Different clinical, virological, serological and tissue tropism outcomes of two new and one old Belgian type 1 subtype 1 porcine reproductive and respiratory virus (PRRSV) isolates

Veterinary Research, Mar 2015

In this study, the pathogenic behavior of PRRSV 13V091 and 13V117, isolated in 2013 from two different Belgian farms with enzootic respiratory problems shortly after weaning in the nursery, were compared with the Belgian strain 07V063 isolated in 2007. Full-length genome sequencing was performed to identify their origin. Twelve weeks-old pigs were inoculated intranasally (IN) with 13V091, 13V117 or 07V063 (9 pigs/group). At 10 days post inoculation (dpi), 4 animals from each group were euthanized and tissues were collected for pathology, virological and serological analysis. 13V091 infection resulted in the highest respiratory disease scores and longest period of fever. Gross lung lesions were more pronounced for 13V091 (13%), than for 13V117 (7%) and 07V063 (11%). The nasal shedding and viremia was also most extensive with 13V091. The 13V091 group showed the highest virus replication in conchae, tonsils and retropharyngeal lymph nodes. 13V117 infection resulted in the lowest virus replication in lymphoid tissues. 13V091 showed higher numbers of sialoadhesin − infected cells/mm 2 in conchae, tonsils and spleen than 13V117 and 07V063. Neutralizing antibody response with 07V063 was stronger than with 13V091 and 13V117. It can be concluded that (i) 13V091 is a highly pathogenic type 1 subtype 1 PRRSV strain that replicates better than 07V063 and 13V117 and has a strong tropism for sialoadhesin − cells and (ii) despite the close genetic relationship between 13V117 and 07V063, 13V117 has an increased nasal replication and shedding, but a decreased replication in lymphoid tissues compared to 07V063.

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Different clinical, virological, serological and tissue tropism outcomes of two new and one old Belgian type 1 subtype 1 porcine reproductive and respiratory virus (PRRSV) isolates

Frydas et al. Veterinary Research Different clinical, virological, serological and tissue tropism outcomes of two new and one old Belgian type 1 subtype 1 porcine reproductive and respiratory virus (PRRSV) isolates Ilias S Frydas 0 Ivan Trus 0 Lise K Kvisgaard 1 Caroline Bonckaert 0 Vishwanatha RAP Reddy 0 Yewei Li 0 Lars E Larsen 1 Hans J Nauwynck 0 0 Laboratory of Virology, Department of Virology, Immunology and Parasitology, Faculty of Veterinary Medicine, Ghent University , Salisburylaan 133, B-9820 Merelbeke, Ghent , Belgium 1 National Veterinary Institute, Technical University of Denmark , Frederiksberg C , Denmark In this study, the pathogenic behavior of PRRSV 13V091 and 13V117, isolated in 2013 from two different Belgian farms with enzootic respiratory problems shortly after weaning in the nursery, were compared with the Belgian strain 07V063 isolated in 2007. Full-length genome sequencing was performed to identify their origin. Twelve weeks-old pigs were inoculated intranasally (IN) with 13V091, 13V117 or 07V063 (9 pigs/group). At 10 days post inoculation (dpi), 4 animals from each group were euthanized and tissues were collected for pathology, virological and serological analysis. 13V091 infection resulted in the highest respiratory disease scores and longest period of fever. Gross lung lesions were more pronounced for 13V091 (13%), than for 13V117 (7%) and 07V063 (11%). The nasal shedding and viremia was also most extensive with 13V091. The 13V091 group showed the highest virus replication in conchae, tonsils and retropharyngeal lymph nodes. 13V117 infection resulted in the lowest virus replication in lymphoid tissues. 13V091 showed higher numbers of sialoadhesin infected cells/mm2 in conchae, tonsils and spleen than 13V117 and 07V063. Neutralizing antibody response with 07V063 was stronger than with 13V091 and 13V117. It can be concluded that (i) 13V091 is a highly pathogenic type 1 subtype 1 PRRSV strain that replicates better than 07V063 and 13V117 and has a strong tropism for sialoadhesin cells and (ii) despite the close genetic relationship between 13V117 and 07V063, 13V117 has an increased nasal replication and shedding, but a decreased replication in lymphoid tissues compared to 07V063. - Introduction Porcine reproductive and respiratory syndrome (PRRS) is a devastating disease that continuously hits swine industry all over the world [1]. A recent economic analysis in the US demonstrated that the amount of total annual losses increased from $560 million in 2005 to $664 million in 2011 [2]. The disease first appeared in the US in the late eighties and then a few years later in Europe and Asia [3]. The causative agent is a positive singlestranded enveloped RNA virus classified together with lactate dehydrogenase virus (LDV), simian hemorrhagic fever virus (SDHF) and equine arteritis virus (EAV) in the family of the Arteriviridae within the order of the Nidovirales [4]. PRRSV causes reproductive failure in late-term gestation sows with an increased number of stillborn, mummified and weak-born piglets. Respiratory disorders are characterized mainly by dyspnea and tachypnea in young animals [5,6]. The PRRSV genome is approximately 15 kb in length and contains nine open reading frames (ORFs) [3]. Open reading frames 1a and 1b constitute 75% of the viral genome and encode viral replicase polyproteins, which are processed by self-encoded proteases into 14 nonstructural proteins (nsp) [3]. Major (GP5, M, N) and minor (GP2, GP3, GP4, ORF5a-protein, E) structural proteins are being encoded at the 3 end of the genome by ORFs 2a, 2b, 3, 4, 5, 5a, 6 and 7 [7]. Like with other nidoviruses, transcription of the PRRSV genome is characterized by the formation of a 3-co-terminal nested set of subgenomic messenger RNAs, each of them with a common 5-leader sequence [8]. Two distinct genotypes were identified, and designated as European type 1 (prototype LV-Lelystad, GenBank: M96262) and American type 2 (prototype VR2332, GenBank: AY150564), with 40% differences at the nucleotide level [7]. A large genetic variability has been shown within both subtypes [9]. Genetic heterogeneity is one of the main reasons why current commercial attenuated and inactivated vaccines provide incomplete protection against heterologous strains and as a result there is an urgent need for a novel generation of vaccines [10,11]. Starting from 2006, new highly pathogenic strains emerged, causing large-scale outbreaks in Eastern Europe (type 1, prototype Lena, GenBank: JF802085), and Southeastern Asia (type 2, prototype JXA1, GenBank: EF112445). These isolates are characterized by high viral loads in blood and tissues, high fever, severe general clinical signs and increased mortality [12-14]. A common genetic characteristic of highly pathogenic strains of both PRRSV type 1 and 2 is a discontinuous 30-amino acid deletion in the nonstructural protein 2 (nsp2) (Lena: aa 710739, JXA1: aa 534563) [13,14]. However, this deletion is m (...truncated)


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Ilias S Frydas, Ivan Trus, Lise K Kvisgaard, Caroline Bonckaert, Vishwanatha RAP Reddy, Yewei Li, Lars E Larsen, Hans J Nauwynck. Different clinical, virological, serological and tissue tropism outcomes of two new and one old Belgian type 1 subtype 1 porcine reproductive and respiratory virus (PRRSV) isolates, Veterinary Research, 2015, pp. 37, 46, DOI: 10.1186/s13567-015-0166-3