Deletion in the S1 Region of Porcine Epidemic Diarrhea Virus Reduces the Virulence and Influences the Virus-Neutralizing Activity of the Antibody Induced

Abstract

Porcine epidemic diarrhea virus (PEDV) causes severe diarrhea and a high rate of mortality in suckling pigs. The epidemic of PEDV that occurred after 2013 was caused by non-insertion and deletion of S gene (S-INDEL) PEDV strains. During this epidemic, a variant of the non-S-INDEL PEDV strain with a large deletion of 205 amino acids on the spike gene (5-17-V) was also found to co-exist with a non-S-INDEL PEDV without deletion (5-17-O). Herein, we describe the differences in the complete genome, distribution, virulence, and antigenicity between strain 5-17-O and variant strain 5-17-V. The deletion of 205 amino acids was primarily located in the S1O domain and was associated with milder clinical signs and lower mortality in suckling pigs than those of the 5-17-O strain. The 5-17-V strain-induced antibody did not completely cross-neutralize the 5-17-O strain. In conclusion, the deletion in the S1 region reduces the virulence of PEDV and influences the virus-neutralizing activities of the antibody it induces.

Antibody Evaluation and Mutations of Antigenic Epitopes in the Spike Protein of the Porcine Epidemic Diarrhea Virus from Pig Farms with Repeated Intentional Exposure (Feedback)

“…The lactogenic immunity to protect neonatal suckling piglets via colostrum and milk is critical in the prevention and control of PEDV infection [ 26 ]. Several studies support that exposure to infected PEDV tissues can induce a significant increase in specific IgA and IgG levels [ 17 , 18 , 19 ]. Our data from the SL farm are consistent with these reports.…”

“…Phylogenetic analysis categorized the five PEDV strains identified from the SL farm into two groups, showing that two variants coexist in the pig population. The coexistence of different PEDV variants within pig herds or even individual pigs with high frequency has been reported [ 18 , 39 ]. The repeated feedback practices implemented in the SL farm might promote the emergence of new PEDV variants.…”

“…The neutralizing antibody titers of PEDV in sera and colostra were evaluated following a previous study [ 18 ], with some modifications. The sera and milk of the sows were diluted in two-fold serial dilution in serum-free DMEM medium before mixing with an equal volume of 200 TCID 50 PEDV and incubated for 1 h at 37 °C, then transferred to 96-well plates containing confluent Vero cell monolayers.…”

Porcine epidemic diarrhea virus: an update overview of virus epidemiology, vaccines, and control strategies in South Korea

“…As with other CoV S proteins, the PEDV S glycoprotein (consisting of S1 and S2 subunits) plays pivotal roles in infection by interacting with the cellular receptor to mediate viral entry and by inducing neutralizing antibodies [ 5 6 ]. Genetic mutations, including insertions (IN) and deletions (DEL), and recombination in the S gene can drive alterations in viral pathogenicity and tissue or species tropism [ 33 34 35 36 37 38 39 40 ]. Considering the phenotypic and genotypic traits, the S gene is a suitable locus for sequencing to investigate the genetic relatedness (i.e., genotyping) and molecular epidemiology of PEDV [ 23 27 41 42 43 44 45 46 47 ].…”

Porcine Epidemic Diarrhea: Insights and Progress on Vaccines

“…The evolution of PEDV has been complex and rapid, with potential recombination events occurring between the G1a and G2 lineages and leading to new lineages such as S-INDEL (G1b) and the newly identified G2c [ 10 , 27 , 28 , 29 ]. Changes in the S gene through mutation and recombination can alter the pathogenicity of the virus and its ability to infect different tissues or species [ 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 ]. The S protein is also vital for infection, as it induces the production of neutralizing antibodies and is a key target for vaccine development, both for live attenuated and subunit vaccines [ 22 ].…”