Immunological Responses of Swine to Porcine Reproductive and Respiratory Syndrome Virus Infection

Abstract

The immunology of porcine reproductive and respiratory syndrome virus (PRRS) begins with an initial encounter of PRRSV with the pig. Regardless of the route of entry of PRRSV--via inhalation, intramuscular vaccination, insemination, or other routes--productive infection occurs predominately in alveolar macrophages of the lung. Thus, innate responses of the lung and the alveolar macrophage comprise the initial defense against PRRSV. The virus appears not to elicit innate interferon and cytokine responses characteristic of other strongly immunogenic viral pathogens, and its effects are consistent with induction of a weak adaptive immune response. Humoral and cell-mediated immunity is induced in due course, and results in clearance of virus from the circulation but not from lymphoid tissues, where the infection becomes persistent. Subsequent reexposure to PRRSV elicits an anamnestic response that is partially to completely protective. Within this unconventional picture of anti-PRRSV immunity lie a variety of unresolved issues, including the nature of protective immunity within individual pigs and among pigs in commercial populations, the efficacy of protective immunity against genetically different PRRSV isolates, the effects of developmental age, sex, genetics, and other host factors on the immune response to PRRSV, and the possible suppression of host immunity to other pathogens.

Alternative codon usage of PRRS virus ORF5 gene increases eucaryotic expression of GP5 glycoprotein and improves immune response in challenged pigs

“…The higher reactivity to GP5, as well as the higher VN activity of pigs sera that have been vaccinated either with hAdV/wtORF5 or hAdV/synORF5 is in agreement with previous findings indicating that GP5 is the primary structural glycoprotein of PRRSV involved in virus neutralization activity [6,7,25]. Even if high titers of VN antibodies appeared at day 10 post-challenge, the viremia could not be prevented (data not shown) as previously observed [10,26,27]. Nevertheless, one report has demonstrated the protective effect of neutralizing antibodies and their potential to prevent viremia [9].…”

“…The viral genome consists of a positive single-stranded RNA molecule of approximately 15 kb in length, composed of nine open reading frames [2][3][4]. The ORFs 5 to 7 encode the three major structural proteins of virions which are the envelope glycoprotein GP5 (25)(26), the non-glycosylated membrane protein M (18-19 kDa) and the nucleocapsid protein N (14-15 kDa) [5]. These PRRSV structural proteins are closely associated, GP5 and M proteins being associated in the form of heterodimers [5].…”

Clinical and pathological responses of pigs from two genetically diverse commercial lines to porcine reproductive and respiratory syndrome virus infection1

“…There is ample evidence for genetic variation in the response of animals to the infection (e.g., Halbur et al, 1998;Petry et al, 2005Petry et al, , 2007Vincent et al, 2005Vincent et al, , 2006 and for the existence of indicative biomarkers that could be targeted for selection (Galina-Pantoja et al, 2006;Petry et al, 2007). The immune response to PRRSV appears to be manifold, and there are many facets of resistance to the virus that could be targeted by genetic selection (Murtaugh et al, 2002). However, to date there is a lack of understanding of the relationships between traits associated with PRRSV susceptibility and performance traits, such as growth in the face of PRRSV infection.…”

The role of mathematical models of host–pathogen interactions for livestock health and production – a review

“…Compared with other common viruses, PRRSV fails to elicit any of the typical innate immune response mechanisms (van Reeth and Nauwynck, 2000;Murtaugh et al, 2002), and the adaptive immune response is delayed and weak (Molitor et al, 1997;Mulupuri et al, 2008; Figure 3b). …”

“…The model describes how pathogen load, severity of infection and target cell numbers change over time in the absence of an immune response. For a more comprehensive model of PRRSV infection that includes immune response mechanisms, see Doeschl-Wilson and Galina-Pantoja (2010 unusual pathogenesis and the atypical immune response it invokes (Murtaugh et al, 2002). PRRSV targets primarily a subpopulation of macrophages in the lung and other tissues that have reached a specific stage of differentiation that renders them permissive to the virus (Duan et al, 1997;Gaudrealt et al, 2009).…”