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Sant Cugat del Vallès, Spain
Sant Cugat del Vallès, Spain
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Wells K.D.,University of Missouri | Bardot R.,Kansas State University | Whitworth K.M.,University of Missouri | Trible B.R.,Kansas State University | And 6 more authors.
Journal of Virology | Year: 2017

CD163 knockout (KO) pigs are resistant to infection with genotype 2 (type 2) porcine reproductive and respiratory syndrome virus (PRRSV). Furthermore, the substitution of CD163 scavenger receptor cysteine-rich (SRCR) domain 5 with a homolog of human CD163-like (hCD163L1) SRCR 8 domain confers resistance of transfected HEK cells to type 1 PRRSV. As a means to understand the role of domain 5 in PRRSV infection with both type 1 and type 2 viruses, pigs were genetically modified (GM) to possess one of the following genotypes: complete knockout (KO) of CD163, deletions within SRCR domain 5, or replacement (domain swap) of SRCR domain 5 with a synthesized exon encoding a homolog of hCD163L1 SRCR domain 8. Immunophenotyping of porcine alveolar macrophages (PAMs) showed that pigs with the KO or SRCR domain 5 deletion did not express CD163. When placed in culture, PAMs from pigs with the CD163 KO phenotype were completely resistant to a panel consisting of six type 1 and nine type 2 isolates. PAMs from pigs that possessed the hCD163L1 domain 8 homolog expressed CD163 and supported the replication of all type 2 isolates, but no type 1 viruses. Infection of CD163-modified pigs with representative type 1 and type 2 viruses confirmed the in vitro results. The results confirm that CD163 is the likely receptor for all PRRS viruses. Even though type 1 and type 2 viruses are considered phenotypically similar at several levels, there is a distinct difference between the viral genotypes in the recognition of CD163. © 2017 American Society for Microbiology.


Popescu L.,Kansas State University | Gaudreault N.N.,Kansas State University | Whitworth K.M.,University of Missouri | Murgia M.V.,Kansas State University | And 6 more authors.
Virology | Year: 2017

African swine fever is a highly contagious, often fatal disease of swine for which there is no vaccine or other curative treatment. The macrophage marker, CD163, is a putative receptor for African swine fever virus (ASFV). Pigs possessing a complete knockout of CD163 on macrophages were inoculated with Georgia 2007/1, a genotype 2 isolate. Knockout and wild type pen mates became infected and showed no differences in clinical signs, mortality, pathology or viremia. There was also no difference following in vitro infection of macrophages. The results do not rule out the possibility that other ASFV strains utilize CD163, but demonstrate that CD163 is not necessary for infection with the Georgia 2007/1 isolate. This work rules out a significant role for CD163 in ASFV infection and creates opportunities to focus on alternative receptors and entry mechanisms. © 2016 The Authors


Trademark
Ites and Genus | Date: 2017-01-12

Hats; Pants; T-shirts; Dress shirts; Short-sleeved or long-sleeved t-shirts; Toboggan hats; Toboggan hats, pants and caps.


Whitworth K.M.,University of Missouri | Lee K.,University of Missouri | Lee K.,Virginia Polytechnic Institute and State University | Benne J.A.,University of Missouri | And 13 more authors.
Biology of Reproduction | Year: 2014

Targeted modification of the pig genome can be challenging. Recent applications of the CRISPR/Cas9 system hold promise for improving the efficacy of genome editing. When a designed CRISPR/Cas9 system targeting CD163 or CD1D was introduced into somatic cells, it was highly efficient in inducing mutations. When these mutated cells were used with somatic cell nuclear transfer, offspring with these modifications were created. When the CRISPR/Cas9 system was delivered into in vitro produced presumptive porcine zygotes, the system was effective in creating mutations in eGFP, CD163, and CD1D (100% targeting efficiency in blastocyst stage embryos); however, it also presented some embryo toxicity. We could also induce deletions in CD163 or CD1D by introducing two types of CRISPRs with Cas9. The system could also disrupt two genes, CD163 and eGFP, simultaneously when two CRISPRs targeting two genes with Cas9 were delivered into zygotes. Direct injection of CRISPR/Cas9 targeting CD163 or CD1D into zygotes resulted in piglets that have mutations on both alleles with only one CD1D pig having a mosaic genotype. We show here that the CRISPR/Cas9 system can be used by two methods. The system can be used to modify somatic cells followed by somatic cell nuclear transfer. System components can also be used in in vitro produced zygotes to generate pigs with specific genetic modifications. © 2014 by the Society for the Study of Reproduction, Inc.


