BACKGROUND: Individuals are reinfected with respiratory syncytial virus (RSV) repeatedly. The nature of reinfection, in relation to RSV genetic and antigenic diversity, is ill defined and has implications for persistence and vaccine control. METHODS: We examined the molecular relatedness of RSV causing primary and repeat infections, by phylogenetic analysis of the attachment (G) gene in 12 infants from a birth cohort in rural Kenya, using nasal wash samples collected during a 16-month period in 2002-2003, which spanned 2 successive epidemics. RESULTS: Six infants were infected during both epidemics, 4 with RSV-A in the first epidemic followed by RSV-B during the second epidemic and 2 with RSV-A during both epidemics, with no significant G gene sequence variability between samples. Two infants were infected and reinfected with different RSV-A strains during the same epidemic. Possible viral persistence was suspected in the remaining 4 infants, although reinfection with the same variant cannot be excluded. CONCLUSIONS: These are the first data that specifically address strain-specific reinfections in infancy in relation to the primary infecting variant. The data strongly suggest that, following primary infection, some infants lose strain-specific immunity within 7-9 months (between epidemics) and group-specific immunity within 2-4 months (during an epidemic period).
BACKGROUND: Individuals are reinfected with respiratory syncytial virus (RSV) repeatedly. The nature of reinfection, in relation to RSV genetic and antigenic diversity, is ill defined and has implications for persistence and vaccine control. METHODS: We examined the molecular relatedness of RSV causing primary and repeat infections, by phylogenetic analysis of the attachment (G) gene in 12 infants from a birth cohort in rural Kenya, using nasal wash samples collected during a 16-month period in 2002-2003, which spanned 2 successive epidemics. RESULTS: Six infants were infected during both epidemics, 4 with RSV-A in the first epidemic followed by RSV-B during the second epidemic and 2 with RSV-A during both epidemics, with no significant G gene sequence variability between samples. Two infants were infected and reinfected with different RSV-A strains during the same epidemic. Possible viral persistence was suspected in the remaining 4 infants, although reinfection with the same variant cannot be excluded. CONCLUSIONS: These are the first data that specifically address strain-specific reinfections in infancy in relation to the primary infecting variant. The data strongly suggest that, following primary infection, some infants lose strain-specific immunity within 7-9 months (between epidemics) and group-specific immunity within 2-4 months (during an epidemic period).
Authors: Maria P Loscertales; Anna Roca; Pere J Ventura; Fátima Abacassamo; Francisco Dos Santos; Mariano Sitaube; Clara Men ndez; Brian M Greenwood; Juan C Saiz; Pedro L Alonso Journal: Pediatr Infect Dis J Date: 2002-02 Impact factor: 2.129
Authors: D James Nokes; Emelda A Okiro; Mwanajuma Ngama; Lisa J White; Rachel Ochola; Paul D Scott; Patricia A Cane; Graham F Medley Journal: J Infect Dis Date: 2004-10-08 Impact factor: 5.226
Authors: Paul D Scott; Rachel Ochola; Mwanajuma Ngama; Emelda A Okiro; D James Nokes; Graham F Medley; Patricia A Cane Journal: J Med Virol Date: 2004-10 Impact factor: 2.327
Authors: Kate L Stokes; Michael H Chi; Kaori Sakamoto; Dawn C Newcomb; Michael G Currier; Matthew M Huckabee; Sujin Lee; Kasia Goleniewska; Carla Pretto; John V Williams; Anne Hotard; Taylor P Sherrill; R Stokes Peebles; Martin L Moore Journal: J Virol Date: 2011-04-06 Impact factor: 5.103
Authors: Paul D Scott; Rachel Ochola; Charles Sande; Mwanajuma Ngama; Emelda A Okiro; Graham F Medley; D James Nokes; Patricia A Cane Journal: J Med Virol Date: 2007-12 Impact factor: 2.327