Subgrouping of respiratory syncytial virus strains from Australia and Papua New Guinea by biological and antigenic characteristics

• Published in: Archives of virology Vol. 136; no. 1-2; pp. 133 - 147
• Main Authors: HIERHOLZER, J. C, TANNOCK, G. A, HIERHOLZER, C. M, COOMBS, R. A, KENNETT, M. L, PHILLIPS, P. A, GUST, I. D
• Format: Journal Article
• Language: English
• Published: Wien Springer 01-03-1994; New York, NY
• Subjects: Antigens, Viral - immunology; Australia - epidemiology; Biological and medical sciences; Cells, Cultured; Child, Preschool; Epidemiology; Fundamental and applied biological sciences. Psychology; Genetic Variation; Humans; Infant; Infant, Newborn; Microbiology; Papua New Guinea - epidemiology; Respiratory Syncytial Virus Infections - epidemiology; Respiratory Syncytial Virus Infections - microbiology; Respiratory Syncytial Virus, Human - classification; Respiratory Syncytial Virus, Human - immunology; Respiratory Syncytial Virus, Human - physiology; Serotyping; Virology; Virus Replication; Papua New Guinea; Australia; Melanesia; Oceania; Human; Typing; Respiratory disease; Infant; Strain specificity; Paramyxoviridae; Infection; Virus; Respiratory syncytial virus; Antigenicity; Antigenic variation; Viral disease; Molecular epidemiology; Pneumovirus; Child; Clinical isolate
• ISSN: 0304-8608; 1432-8798
• DOI: 10.1007/bf01538823

Strains of respiratory syncytial virus from 3 major areas of Australia and Papua New Guinea (PNG) were analyzed for variations in their antigenic and biological properties and in the molecular weights of their major structural proteins. Seventy-eight strains from infants and young children with LRI were collected from 1981-1984. The RSV season in the Australian cities lasted from April through September, with major peaks in July of each year, while the RSV season in tropical PNG was year-round, with small peaks in March and October of each year coinciding with excessive rainfall. Fifty-six strains were analyzed in detail; 40 were typed by time-resolved fluoroimmunoassay with monoclonal antibodies as group A strains and 16 were group B; both groups were concurrent. Three children of one family had sequential RSV infections 13 months apart, and the etiologic group A strain was identical both years in terms of growth and antigenic properties with strain-specific ferret antisera; the second infection was milder in all three children. On average, the group A strains replicated considerably better than group B strains in HEp2 cells, producing 53% more syncytia and 99% higher infectious virus titers in 31% less time in culture. Ten group A and B reference strains exhibited the same growth patterns as the A and B regional strains, respectively. Differences in antigenicity as measured with hyperimmune antisera to prototype Long strain were even greater. Group A strains exhibited a mean 68% greater IFA staining than B strains, a 71% greater EIA reaction, and were neutralized to 69% higher serum titers than B strains. Again, the reference A and B strains included as controls gave patterns identical to those of the regional strains. Finally, the P phosphoprotein had consistently higher molecular weight in A strains (mean 35,900) than B strains (mean 33,100). Small variations in the sizes of the F and G glycoproteins were not sufficient to suggest grouping on this basis.