Characterization of homologous and heterologous adaptive immune responses in porcine reproductive and respiratory syndrome virus infection

Abstract

The present study characterized the homologous and heterologous immune response in type-I porcine reproductive and respiratory syndrome virus (PRRSV) infection. Two experiments were conducted: in experiment 1, eight pigs were inoculated with PRRSV strain 3262 and 84 days post-inoculation (dpi) they were challenged with either strain 3262 or strain 3267 and followed for the next 14 days (98 dpi). In experiment 2, eight pigs were inoculated with strain 3267 and challenged at 84 dpi as above. Clinical course, viremia, humoral response (neutralizing and non-neutralizing antibodies, NA) and virus-specific IFN-γ responses (ELISPOT) were evaluated all throughout the study. Serum levels of IL-1, IL-6, IL-8, TNF-α and TGF-β were determined (ELISA) after the second challenge. In experiment 1 primo-inoculation with strain 3262 induced viremia of ≤ 28 days, low titres of homologous NA but strong IFN-γ responses. In contrast, strain 3267 induced longer viremias (up to 56 days), higher NA titres (≤ 6 log2) and lower IFN-γ responses. Inoculation with 3267 produced higher serum IL-8 levels. After the re-challenge at 84 dpi, pigs in experiment 1 developed mostly a one week viremia regardless of the strain used. In experiment 2, neither the homologous nor the heterologous challenge resulted in detectable viremia although PRRSV was present in tonsils of some animals. Homologous re-inoculation with 3267 produced elevated TGF-β levels in serum for 7–14 days but this did not occur with the heterologous re-inoculation. In conclusion, inoculation with different PRRSV strains result in different virological and immunological outcomes and in different degrees of homologous and heterologous protection.

Vaccination with a genotype 1 modified live vaccine against porcine reproductive and respiratory syndrome virus significantly reduces viremia, viral shedding and transmission of the virus in a quasi-natural experimental model

“…Thus, despite we are assuming again the worst case scenario for V pigs, the impact of vaccination on the viral transmission is still evident. Regarding the challenge strain 3267, when used in previous experiments (Díaz et al, 2012) it was shown that most animals developed a viremia long enough to cover the entire exposure phase, being thus adequate for the purpose of the present study. The results of the infection with strain 3267 can be considered as typical of an average genotype 1 subtype 1 isolate when inoculated in young pigs (Martínez-Lobo et al, 2011).…”

“…Group NV was left unvaccinated and remained as naïve controls. On the 35th day postvaccination (dpv), 14 NV pigs were separated, housed in an isolated room and inoculated intranasally with 2 ml (1 ml/ nostril) of a suspension containing 10 5.5 TCID 50 /ml of a genotype 1 PRRSV strain designated as 3267 Díaz et al, 2012;Gimeno et al, 2011). The inoculated animals were designated as ''seeder'' pigs (SP).…”

“…The inoculation of SP pigs was done with a genotype 1 subtype 1 PRRSV 3267 strain [Genbank accession number JF276435] that has been described in previous studies Díaz et al, 2012;Gimeno et al, 2011). The strain was isolated in 2006 from the serum of a boar of a Portuguese farm and causes a mild respiratory process in piglets and a viremia lasting three or more weeks.…”

“…The VNT was performed following a previously described method (Díaz et al, 2012), using either MARC-145 cells or PAM for vaccine and challenge virus, respectively (the vaccine virus replicates poorly in PAM). Briefly, sera were inactivated at 56 8C for 30 min, diluted (in duplicate) in a serial dilution from 1/2 to 1/256 and incubated overnight at 4 8C with an equal volume (50 ml) of either the vaccine or the challenge virus (2000 TCID 50 /ml).…”

Predicted Peptides from Non-Structural Proteins of Porcine Reproductive and Respiratory Syndrome Virus Are Able to Induce IFN-γ and IL-10

“…PRRSV control has proven to be difficult, among other causes because immunity against one strain does not preclude protective immunity against a different one [17,18,19]. The ideal of a universally effective vaccine, namely, one that could protect against all existing PRRSV strains, is far from reach.…”