Jason Sousa, Jenny Nicholds, Erich Linnemann, Robin Gilbert, Tiffani Allen, Cole Taylor, Holly S Sellers
{"title":"灭活鸡星状病毒接种白鸡综合征雏鸡的抗体应答。","authors":"Jason Sousa, Jenny Nicholds, Erich Linnemann, Robin Gilbert, Tiffani Allen, Cole Taylor, Holly S Sellers","doi":"10.1637/aviandiseases-D-25-00036","DOIUrl":null,"url":null,"abstract":"<p><p>White chick syndrome (WCS), a vertically transmitted disease caused by chicken astrovirus (CAstV), causes decreased hatchability of broiler breeder progeny and increased hatch of weak, white chicks. In the absence of a commercial vaccine, control measures for WCS have included serological surveillance of pullets, then movement of litter from farms with confirmed CAstV seroconversion to farms with seronegative birds. However, litter movement carries the risk of introducing other pathogens to farms, such as <i>Salmonella</i>. CAstVs have been isolated from clinical cases of WCS and genetically characterized as chicken astrovirus, group Biv based on sequencing of the capsid protein. Autogenous vaccines (AVs) have included CAstVs, but no data exist to validate their ability to stimulate adequate immunity in breeders to prevent WCS. The objectives of this study were to 1) develop a CAstV Biv-inactivated oil emulsion vaccine using a CAstV isolate from a clinical case of WCS and 2) evaluate antibody production following injection into 3-wk-old specific-pathogen-free (SPF) leghorns. The CAstV isolate was propagated and titrated in leghorn male hepatoma cells, inactivated using beta-propriolactone, formulated into an oil emulsion with Montanide® ISA 70 VG adjuvant and then injected intramuscularly into 3-wk-old SPF leghorns. Birds received a second injection at approximately 9 wk of age. A negative control group received no vaccination at either time point. Serum was collected at 0, 2, 4, 8, 10, 12, and 14 wk post-initial vaccination (wpiv) for CAstV ELISA (BioChek®) and CAstV virus neutralization assay (VN). At 0, 2, and 4 wpiv no vaccinated birds had measurable antibody levels via enzyme-linked immunosorbent assay (ELISA) and VN tests. At 8, 10, 12, and 14 wpiv CAstV-specific antibodies were not detected by ELISA in either group; however, seroconversion was observed by VN in CAstV-vaccinated birds. Serum samples collected from breeder flocks with progeny that were clinically affected with WCS had consistently high ELISA titers, but the VN titers, while positive, were more variable. Control of WCS with a CAstV AV may be an option for use in broiler breeders. Progeny studies to detect maternal antibody transfer after vaccination would be useful in confirming this assertion. Based on this study, VN serology using a genetically similar CAstV as antigen is the preferred method of monitoring vaccinated flocks for seroconversion given the lack of antibody detection by ELISA. The ability to determine efficacy of any vaccine would rely solely on field observations as there is no established challenge model for WCS.</p>","PeriodicalId":516846,"journal":{"name":"Avian diseases","volume":"69 3","pages":"314-318"},"PeriodicalIF":1.3000,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Antibody Response in Pullets Vaccinated with Inactivated Chicken Astrovirus for White Chick Syndrome.\",\"authors\":\"Jason Sousa, Jenny Nicholds, Erich Linnemann, Robin Gilbert, Tiffani Allen, Cole Taylor, Holly S Sellers\",\"doi\":\"10.1637/aviandiseases-D-25-00036\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>White chick syndrome (WCS), a vertically transmitted disease caused by chicken astrovirus (CAstV), causes decreased hatchability of broiler breeder progeny and increased hatch of weak, white chicks. In the absence of a commercial vaccine, control measures for WCS have included serological surveillance of pullets, then movement of litter from farms with confirmed CAstV seroconversion to farms with seronegative birds. However, litter movement carries the risk of introducing other pathogens to farms, such as <i>Salmonella</i>. CAstVs have been isolated from clinical cases of WCS and genetically characterized as chicken astrovirus, group Biv based on sequencing of the capsid protein. Autogenous vaccines (AVs) have included CAstVs, but no data exist to validate their ability to stimulate adequate immunity in breeders to prevent WCS. The objectives of this study were to 1) develop a CAstV Biv-inactivated oil emulsion vaccine using a CAstV isolate from a clinical case of WCS and 2) evaluate antibody production following injection into 3-wk-old specific-pathogen-free (SPF) leghorns. The CAstV isolate was propagated and titrated in leghorn male hepatoma cells, inactivated using beta-propriolactone, formulated