Simulating the Commercial Implementation of Gene-Editing for Influenza A Virus Resistance in Pigs: An Economic and Genetic Analysis.

The development of swine Influenza A Virus resistance along with genetic technologies could complement current control measures to help to improve animal welfare standards and the economic efficiency of pig production. We have created a simulation model to assess the genetic and economic implications of various gene-editing methods that could be implemented in a commercial, multi-tiered swine breeding system. Our results demonstrate the length of the gene-editing program was negatively associated with genetic progress in commercial pigs and that the time required to reach fixation of resistance alleles was reduced if the efficiency of gene-editing is greater.

Characterisation of autophagy disruption in the ileum of pigs infected with Lawsonia intracellularis.

Lawsonia intracellularis is the aetiological agent of proliferative enteropathy, an enteric disease endemic in swine. Survival in its intracellular niche of the ileum epithelial lining requires the capacity to subvert, repress or exploit the host immune response to create an environment conducive to bacterial propagation. To better understand how L.

Current and prospective control strategies of influenza A virus in swine.

Background: Influenza A Viruses (IAV) are endemic pathogens of significant concern in humans and multiple keystone livestock species. Widespread morbidity in swine herds negatively impacts animal welfare standards and economic performance whilst human IAV pandemics have emerged from pigs on multiple occasions. To combat the rising prevalence of swine IAV there must be effective control strategies available.

Swine ANP32A Supports Avian Influenza Virus Polymerase.

Avian influenza viruses occasionally infect and adapt to mammals, including humans. Swine are often described as "mixing vessels," being susceptible to both avian- and human-origin viruses, which allows the emergence of novel reassortants, such as the precursor to the 2009 H1N1 pandemic. ANP32 proteins are host factors that act as influenza virus polymerase cofactors.