PMID- 28215617
OWN - NLM
STAT- MEDLINE
DCOM- 20180403
LR  - 20180403
IS  - 1873-2542 (Electronic)
IS  - 0378-1135 (Linking)
VI  - 209
DP  - 2017 Sep
TI  - Genetic engineering alveolar macrophages for host resistance to PRRSV.
PG  - 124-129
LID - S0378-1135(16)30437-0 [pii]
LID - 10.1016/j.vetmic.2017.01.036 [doi]
AB  - Standard strategies for control of porcine reproductive and respiratory syndrome 
      virus (PRRSV) have not been effective, as vaccines have not reduced the 
      prevalence of disease and many producers depopulate after an outbreak. Another 
      method of control would be to prevent the virus from infecting the pig. The virus 
      was thought to infect alveolar macrophages by interaction with a variety of cell 
      surface molecules. One popular model had PRRSV first interacting with heparin 
      sulfate followed by binding to sialoadhesin and then being internalized into an 
      endosome. Within the endosome, PRRSV was thought to interact with CD163 to uncoat 
      the virus so the viral genome could be released into the cytosol and infect the 
      cell. Other candidate receptors have included vimentin, CD151 and CD209. By using 
      genetic engineering, it is possible to test the importance of individual entry 
      mediators by knocking them out. Pigs engineered by knockout of sialoadhesin were 
      still susceptible to infection, while CD163 knockout resulted in pigs that were 
      resistant to infection. Genetic engineering is not only a valuable tool to 
      determine the role of specific proteins in infection by PRRSV (in this case), but 
      also provides a means to create animals resistant to disease. Genetic engineering 
      of alveolar macrophages can also illuminate the role of other proteins in 
      response to infection. We suggest that strategies to prevent infection be pursued 
      to reduce the reservoir of virus.
CI  - Copyright (c) 2017 Elsevier B.V. All rights reserved.
FAU - Prather, Randall S
AU  - Prather RS
AD  - Division of Animal Sciences, University of Missouri, Columbia, MO 65211, United 
      States. Electronic address: PratherR@Missouri.Edu.
FAU - Whitworth, Kristin M
AU  - Whitworth KM
AD  - Division of Animal Sciences, University of Missouri, Columbia, MO 65211, United 
      States.
FAU - Schommer, Susan K
AU  - Schommer SK
AD  - Division of Animal Sciences, University of Missouri, Columbia, MO 65211, United 
      States.
FAU - Wells, Kevin D
AU  - Wells KD
AD  - Division of Animal Sciences, University of Missouri, Columbia, MO 65211, United 
      States.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20170210
PL  - Netherlands
TA  - Vet Microbiol
JT  - Veterinary microbiology
JID - 7705469
RN  - 0 (Antigens, CD)
RN  - 0 (Antigens, Differentiation, Myelomonocytic)
RN  - 0 (CD163 antigen)
RN  - 0 (Receptors, Cell Surface)
SB  - IM
MH  - Animals
MH  - Antigens, CD/genetics
MH  - Antigens, Differentiation, Myelomonocytic/genetics
MH  - Gene Knockout Techniques
MH  - *Genetic Engineering
MH  - Immunity, Innate/*genetics
MH  - Macrophages, Alveolar/*immunology/virology
MH  - Porcine Reproductive and Respiratory Syndrome/*genetics/*immunology/prevention & 
      control
MH  - Porcine respiratory and reproductive syndrome virus/immunology
MH  - Receptors, Cell Surface/genetics
MH  - Swine
OTO - NOTNLM
OT  - CD163
OT  - Genetic engineering
OT  - PRRSV
OT  - Receptor
OT  - Resistance
EDAT- 2017/02/22 06:00
MHDA- 2018/04/04 06:00
CRDT- 2017/02/21 06:00
PHST- 2016/10/10 00:00 [received]
PHST- 2016/12/28 00:00 [revised]
PHST- 2017/01/30 00:00 [accepted]
PHST- 2017/02/22 06:00 [pubmed]
PHST- 2018/04/04 06:00 [medline]
PHST- 2017/02/21 06:00 [entrez]
AID - S0378-1135(16)30437-0 [pii]
AID - 10.1016/j.vetmic.2017.01.036 [doi]
PST - ppublish
SO  - Vet Microbiol. 2017 Sep;209:124-129. doi: 10.1016/j.vetmic.2017.01.036. Epub 2017 
      Feb 10.