into an oil emulsion with Montanide® ISA 70 VG adjuvant and then injected intramuscularly into 3-wk-old SPF leghorns. Birds received a second injection at approximately 9 wk of age. A negative control group received no vaccination at either time point. Serum was collected at 0, 2, 4, 8, 10, 12, and 14 wk post-initial vaccination (wpiv) for CAstV ELISA (BioChek®) and CAstV virus neutralization assay (VN). At 0, 2, and 4 wpiv no vaccinated birds had measurable antibody levels via enzyme-linked immunosorbent assay (ELISA) and VN tests. At 8, 10, 12, and 14 wpiv CAstV-specific antibodies were not detected by ELISA in either group; however, seroconversion was observed by VN in CAstV-vaccinated birds. Serum samples collected from breeder flocks with progeny that were clinically affected with WCS had consistently high ELISA titers, but the VN titers, while positive, were more variable. Control of WCS with a CAstV AV may be an option for use in broiler breeders. Progeny studies to detect maternal antibody transfer after vaccination would be useful in confirming this assertion. Based on this study, VN serology using a genetically similar CAstV as antigen is the preferred method of monitoring vaccinated flocks for seroconversion given the lack of antibody detection by ELISA. The ability to determine efficacy of any vaccine would rely solely on field observations as there is no established challenge model for WCS.</p>\",\"PeriodicalId\":516846,\"journal\":{\"name\":\"Avian diseases\",\"volume\":\"69 3\",\"pages\":\"314-318\"},\"PeriodicalIF\":1.3000,\"publicationDate\":\"2025-09-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Avian diseases\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1637/aviandiseases-D-25-00036\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Avian diseases","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1637/aviandiseases-D-25-00036","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Antibody Response in Pullets Vaccinated with Inactivated Chicken Astrovirus for White Chick Syndrome.
White chick syndrome (WCS), a vertically transmitted disease caused by chicken astrovirus (CAstV), causes decreased hatchability of broiler breeder progeny and increased hatch of weak, white chicks. In the absence of a commercial vaccine, control measures for WCS have included serological surveillance of pullets, then movement of litter from farms with confirmed CAstV seroconversion to farms with seronegative birds. However, litter movement carries the risk of introducing other pathogens to farms, such as Salmonella. CAstVs have been isolated from clinical cases of WCS and genetically characterized as chicken astrovirus, group Biv based on sequencing of the capsid protein. Autogenous vaccines (AVs) have included CAstVs, but no data exist to validate their ability to stimulate adequate immunity in breeders to prevent WCS. The objectives of this study were to 1) develop a CAstV Biv-inactivated oil emulsion vaccine using a CAstV isolate from a clinical case of WCS and 2) evaluate antibody production following injection into 3-wk-old specific-pathogen-free (SPF) leghorns. The CAstV isolate was propagated and titrated in leghorn male hepatoma cells, inactivated using beta-propriolactone, formulated into an oil emulsion with Montanide® ISA 70 VG adjuvant and then injected intramuscularly into 3-wk-old SPF leghorns. Birds received a second injection at approximately 9 wk of age. A negative control group received no vaccination at either time point. Serum was collected at 0, 2, 4, 8, 10, 12, and 14 wk post-initial vaccination (wpiv) for CAstV ELISA (BioChek®) and CAstV virus neutralization assay (VN). At 0, 2, and 4 wpiv no vaccinated birds had measurable antibody levels via enzyme-linked immunosorbent assay (ELISA) and VN tests. At 8, 10, 12, and 14 wpiv CAstV-specific antibodies were not detected by ELISA in either group; however, seroconversion was observed by VN in CAstV-vaccinated birds. Serum samples collected from breeder flocks with progeny that were clinically affected with WCS had consistently high ELISA titers, but the VN titers, while positive, were more variable. Control of WCS with a CAstV AV may be an option for use in broiler breeders. Progeny studies to detect maternal antibody transfer after vaccination would be useful in confirming this assertion. Based on this study, VN serology using a genetically similar CAstV as antigen is the preferred method of monitoring vaccinated flocks for seroconversion given the lack of antibody detection by ELISA. The ability to determine efficacy of any vaccine would rely solely on field observations as there is no established challenge model for WCS.