PMID- 9823592
OWN - NLM
STAT- MEDLINE
DCOM- 19990113
LR  - 20170214
IS  - 0300-9858 (Print)
IS  - 0300-9858 (Linking)
VI  - 35
IP  - 6
DP  - 1998 Nov
TI  - Apoptosis induced in vivo during acute infection by porcine reproductive and 
      respiratory syndrome virus.
PG  - 506-14
AB  - We studied apoptosis caused by porcine reproductive and respiratory syndrome 
      virus (PRRSV) in vivo, focusing on the tissues that constitute the main targets 
      for infection: lung and lymphoid tissues. Previous investigators have shown that 
      the PRRSV glycoprotein p25, encoded by PRRSV open reading frame 5, induces 
      apoptosis when expressed in COS-1 cells. Results of studies conducted in our 
      laboratory indicate the simultaneous occurrence of PRRSV-induced alterations of 
      spermatogenesis and apoptotic death of germinal epithelial cells in the testicle. 
      In this study, the goal was to determine whether virus-induced apoptosis is a 
      direct mechanism of cell death caused by PRRSV in infected pigs. Eight 3-week-old 
      pigs were intranasally inoculated with PRRSV 16244B, a highly virulent field 
      strain. Lung, tonsil, bronchial lymph node, spleen, and heart were assessed 
      histologically at 4 and 7 days postinfection. To characterize PRRSV-infected 
      cells and apoptotic cell death, we used immunohistochemical methods for detection 
      of viral antigen, DNA electrophoresis for detection of DNA fragmentation, the 
      terminal deoxynucleotidyl transferase-mediated deoxyuridine 
      triphosphate-fluorescein nick end labeling method for in situ detection of DNA 
      strand breaks, and electron microscopy for ultrastructural morphologic studies. 
      PRRSV infection resulted in widespread apoptosis in the lungs and lymphoid 
      tissues of infected pigs. Virus infection-induced apoptotic cells were more 
      abundant than PRRSV-infected cells in all tissues. DNA laddering was detected in 
      lung and lymphoid tissues. However, double-labeling experiments demonstrated that 
      the majority of apoptotic cells did not colocalize with PRRSV-infected cells. Our 
      findings suggest the presence of an indirect mechanism in the induction of 
      apoptosis for PRRSV.
FAU - Sur, J H
AU  - Sur JH
AD  - Department of Veterinary and Biomedical Sciences, University of Nebraska, 
      Lincoln, USA.
FAU - Doster, A R
AU  - Doster AR
FAU - Osorio, F A
AU  - Osorio FA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Vet Pathol
JT  - Veterinary pathology
JID - 0312020
RN  - 0 (Antigens, Viral)
RN  - 0 (DNA, Viral)
SB  - IM
MH  - Acute Disease
MH  - Animals
MH  - Antigens, Viral/analysis
MH  - *Apoptosis
MH  - Cell Nucleus/ultrastructure
MH  - DNA, Viral/analysis
MH  - Electrophoresis, Agar Gel/veterinary
MH  - Immunoenzyme Techniques/veterinary
MH  - In Situ Nick-End Labeling/veterinary
MH  - Lung/pathology/virology
MH  - Lymphoid Tissue/pathology/virology
MH  - Macrophages, Alveolar/ultrastructure
MH  - Porcine Reproductive and Respiratory Syndrome/*pathology/virology
MH  - Porcine respiratory and reproductive syndrome 
      virus/genetics/immunology/*pathogenicity
MH  - Swine
EDAT- 1998/11/21 00:00
MHDA- 1998/11/21 00:01
CRDT- 1998/11/21 00:00
PHST- 1998/11/21 00:00 [pubmed]
PHST- 1998/11/21 00:01 [medline]
PHST- 1998/11/21 00:00 [entrez]
AID - 10.1177/030098589803500605 [doi]
PST - ppublish
SO  - Vet Pathol. 1998 Nov;35(6):506-14. doi: 10.1177/030098589803500605.