CD163 knockout (KO) pigs are resistant to infection with genotype 2 (type 2) porcine reproductive and respiratory syndrome virus (PRRSV). Furthermore, the substitution of CD163 scavenger receptor cysteine-rich (SRCR) domain 5 with a homolog of human CD163-like (hCD163L1) SRCR 8 domain confers resistance of transfected HEK cells to type 1 PRRSV. As a means to understand the role of domain 5 in PRRSV infection with both type 1 and type 2 viruses, pigs were genetically modified (GM) to possess one of the following genotypes: complete knockout (KO) of CD163, deletions within SRCR domain 5, or replacement (domain swap) of SRCR domain 5 with a synthesized exon encoding a homolog of hCD163L1 SRCR domain 8. Immunophenotyping of porcine alveolar macrophages (PAMs) showed that pigs with the KO or SRCR domain 5 deletion did not express CD163. When placed in culture, PAMs from pigs with the CD163 KO phenotype were completely resistant to a panel consisting of six type 1 and nine type 2 isolates. PAMs from pigs that possessed the hCD163L1 domain 8 homolog expressed CD163 and supported the replication of all type 2 isolates, but no type 1 viruses. Infection of CD163-modified pigs with representative type 1 and type 2 viruses confirmed the in vitro results. The results confirm that CD163 is the likely receptor for all PRRS viruses. Even though type 1 and type 2 viruses are considered phenotypically similar at several levels, there is a distinct difference between the viral genotypes in the recognition of CD163.Genetic modification of the CD163 gene creates the opportunity to develop production animals that are resistant to PRRS, the costliest viral disease to ever face the swine industry. The results create further opportunities to develop refinements in the modification of CD163 with the goal of making pigs refractory to infection while retaining important CD163 functions.


PubMed | University of Missouri, Kansas State University and Genus
Type: | Journal: Virology | Year: 2016

African swine fever is a highly contagious, often fatal disease of swine for which there is no vaccine or other curative treatment. The macrophage marker, CD163, is a putative receptor for African swine fever virus (ASFV). Pigs possessing a complete knockout of CD163 on macrophages were inoculated with Georgia 2007/1, a genotype 2 isolate. Knockout and wild type pen mates became infected and showed no differences in clinical signs, mortality, pathology or viremia. There was also no difference following in vitro infection of macrophages. The results do not rule out the possibility that other ASFV strains utilize CD163, but demonstrate that CD163 is not necessary for infection with the Georgia 2007/1 isolate. This work rules out a significant role for CD163 in ASFV infection and creates opportunities to focus on alternative receptors and entry mechanisms.


Novel mutations in cytochrome P450C17 (CYP17) and cytochrome b5 (CYB5) affecting 16-androstene steroid synthesis are disclosed. The novel mutations result in alterations in production of critical intermediaries in the synthesis of 16-androstene steroids. Altering the activity of these enzymes may be useful in enhancing reducing androstenone synthesis and reducing boar taint. The identification of these novel mutations also allows for the development of transgenic pigs bearing mutations in these enzymes or for genetic screening to identify pigs on the basis of their CYP17 and/or CYB5 genotype. Pigs having these mutations may be selected and bred to produce pigs that have a lower incidence of boar taint.


Novel mutations in cytochrome P450C17 (CYP17) and cytochrome b5 (CYB5) affecting 16-androstene steroid synthesis are disclosed. The novel mutations result in alterations in production of critical intermediaries in the synthesis of 16-androstene steroids. Altering the activity of these enzymes may be useful in enhancing reducing androstenone synthesis and reducing boar taint. The identification of these novel mutations also allows for the development of transgenic pigs bearing mutations in these enzymes or for genetic screening to identify pigs on the basis of their CYP17 and/or CYB5 genotype. Pigs having these mutations may be selected and bred to produce pigs that have a lower incidence of boar taint.


Berry E.A.,Ryelands | Scrivens M.,Genus | Hillerton J.E.,Drumlanrig
International Journal of Dairy Technology | Year: 2016

A review of milking machine tests on 640 dairy farms in England and Wales between 2012 and 2014 suggests more machines now comply with installation and operation standards than 10 years ago. However, approximately 60% of systems tested failed to meet the milking machine requirements of the farm assurance standards in the UK, with most failing to reach operational requirements on one aspect. The most common problem (47%) was that the systems had excessive vacuum line losses, with other vacuum/airline losses also common. Many machines failed on more than one aspect. © 2016 Society of Dairy Technology

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