Public health measures have successfully identified and contained outbreaks of the severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV), but concerns remain over the possibility of future recurrences. Finding a vaccine for this virus therefore remains a high priority. Here, we show that a DNA vaccine encoding the spike (S) glycoprotein of the SARS-CoV induces T cell and neutralizing antibody responses, as well as protective immunity, in a mouse model. Alternative forms of S were analysed by DNA immunization. These expression vectors induced robust immune responses mediated by CD4 and CD8 cells, as well as significant antibody titres, measured by enzyme-linked immunosorbent assay. Moreover, antibody responses in mice vaccinated with an expression vector encoding a form of S that includes its transmembrane domain elicited neutralizing antibodies. Viral replication was reduced by more than six orders of magnitude in the lungs of mice vaccinated with these S plasmid DNA expression vectors, and protection was mediated by a humoral but not a T-cell-dependent immune mechanism. Gene-based vaccination for the SARS-CoV elicits effective immune responses that generate protective immunity in an animal model.

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A DNA vaccine induces SARS coronavirus neutralization and protective immunity in mice

Manual of Standards for Diagnostic Tests and Vaccines

During the 10 days commencing April 29, 2013, the Iowa State University Veterinary Diagnostic Laboratory received the first 4 of many submissions from swine farms experiencing explosive epidemics of diarrhea and vomiting affecting all ages, with 90-95% mortality in suckling pigs. Histology revealed severe atrophy of villi in all segments of the small intestines with occasional villus-epithelial syncytial cells, but testing for rotaviruses and Transmissible gastroenteritis virus (Alphacoronavirus 1) were negative. Negative-staining electron microscopy of feces revealed coronavirus-like particles and a pan-coronavirus polymerase chain reaction (PCR) designed to amplify a conserved region of the polymerase gene for all members in the family Coronaviridae produced expected 251-bp amplicons. Subsequent sequencing and analysis revealed 99.6-100% identity among the PCR amplicons from the 4 farms and 97-99% identity to the corresponding portion of the polymerase gene of Porcine epidemic diarrhea virus (PEDV) strains, with the highest identity (99%) to strains from China in 2012. Findings were corroborated at National Veterinary Services Laboratories using 2 nested S-gene and 1 nested N-gene PCR tests where the sequenced amplicons also had the highest identity with 2012 China strains. Whole genome sequence for the virus from 2 farms in 2 different states using next-generation sequencing technique was compared to PEDV sequences available in GenBank. The 2013 U.S. PEDV had 96.6-99.5% identity with all known PEDV strains and the highest identity (>99.0%) to some of the 2011-2012 Chinese strains. The nearly simultaneous outbreaks of disease, and high degree of homology (99.6-100%) between the PEDV strains from the 4 unrelated farms, suggests a common source of virus.

https://journals.sagepub.com/doi/pdf/10.1177/1040638713501675

Emergence of Porcine epidemic diarrhea virus in the United States: clinical signs, lesions, and viral genomic sequences.

This review is focused on the acute form of infectious bursal disease (IBD) caused by very virulent IBD virus (vvIBDV). First described in Europe about 10 years ago, this new form of the disease has rapidly spread all over the world, causing dramatic losses; after a decade, it still represents a considerable threat to the poultry industry. Emergence of the acute forms of the disease has drastically changed the epidemiology of IBD. Although their origin is still under investigation, vvIBDVs have spread all over the world in a very explosive but conserved manner. This raises the question of the origin of vvIBDVs, of the possible existence of reservoirs and of the possible emergence of new, distinct lineages in the future. While it has become clear that amino acids within the variable region of virus protein VP2 account for the molecular basis of antigenic variation, no definite hot spot that determines pathogenicity has been identified. Fingerprints of VP2 on vvIBDVs have to be considered more as common evo...

https://www.tandfonline.com/doi/pdf/10.1080/03079450050045431

Acute infectious bursal disease in poultry: A review

Infectious bursal disease (IBD), caused by an avibirnavirus, has been an economically significant, widely distributed condition affecting immature chickens since 1960. The classical type 1 conventi...

Infectious bursal disease.

