Subgrouping of respiratory syncytial virus strains from Australia and Papua New Guinea by biological and antigenic characteristics.
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.
Hierholzer
J C
JC
Respiratory and Enteric Viruses Branch, CDC, Altanta, Georgia.
Tannock
G A
GA
Hierholzer
C M
CM
Coombs
R A
RA
Kennett
M L
ML
Phillips
P A
PA
Gust
I D
ID
D000956:Antigens, Viral / Q000276:immunology*; D001315:Australia / Q000453:epidemiology; D002478:Cells, Cultured; D002675:Child, Preschool; D014644:Genetic Variation; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D010219:Papua New Guinea / Q000453:epidemiology; D018357:Respiratory Syncytial Virus Infections / Q000453:epidemiology / Q000382:microbiology*; D018113:Respiratory Syncytial Virus, Human / Q000145:classification* / Q000276:immunology / Q000502:physiology; D012703:Serotyping; D014779:Virus Replication
D000956:Antigens, Viral