Abstract
Porcine reproductive and respiratory syndrome (PRRS) is considered one of the most relevant diseases of swine. The condition is caused by PRRS virus (PRRSV), an extremely variable virus of the Arteriviridae family. Its heterogeneity can be responsible, at least partially, of the poor cross-protection observed between PRRSV isolates. Neutralizing antibodies (NAs), known to play a role in protection, usually poorly recognize heterologous PRRSV isolates, indicating that most NAs are strain-specific. However, some pigs develop broadly reactive NAs able to recognize a wide range of heterologous isolates. The aim of this study was to determine whether PRRSV isolates that induce broadly reactive NAs as determined in vitro are able to confer a better protection in vivo. For this purpose two in vivo experiments were performed. Initially, 40 pigs were immunized with a PRRSV-1 isolate known to induce broadly reactive NAs and 24 additional pigs were used as controls. On day 70 after immunization, the pigs were divided into eight groups composed by five immunized and three control pigs and exposed to one of the eight different heterologous PRRSV isolates used for the challenge. In the second experiment, the same experimental design was followed but the pigs were immunized with a PRRSV-1 isolate, which is known to generate mostly strain-specific NAs. Virological parameters, specifically viremia and the presence of challenge virus in tonsils, were used to determine protection. In the first experiment, sterilizing immunity was obtained in three groups, prevention of viremia was observed in two additional groups, although the challenge virus was detected occasionally in the tonsils of immunized pigs, and partial protection, understood as a reduction in the frequency of viremia compared with controls, was recorded in the remaining three groups. On the contrary, only partial protection was observed in all groups in the second experiment. The results obtained in this study confirm that PRRSV-1 isolates differ in their ability to induce cross-reactive NAs and, although other components of the immune response might have contributed to protection, pigs with cross-reactive NAs at the time of challenge exhibited better protection, indicating that broadly reactive NAs might play a role in protection against heterologous reinfections.
Highlights
Porcine reproductive and respiratory syndrome (PRRS) remains one of the most important diseases of swine
The results reported here confirm that porcine reproductive and respiratory syndrome virus (PRRSV)-1 isolates differ in their ability to induce cross-reactive NAs and in their ability to confer protection against heterologous reinfections
It has to be mentioned that the correlation between the level of NAs and protection was not perfect and that a few pigs without measurable titers of NAs or with NA titers lower than those established as the threshold for protection in passive transfer studies were protected
Summary
Porcine reproductive and respiratory syndrome (PRRS) remains one of the most important diseases of swine. The condition is characterized by reproductive failure in sows and boars and respiratory disease in growing pigs, leading to important economic losses in the vast majority of pork-producing countries (1). The etiological agent of PRRS is a small, enveloped, RNA virus, commonly known as porcine reproductive and respiratory syndrome virus (PRRSV), which has been recently classified in the genus Betaarterivirus within the family Arteriviridae in the order Nidovirales (2). The huge genomic variability of PRRSV isolates has led to their classification into two different species: Betaarterivirus suid 1, known as PRRSV-1, which predominates in European countries, and Betaarterivirus suid 2, known as PRRSV-2, widely spread in American and Asian countries (3). A significant genomic variability has been described within each species, and several subtypes and lineages have been identified (3–5). Genomic variability translates into high antigenic variability, which is considered as one of the main factors, which could explain the poor or, in the best case, the partial cross-protection observed upon heterologous virus exposure (6–9)
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