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2003 JUL 2 - (NewsRx.com & NewsRx.net) -- The immune responses to the nonglycosylated ectodomain of respiratory syncytial virus attachment glycoprotein mediated pulmonary eosinophilia in inbred strains of mice with different MHC haplotypes.
According to recent research published in the Journal of Medical Virology, "Development of subunit vaccines against respiratory syncytial virus (RSV) for naive human infants is hindered by concerns that immunization with the fusion or attachment (G) proteins will elicit polarized Type 2 T cell responses and cause immunopotentiation upon subsequent natural infection. We investigated the regions of G protein responsible for inducing a Type 2 T cell phenotype in inbred mice of different MHC haplotype toward development of vaccines with improved safety."
"As demonstrated by IL-5-dependent pulmonary eosinophilia after challenge and serum anti-G protein IgG1 to IgG2 ratios, highly purified native G protein sensitized all strains for a Type 2T cell phenotype," reported Gerald E. Hancock and colleagues at Wyeth Vaccines. "Stimulation of G protein-primed splenocytes with synthetic overlapping peptides indicated that the nonglycosylated ectodomain was primarily responsible."
"Respectively the recall responses of BALB/c (H2[superscript]d), C57BL/6 (H-2[superscript]b), SJL (H-2[superscript]s), and C3H/HeJ (H-2[superscript]k) mice were directed against epitopes within peptides spanning amino acids 184-198 (pep[subscript]184-198), 168-181 (pep[subscript]168-181) or 171-185 (pep[subscript]171-185), 176-190 (pep[subscript]176-190), and 104-118 (pep[subscript]104-118) or 159-173 ...
Source: HighBeam Research, RSV attachment glycoprotein mediates pulmonary eosinophilia.