6 transiently increased during acute 
      infection. All virus strains caused gross lesions including multifocal 
      interstitial pneumonia and hyperplasia of lymph nodes. Inflammation of the 
      stomach and small intestine was also observed. Lesions in the group infected with 
      GX-1/2008F were more serious than in other groups. Transmission electron 
      microscopy revealed that alveolar macrophages, plasmacytes and lymphocytes had 
      fractured cytomembranes, and hepatocytes had disrupted organelles and swollen 
      mitochondria. CONCLUSIONS: The pathogenicity of the PRRSV field isolate became 
      attenuated when propagated in MARC-145 cells. Tissue tropism of highly pathogenic 
      strains prevailing in China was altered compared with classical PRRSV strains. 
      The observed damage to immune cells and modulation of cytokine production could 
      be mechanisms that PRRSV employs to evade host immune responses.
FAU - Shang, Youjun
AU  - Shang Y
AD  - State Key Laboratory of Veterinary Etiological Biology, National Foot and Mouth 
      Disease Reference Laboratory, Lanzhou Veterinary Research Institute, Chinese 
      Academy of Agricultural Sciences, Xujiaping 1, Chengguan District, Lanzhou 
      730046, The People's Republic of China.
FAU - Wang, Guangxiang
AU  - Wang G
FAU - Yin, Shuanghui
AU  - Yin S
FAU - Tian, Hong
AU  - Tian H
FAU - Du, Ping
AU  - Du P
FAU - Wu, Jinyan
AU  - Wu J
FAU - Chen, Yan
AU  - Chen Y
FAU - Yang, Shunli
AU  - Yang S
FAU - Jin, Ye
AU  - Jin Y
FAU - Zhang, Keshan
AU  - Zhang K
FAU - Lu, Zengjun
AU  - Lu Z
FAU - Liu, Xiangtao
AU  - Liu X
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130103
PL  - England
TA  - Virol J
JT  - Virology journal
JID - 101231645
RN  - 0 (Cytokines)
SB  - IM
MH  - Animals
MH  - China
MH  - Cytokines/immunology
MH  - Genotype
MH  - Porcine Reproductive and Respiratory Syndrome/immunology/*virology
MH  - Porcine respiratory and reproductive syndrome 
      virus/classification/*genetics/isolation & purification/*pathogenicity
MH  - Swine
MH  - Swine Diseases/immunology/*virology
MH  - Virulence
PMC - PMC3616938
EDAT- 2013/01/04 06:00
MHDA- 2013/09/13 06:00
PMCR- 2013/01/03
CRDT- 2013/01/04 06:00
PHST- 2011/08/18 00:00 [received]
PHST- 2012/12/24 00:00 [accepted]
PHST- 2013/01/04 06:00 [entrez]
PHST- 2013/01/04 06:00 [pubmed]
PHST- 2013/09/13 06:00 [medline]
PHST- 2013/01/03 00:00 [pmc-release]
AID - 1743-422X-10-7 [pii]
AID - 10.1186/1743-422X-10-7 [doi]
PST - epublish
SO  - Virol J. 2013 Jan 3;10:7. doi: 10.1186/1743-422X-10-7.