Two serotypes of infectious bursal disease virus (IBDV) were distinguished using the virus-neutralization test. An IBDV isolate from chickens, two commercial IBDV vaccine viruses, and an IBDV isolate from turkeys were designated serotype I. Two IBDV isolates from turkeys were designated serotype II. A common antigen shared by serotype I and serotype II viruses was detected using an indirect immunofluorescent assay. The virions of both IBDV serotypes were determined to be nonenveloped icosahedrons with diameters ranging from 58 to 60 nm. The virion densities of one serotype I isolate and two serotype II isolates were similar (1.32 g/ml). Twenty-three turkey breeder flocks and 22 commercial turkey flocks from Ohio, North Carolina, and Indiana were tested for antibodies to the two IBDV serotypes. Seventy percent of the 23 breeder flocks had antibody titers to serotype I, and 75% had antibody titers to serotype II. None of the 22 commercial flocks had antibodies to serotype I, and 77% had antibody titers to serotype II. Antibodies to serotype I were detected only in breeder flocks that were vaccinated using a commercial serotype I IBDV vaccine. Only antibodies to serotype II viruses were naturally widespread in the flocks tested.

Characteristics and Serologic Studies of Two Serotypes of Infectious Bursal Disease Virus in Turkeys

The nucleotide sequence of genome segment A cDNA of the STC strain of infectious bursal disease virus (IBDV) was determined and compared with sequences of the homologous genome segment of the 002-73 strain of IBDV and the Jasper strain of infectious pancreatic necrosis virus (IPNV). The STC-IBDV genome segment A was determined to be 3262 base pairs (bp), which is close to the estimated total length of 3300 bp for genome segment A in IBDV, although there is no proof that it is the real length of this genome segment. The STC-IBDV genome segment A contains two major overlapping open reading frames (ORFs). The large ORF of 3036 bp predicts a polyprotein of Mr 109,358, whereas the small ORF is 435 bp and predicts a protein of Mr 16,550 in STC-IBDV. STC-IBDV and 002-73-IBDV polyproteins are closely related (97.4% amino acid homology). Most of the amino acid mismatches are in VP2 sequences, mainly within the area of the conformation-dependent epitope. Comparison with the Jasper-IPNV polyprotein reveals levels of amino acid sequence homology of about 40% in VP2, 32% in VP3 and 21% in VP4. Within the VP2 molecule the conformation-dependent epitope area is again the least homologous, but the heterogeneity is more conspicuous than between the two IBDV strains, which is not surprising since IBDV and IPNV are serologically unrelated. The small ORF proteins have about 88% amino acid sequence homology between STC-IBDV and 002-73-IBDV, and 30% between each IBDV strain and Jasper-IPNV. There is no homology at all in the non-coding regions of IBDV and IPNV. These comparative sequence data will be useful for subgrouping the Birnaviridae family.

Nucleotide sequence analysis of genome segment A of infectious bursal disease virus.

Studies on naturally occurring infectious bursal disease viruses suggest that a single amino acid substitution at position 253 in VP2 increases pathogenicity.

Genetic characteristics of infectious bursal disease viruses from four continents.

Infectious bursal disease virus (IBDV) causes infectious bursal disease (IBD), an immunosuppressive disease of poultry. The current classification scheme of IBDV is confusing because it is based on antigenic types (variant and classical) as well as pathotypes. Many of the amino acid changes differentiating these various classifications are found in a hypervariable region of the capsid protein VP2 (hvVP2), the major host protective antigen. Data from this study were used to propose a new classification scheme for IBDV based solely on genogroups identified from phylogenetic analysis of the hvVP2 of strains worldwide. Seven major genogroups were identified, some of which are geographically restricted and others that have global dispersion, such as genogroup 1. Genogroup 2 viruses are predominately distributed in North America, while genogroup 3 viruses are most often identified on other continents. Additionally, we have identified a population of genogroup 3 vvIBDV isolates that have an amino acid change from alanine to threonine at position 222 while maintaining other residues conserved in this genogroup (I242, I256 and I294). A222T is an important mutation because amino acid 222 is located in the first of four surface loops of hvVP2. A similar shift from proline to threonine at 222 is believed to play a role in the significant antigenic change of the genogroup 2 IBDV strains, suggesting that antigenic drift may be occurring in genogroup 3, possibly in response to antigenic pressure from vaccination.

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Daral J. Jackwood

Papers

Characteristics and Serologic Studies of Two Serotypes of Infectious Bursal Disease Virus in Turkeys

Nucleotide sequence analysis of genome segment A of infectious bursal disease virus.

Studies on naturally occurring infectious bursal disease viruses suggest that a single amino acid substitution at position 253 in VP2 increases pathogenicity.

Genetic characteristics of infectious bursal disease viruses from four continents.

Classification of infectious bursal disease virus into genogroups