Comparison of the antibody response to transmissible gastroenteritis virus and porcine respiratory coronavirus, using monoclonal antibodies to antigenic sites A and X of the S glycoprotein

A. P. van Nieuwstadt From the Central Veterinary Institute, PO Box 365, 8200 AJ Lelystad, The Netherlands.

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J. Boonstra From the Central Veterinary Institute, PO Box 365, 8200 AJ Lelystad, The Netherlands.

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Summary

Pigs were inoculated with various strains of transmissible gastroenteritis virus (tgev) or with porcine respiratory coronavirus (prcv), and antigenic site-specific antibody responses were compared.

A blocking-elisa was used to study to what extent antibodies in convalescent sera interfered with the binding of monoclonal antibodies (mab)57.16 or 57.110 to the attenuated tgev/Purdue virus. Monoclonal antibody 57.16 is directed against the A site on the peplomer, neutralizes virus, and recognizes tgev and prcv. Monoclonal antibody 57.110 is directed against the X site on the peplomer, but does not neutralize virus, and recognizes only tgev. Antibodies directed against tgev and prcv could be detected in a blocking elisa, using mab 57.16 as a conjugate. Antibodies directed against both viruses were detectable as early as 1 week after inoculation. Antibody titers correlated well with those in a virus-neutralization test. Antibodies against tgev could be detected in a blocking elisa, using mab 57.110 as a conjugate. Such antibodies were not induced by a prcv infection. In the blocking elisa, using mab 57.110 as a conjugate, antibodies were detectable as early as 2 weeks after inoculation. There was a significant difference between antibody titers reached after infection with various tgev strains, however. This difference is ascribed to a variation of the antigenic site defined by mab 57.110 in tgev strains.

Conditions for a differential test for TGE serodiagnosis, and for serologic discrimination between tgev- and prcv- infected pigs, are discussed. It is concluded that by using a blocking elisa with mab 57.110, no definite distinction can be made between antibodies directed against tgev and prcv, because low antibody titers develop after infection with some tgev strains, and because antibodies directed against antigenic sites that prcv has in common with tgev may interfere with the binding of mab 57.110 to tgev.

Summary

Pigs were inoculated with various strains of transmissible gastroenteritis virus (tgev) or with porcine respiratory coronavirus (prcv), and antigenic site-specific antibody responses were compared.

A blocking-elisa was used to study to what extent antibodies in convalescent sera interfered with the binding of monoclonal antibodies (mab)57.16 or 57.110 to the attenuated tgev/Purdue virus. Monoclonal antibody 57.16 is directed against the A site on the peplomer, neutralizes virus, and recognizes tgev and prcv. Monoclonal antibody 57.110 is directed against the X site on the peplomer, but does not neutralize virus, and recognizes only tgev. Antibodies directed against tgev and prcv could be detected in a blocking elisa, using mab 57.16 as a conjugate. Antibodies directed against both viruses were detectable as early as 1 week after inoculation. Antibody titers correlated well with those in a virus-neutralization test. Antibodies against tgev could be detected in a blocking elisa, using mab 57.110 as a conjugate. Such antibodies were not induced by a prcv infection. In the blocking elisa, using mab 57.110 as a conjugate, antibodies were detectable as early as 2 weeks after inoculation. There was a significant difference between antibody titers reached after infection with various tgev strains, however. This difference is ascribed to a variation of the antigenic site defined by mab 57.110 in tgev strains.

Conditions for a differential test for TGE serodiagnosis, and for serologic discrimination between tgev- and prcv- infected pigs, are discussed. It is concluded that by using a blocking elisa with mab 57.110, no definite distinction can be made between antibodies directed against tgev and prcv, because low antibody titers develop after infection with some tgev strains, and because antibodies directed against antigenic sites that prcv has in common with tgev may interfere with the binding of mab 57.110 to tgev.

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