Characterization of the stunting syndrome agent: Relatedness to known viruses

Research output: Contribution to journalArticle

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Abstract

An enteric disease of young turkeys, referred to as stunting syndrome (SS), causes reduced growth and impaired feed efficiency. A recently isolated virus, stunting syndrome agent, (SSA) has been found to be the etiologic agent of SS. The objective of the present study was to determine relatedness of the SSA with other viral agents. Serologic (viral neutralization and enzyme-linked immunosorbent assay [ELISA]) assays and a reverse transcriptase-polymerase chain reaction (RT-PCR) were used. The antisera against turkey enteric coronavirus (bluecomb agent), bovine coronavirus (BCV), bovine Breda-1 virus, bovine Breda-2 virus, avian infectious bronchitis virus (IBV), avian influenza virus, Newcastle disease virus (NDV), and transmissible gastroenteritis virus (TGEV) of swine were evaluated by dot-immunobinding avidin-biotin-enhanced ELISA and did not react with SSA. The homologous (anti-SSA) antiserum was positive by ELISA. Similarly, anti-SSA antiserum did not react when NDV, IBV, BCV, or TGEV was used as antigen but did react with the homologous (SSA) virus. The virus neutralization assay was performed by inoculating 24-to-25-day-old turkey embryos via the amniotic route and by assessing the embryo infectivity on the basis of gross intestinal lesions and intestinal maltase activity at 72 hr postinoculation. None of the aforementioned antisera neutralized SSA infectivity in embryos except for the homologous anti-SSA antiserum. A RT-PCR was performed with known primers specific for NDV, IBV, BCV, and TGEV. The known primers failed to amplify SSA genome but amplified their respective viral genomes. We concluded that the SSA was distinct from the viral agents that were evaluated.

Original languageEnglish (US)
Pages (from-to)45-50
Number of pages6
JournalAvian diseases
Volume44
Issue number1
DOIs
StatePublished - Jan 1 2000

Fingerprint

Growth Disorders
growth retardation
Viruses
viruses
Bovine Coronavirus
Transmissible gastroenteritis virus
antiserum
Immune Sera
Infectious bronchitis virus
Bovine coronavirus
Newcastle disease virus
Torovirus
embryo (animal)
Embryonic Structures
Enzyme-Linked Immunosorbent Assay
enzyme-linked immunosorbent assay
neutralization tests
Reverse Transcriptase Polymerase Chain Reaction
Turkey Coronavirus
Turkey coronavirus

Keywords

  • ELISA
  • Enteric virus
  • RT-PCR
  • Serum virus neutralization
  • Stunting syndrome
  • Stunting syndrome agent
  • Turkey embryos

ASJC Scopus subject areas

  • Food Animals
  • Animal Science and Zoology
  • Immunology and Microbiology(all)

Cite this

Characterization of the stunting syndrome agent : Relatedness to known viruses. / Ali, A.; Reynolds, D. L.

In: Avian diseases, Vol. 44, No. 1, 01.01.2000, p. 45-50.

Research output: Contribution to journalArticle

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abstract = "An enteric disease of young turkeys, referred to as stunting syndrome (SS), causes reduced growth and impaired feed efficiency. A recently isolated virus, stunting syndrome agent, (SSA) has been found to be the etiologic agent of SS. The objective of the present study was to determine relatedness of the SSA with other viral agents. Serologic (viral neutralization and enzyme-linked immunosorbent assay [ELISA]) assays and a reverse transcriptase-polymerase chain reaction (RT-PCR) were used. The antisera against turkey enteric coronavirus (bluecomb agent), bovine coronavirus (BCV), bovine Breda-1 virus, bovine Breda-2 virus, avian infectious bronchitis virus (IBV), avian influenza virus, Newcastle disease virus (NDV), and transmissible gastroenteritis virus (TGEV) of swine were evaluated by dot-immunobinding avidin-biotin-enhanced ELISA and did not react with SSA. The homologous (anti-SSA) antiserum was positive by ELISA. Similarly, anti-SSA antiserum did not react when NDV, IBV, BCV, or TGEV was used as antigen but did react with the homologous (SSA) virus. The virus neutralization assay was performed by inoculating 24-to-25-day-old turkey embryos via the amniotic route and by assessing the embryo infectivity on the basis of gross intestinal lesions and intestinal maltase activity at 72 hr postinoculation. None of the aforementioned antisera neutralized SSA infectivity in embryos except for the homologous anti-SSA antiserum. A RT-PCR was performed with known primers specific for NDV, IBV, BCV, and TGEV. The known primers failed to amplify SSA genome but amplified their respective viral genomes. We concluded that the SSA was distinct from the viral agents that were evaluated.",
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