Vaccination with a Porcine Reproductive and Respiratory Syndrome (PRRS) Modified Live Virus Vaccine Followed by Challenge with PRRS Virus and Porcine Circovirus Type 2 (PCV2) Protects against PRRS but Enhances PCV2 Replication and Pathogenesis Compared to Results for Nonvaccinated Cochallenged Controls

Abstract

cCoinfections involving porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2 (PCV2) contribute to a group of disease syndromes known as porcine circovirus-associated disease (PCVAD). Presumably, PRRSV infection enhances PCV2 replication as a result of modulation of host immunity. The purpose of this study was to evaluate PCV2 replication and pathogenesis in pigs vaccinated with a PRRS modified live virus (MLV) vaccine and subsequently challenged with a combination of PRRSV and PCV2. During the early postchallenge period, the number of pigs with PRRSV-associated clinical signs was decreased, and average daily gain (ADG) was increased, in the vaccinated group, demonstrating the protective effect of PRRS vaccination. However, during the later postchallenge period, more pigs in the vaccinated group showed increased PCV2 viremia, decreased ADG, increased PCVAD clinical signs, and increased mortality. In this disease model, the early benefits of PRRSV vaccination were outweighed by the later amplification of PCVAD. P orcine circovirus type 2 (PCV2), a single-stranded DNA virus in the family Circoviridae, contributes to a group of syndromes collectively termed porcine circovirus-associated disease (PCVAD) (1). Two important clinical syndromes associated with PCVAD are PCV2-associated pneumonia and postweaning multisystemic wasting syndrome (PMWS) (1, 2). Management of PCV2 through the use of inactivated and subunit vaccines has led to the effective control of PCVAD in North America and Europe. However, the emergence of new PCV2 strains and the lack of PCV2 vaccination programs in other countries create an uncertain future for continued disease control.Porcine reproductive and respiratory syndrome virus (PRRSV) is a single-stranded RNA virus in the family Arteriviridae (3, 4). For the past 20 years, PRRSV has remained the most costly disease affecting swine production worldwide (5). PRRSV infection contributes to a number of immunological outcomes that increase the susceptibility of the host to secondary infections by primary and secondary pathogens (6-8). PRRSV is frequently isolated along with PCV2 (9) and is one of the major cofactors linked with increasing PCV2 replication and pathogenesis (10-12). Previous work by us and others has shown that a principal contribution of PRRSV is to increase PCV2 viremia (13). Increased PCV2 replication is likely the result of immune stimulation that results in more PCV2-permissive cells combined with PRRSV-induced immunomodulation. The complex etiology of PCVAD, including the role of PRRSV infection, has yet to be fully understood. In an extensive body of work, we identified the aberrant recognition of a nonneutralizing decoy epitope on the PCV2 capsid protein (CP) as a contributing factor in PCVAD immunopathogenesis. Natural PCV2 infection of a population produces a mixture of pigs that recognize the decoy and neutralizing epitopes, which may explain why only a subpopulation of infected pigs goes on to develop PCVAD (13-15).In this study, we to...

Host genetics of response to porcine reproductive and respiratory syndrome in nursery pigs

“…To evaluate host response to PRRS vaccination, half of the pigs in each trial were vaccinated with a modified live PRRSV 28 days prior to co-infection. Details of the design of these experiments, along with results for pathogenesis and the effects of PRRSV vaccination are in Niederwerder et al (2015). Results showed that vaccination to PRRS increased the impact of subsequent exposure to PCV2b, consistent with earlier findings that PRRSV infection weakens the immune system and increases the susceptible of pigs to other pathogens (Yin et al, 2013).…”

Porcine MKRN1 Modulates the Replication and Pathogenesis of Porcine Circovirus Type 2 by Inducing Capsid Protein Ubiquitination and Degradation

“…ORF1 encodes two replication-associated proteins (Rep and Rep=) which are necessary for the rolling-circle replication of viral DNA (5,8). ORF2 encodes the capsid protein (Cap), a unique structural component of the virion and the dominant immunogenic agent (3,4,9). Cap not only is indispensable for encapsulating the viral genome to assemble infectious virions but also is required for transport of the Rep protein and viral DNA between the cytoplasm and nucleus (10)(11)(12).…”

Pathogenic characterization of porcine reproductive and respiratory syndrome virus of Indian origin in experimentally infected piglets

“…For lungs, scores for microscopic lesions were assigned as described previously (Niederwerder et al., ) with minor modifications. Briefly, the scoring system is as follows: 0, no significant microscopic lesions; 1, mild interstitial pneumonia with <50% involvement in a single lobe; 2, mild to moderate multifocal interstitial pneumonia with 50%–75% involvement in one or two lobes; 3, severe multifocal interstitial pneumonia with 50%–75% involvement in one or two lobes; 4, severe diffuse interstitial pneumonia with >75% involvement in multiple lobes.…”