Gradual development of the interferon-γ response of swine to porcine reproductive and respiratory syndrome virus infection or vaccination

Abstract

Infection of swine with virulent porcine reproductive and respiratory syndrome (PRRS) virus induced a rapid, robust antibody response that comprised predominantly nonneutralizing antibodies and waned after approximately 3 months. In contrast, the initial onset of virus-specific interferon (IFN)-gamma-secreting cells (SC) in the pig lymphocyte population remained at a fairly low level during this period and then increased gradually in frequency, plateauing at 6 months postinfection. A similar polarization of the host humoral and cellular immune responses was also observed in pigs immunized with a PRRS-modified live virus (MLV) vaccine. Even coadministration of an adjuvant that enhanced the immune response to a pseudorabies (PR) MLV vaccine failed to alter the induction of PRRS virus-specific IFN-gamma SC (comprising predominantly CD4/CD8 alpha double positive memory T cells with a minority being typical CD4(-)/CD8 alpha beta(+) T cells) and the generation of neutralizing antibodies. Moreover, unlike inactivated PR virus, nonviable PRRS virus did not elicit virus-neutralizing antibody production. Presumably, an intrinsic property of this pathogen delays the development of the host IFN-gamma response and preferentially stimulates the synthesis of antibodies incapable of neutralization.

Immunostimulatory properties of a novel adjuvant administered with inactivated influenza virus vaccine

“…These cells are memory cells that proliferate specifically and produce IFN-γ [22,31,39] [36]. For the groups (Ag+BioMed) and (Ag+Alhydrogel), a decrease in relative percentage of doubly marked cells was observed on day 4 postchallenge.…”

Regulatory T Cells and Viral Disease

“…Additionally, both PRRSV infection and vaccination decreases the efficiency of vaccines against Mycoplasma hyopneumoniae (Thacker EL, 2000) and porcine pestivirus (Suradhat S, 2006). Infection and vaccination with PRRSV induces a rapid, non-neutralizing antibody response, and an early, weak gamma interferon (IFN-) response (Meier WA, 2003;Wesley RD, 2006). The initial IFN- response is not PRRSV-specific and may be a result of activation of natural killer cells (Wesley RD, 2006).…”

“…A PRRSV-specific T lymphocyte IFN- response does not appear until at least 2 weeks after infection (Xiao Z, 2004). The IFN- response gradually increases and plateaus at 6 months postinfection, and is associated with a slow increase in neutralizing antibody (Lopez OJ, 2004;Meier WA, 2003). Protective immunity is associated with both an IFN- and neutralizing antibody response; however, peak viremia and shedding occur before development of neutralizing antibody and IFN- (Lopez OJ, 2004).…”

“…The cause of the delayed IFN- and neutralizing antibody response resulting in persistent infection is unknown. Meier et al were unable to enhance the induction of PRRSV-specific IFN- secreting cells and generation of neutralizing antibody using an adjuvant that enhances the immune response to pseudorabies modified live vaccine (Meier WA, 2003). These data suggest that the virus somehow modulates the immune response to not only delay the response to the virus itself, but to also decrease the ability to mount a protective response against secondary infection.…”

Different immunological features of two genetically distinct type 2 porcine reproductive and respiratory syndrome (PRRS) viruses

“…Thus, it stimulates delayed and weak protective immunity [i.e., serum virus neutralizing (SVN) antibody and interferon (IFN)-γ secreting T cells] which seldom appears until 3 to 4 weeks after infection (Meier et al, 2003;Faaberg et al, 2006;Vanhee et al, 2009). Passively acquired SVN antibody alone was proven to prevent viremia and reproductive failure in pigs challenged with virulent PRRSV strains (Osorio et al, 2002), suggesting the critical role of SVN antibody in the control of virus infection.…”