Host–pathogen interactions during porcine reproductive and respiratory syndrome virus 1 infection of piglets

Abstract

Porcine reproductive and respiratory syndrome (PRRS) is a major disease affecting pigs worldwide and resulting in considerable economic losses. While PRRS is a global phenomenon, the causative viruses PRRSV-1 (first detected in Europe) and PRRSV-2 (isolated in North America) are genetically and biologically distinct. In addition, the disease outcome is directly linked to co-infections associated with the porcine respiratory disease complex and the host response is variable between different breeds of pigs. It is therefore warranted when studying the pathogenesis of PRRS to consider each viral genotype separately and apply careful consideration to the disease model studied. We here review the respiratory pig model for PRRSV-1, with a focus on a recent set of studies conducted with carefully selected virus strains and pigs, which may serve as both a baseline and benchmark for future investigation.

Pathogenicity of three genetically diverse strains of PRRSV Type 1 in specific pathogen free pigs

“…It has been shown that, in terms of virulence, antigenic characteristics and immunological responses following experimental infection, the Belarusian Lena subtype 3 strain differed from subtype 1 strains from Western Europe being generally more pathogenic for pigs (Karniychuk et al, 2010;Weesendorp et al, 2013aWeesendorp et al, , 2014. Later, another subtype 3 Belarusian strain SU1-bel, which was characterized in vitro and in in vivo challenge experiments also proved to be significantly more virulent than Western European strains (Morgan et al, 2014(Morgan et al, , 2013Salguero et al, 2015). At present, no data are available about the biological characteristics of East European PRRSV-1 strains from other genetic subtypes, e.g.…”

Thymic depletion of lymphocytes is associated with the virulence of PRRSV-1 strains

“…These results suggest the presence of alternatively activated M2 macrophages and reflect the requirement for enhanced phagocytosis after the increased cell death (tissue remodelling). The reduced generation of T cells could result in an impaired T cell response, as previously suggested (Rodríguez-Gómez et al, 2013;Salguero et al, 2015).…”

“…More recently, HP-PRRSV strains were also identified in Eastern Europe (Karniychuk et al, 2010). The emergence of HP-PRRSV in Asia and Eastern Europe have revived the interest in understanding the immunobiology of PRRSV strains of differing virulence Salguero et al, 2015).…”

“…Differences in the virulence among PRRSV-1 strains have been associated with either an enhanced pro-inflammatory immune response, mainly associated to an increased pulmonary expression of IL-1α/β, or to higher levels of virus replication (Gómez-Laguna et al, 2010;Karniychuk et al, 2010;Morgan et al, 2013Morgan et al, , 2014Weesendorp et al, 2013;Amarilla et al, 2015;Salguero et al, 2015). However, the exact mechanisms by which PRRSV-1 exert its virulence are unknown.…”

Expression of peptide nanoparticles containing a porcine reproductive and respiratory syndrome (PRRS) virus epitope in plants

“…However, development of new PRRSV vaccines faces many challenges because of the high variability and the diverse mechanisms that the virus employs to evade the immune Uribe-Campero et al 1601 response (Huang et al, 2015;Salguero et al, 2015). A number of strategies including recombinant production of different PRRSV antigens in various systems have been tested (Qiu et al, 2005;Jiang et al, 2006;Zheng et al, 2007;Li et al, 2009a, b;Cruz et al, 2010;Chen and Liu, 2011;Chia et al, 2011;Vimolmangkang et al, 2012;Chan et al, 2013;Nam et al, 2013).…”