title: Species-specific but not genotype-specific primary and secondary isotype-specific NSP4 antibody responses in gnotobiotic calves and piglets infected with homologous host bovine (NSP4[A]) or porcine (NSP4[B]) rotavirus.
abstract: Using recombinant baculoviruses expressing rotavirus NSP4 [A], [B], [C], and [D] genotypes of bovine, porcine, human, simian, or murine origin, we analyzed serum antibody responses to NSP4s in gnotobiotic calves and piglets infected by the oral/alimentary or intraamniotic route with bovine (NSP4[A]) (Wyatt, R.G., Mebus, C.A., Yolken, R.H., Kalica, A.R., James, H.D., Jr., Kapikian, A.Z., Chanock, R.M., 1979. Rotaviral immunity in gnotobiotic calves: heterologous resistance to human virus induced by bovine virus. Science 203(4380), 548-550) or porcine (NSP4[B]) (Hoshino, Y., Saif, L.J., Sereno, M.M., Chanock, R.M., Kapikian, A.Z., 1988. Infection immunity of piglets to either VP3 or VP7 outer capsid protein confers resistance to challenge with a virulent rotavirus bearing the corresponding antigen. J. Virol. 62(3), 744-748) rotaviruses. Following primary infection and challenge with virulent rotaviruses, the animals developed higher or significantly higher antibody titers to homologous host homotypic NSP4s than to heterologous host homotypic or heterologous host heterotypic NSP4s, indicating that antibody responses were species specific rather than genotype specific. Antibody responses to NSP4s corresponded closely with the phylogenetic relationships of NSP4s within a species-specific region of amino acids (aa) 131-141. In contrast, NSP4 genotypes determined by amino acid full-length sequence identity predicted poorly their "serotypes". In piglets, antibodies to NSP4 induced by previous oral infection failed to confer protection against challenge from a porcine rotavirus bearing serotypically different VP4 and VP7 but essentially identical NSP4 to the porcine rotavirus in primary infection. Thus, in an approach to immunization with a live oral rotavirus vaccine, the NSP4 protein does not appear to play an important role in protection against rotavirus disease and infection.
authors.affiliation: Epidemiology Section, Laboratory of Infectious Disease, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
authors.forename: Lijuan
authors.initials: L
authors.lastname: Yuan
authors.forename: Shinjiro
authors.initials: S
authors.lastname: Honma
authors.forename: Shin-Ichi
authors.initials: S
authors.lastname: Ishida
authors.forename: Xiao-Yi
authors.initials: XY
authors.lastname: Yan
authors.forename: Albert Z
authors.initials: AZ
authors.lastname: Kapikian
authors.forename: Yasutaka
authors.initials: Y
authors.lastname: Hoshino
mesh_terms: D000595:Amino Acid Sequence; D000818:Animals; D000917:Antibody Formation; D002417:Cattle; D017124:Conserved Sequence; D006023:Glycoproteins / Q000235:genetics*; D006801:Humans; D008969:Molecular Sequence Data; D012401:Rotavirus / Q000235:genetics*; D012400:Rotavirus Infections / Q000235:genetics* / Q000276:immunology*; D016415:Sequence Alignment; D017386:Sequence Homology, Amino Acid; D013552:Swine; D014118:Toxins, Biological; D017361:Viral Nonstructural Proteins / Q000235:genetics*
chemical_list: D006023:Glycoproteins; C081369:NS28 protein, rotavirus; D014118:Toxins, Biological; D017361:Viral Nonstructural Proteins