Editorial: Porcine reproductive and respiratory syndrome virus - animal virology, immunology, and pathogenesis

Abstract

Editorial on the Research TopicPorcine reproductive and respiratory syndrome virus -animal virology, immunology, and pathogenesis Porcine reproductive and respiratory syndrome (PRRS) is one of the most important pig diseases causing huge economic losses worldwide. The causative agent, PRRS virus (PRRSV), is an enveloped, single-stranded, positive-sense RNA virus which is classified into the genus Betaarterivirus, subfamily Variarterivirinae, family Arteriviridae along with equine arteritis virus (EAV), lactate dehydrogenase-elevating virus of mice (LDV), and simian hemorrhagic fever virus (SHFV). Its genome is about 15 kb in length and contains at least 11 open reading frames (ORFs) with 5´cap and 3´polyadenylated tail (1-3). The nonstructural proteins (nsp1-12), owning the functions of protease, replicase and regulation of host cell gene expression and responsible for the synthesis of viral RNA, are encoded by ORF1a and ORF1b which occupy approximately two-thirds of the genome (4). The structural proteins including glycoprotein 2 (GP2), GP3, GP4, GP5, envelope protein (E), matrix protein (M), and nucleocapsid protein (N), expressed by a series of subgenomic RNAs, are encoded by ORFs 2-7 at the 3´terminus of the genome (5). Due to the lack of proofreading ability of PRRSV RNA-dependent RNA polymerase (RdRp), the viral genome is highly susceptible to mutation and recombination, which causes the emergence of novel PRRSV isolates worldwide (6). At present, PRRSV can be divided into two species: PRRSV-1 (European genotype, Betaarterivirus suid 1) and PRRSV-2 (North American genotype; Betaarterivirus suid 2). Both species show high genetic diversity and share approximately 60% nucleotide sequence identity, and each one can be further divided into several clades, substrains or lineages. In China, the dominant strains are PRRSV-2 and the outbreaks of highly pathogenic variants lead to concerns in the pig industry (7). PRRSV infection causes severe reproductive failure in sows and respiratory disease in pigs of all ages, which often leads to secondary bacterial infections (such as Haemophilus parasuis and Streptococcus suis) with greater clinical manifestations and higher mortality (8).

Pathogenicity of genotype 2.1 classical swine fever virus isolated from Japan in 2019 in pigs

“…This suggests that approximately 70% of the pigs with acquired immunity recuperated from the infection, albeit after experiencing some discomfort (Table 2) and viral excretion. However, secondary infections such as chronic porcine circovirus infection or porcine reproductive and respiratory syndrome virus infection that may exacerbate the condition owing to immunosuppressive effects in pigs 44,45 may also be considered, making some cases appear more virulent in the field. Additionally, regarding the week-age on the virus challenge, CS peaked at the same time for the virus challenge in 10-week-old pigs (#4, 5 and 6) and the challenge at 7-week-old pigs (#9 and 10) but decreased thereafter and was earlier in the 10-weekold group (data not shown).…”

Synthetic Peptides Elicit Humoral Response against Porcine Reproductive and Respiratory Syndrome Virus in Swine

“…The translated polypeptides pp1a and pp1ab (encoded in ORF1a and ORF 1b) are cleaved into 15 Non-Structural Proteins (NSPs), including NSP1α, NSP1β, NSP2-related proteins (NSP2N, NSP2TF, and NSP2), and NSP3–NSP12, which are involved in viral replication [ 13 ]. ORF2a, ORF2b, ORF3, ORF4, ORF5, and ORF5a encode six structural envelope-related proteins, namely, GP2a, GP2b, GP3, GP4, GP5, and GP5a, respectively [ 14 , 15 , 16 , 17 ]. Structural proteins are glycoproteins (GPs) embedded on the lipid envelope, forming protein complexes that provide stability to the viral particle and participate in the recognition and internalization of the virus to its target cell [ 15 , 18 ].…”

“…Moreover, GP5 is highly immunogenic, making it significant in the diagnosis, prevention, and control of PRRSV [ 16 , 34 , 35 , 36 , 37 , 38 , 39 ]. Effective anti-PRRSV immunity may be attained by exposing immunogenic epitopes to induce efficient innate and adaptive immune responses mediated by specific antibodies, cytokines, and T-cell responses [ 17 , 40 ]. Compared to commercial vaccines, peptide vaccines do not contain nucleic acid substances; therefore, they are considered safer [ 41 ].…”