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Genetic relatedness of infecting and reinfecting respiratory syncytial virus strains identified in a birth cohort from rural Kenya.

Agoti CN, Mwihuri AG, Sande CJ, Onyango CO, Medley GF, Cane PA, Nokes DJ - J. Infect. Dis. (2012)

Bottom Line: The extent to which this is a consequence of RSV antigenic diversity is unclear.A positive sample separated from a previous positive by ≥14 days was defined as a reinfection a priori.Heterologous group reinfections were observed in 28 episodes, and homologous group reinfections were observed in 25 episodes; 10 involved homologous genotypes, 5 showed no amino acid changes, and 3 were separated by 21-24 days and were potentially persistent infections.

View Article: PubMed Central - PubMed

Affiliation: Kenya Medical Research Institute, Centre for Geographic Medicine Research, Coast, Kenya. cnyaigoti@kilifi.kemri-wellcome.org

ABSTRACT

Background: Respiratory syncytial virus (RSV) reinfects individuals repeatedly. The extent to which this is a consequence of RSV antigenic diversity is unclear.

Methods: Six-hundred thirty-five children from rural Kenya were closely monitored for RSV infection from birth through 3 consecutive RSV epidemics. RSV infections were identified by immunofluorescence testing of nasal washing samples collected during acute respiratory illnesses, typed into group A and B, and sequenced in the attachment (G) protein. A positive sample separated from a previous positive by ≥14 days was defined as a reinfection a priori.

Results: Phylogenetic analysis was undertaken for 325 (80%) of 409 identified infections, including 53 (64%) of 83 reinfections. Heterologous group reinfections were observed in 28 episodes, and homologous group reinfections were observed in 25 episodes; 10 involved homologous genotypes, 5 showed no amino acid changes, and 3 were separated by 21-24 days and were potentially persistent infections. The temporal distribution of genotypes among reinfections did not differ from that of single infections.

Conclusions: The vast majority of infection and reinfection pairs differed by group, genotype, or G amino acid sequence (ie, comprised distinct viruses). The extent to which this is a consequence of immune memory of infection history or prevalent diversity remains unclear.

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Related in: MedlinePlus

A maximum likelihood tree showing the evolutionary relationship of strains from subjects who experienced homologous group B reinfections. The tree is based on sequences from 11 subjects and reference sequences representing genotypes GB1-4, SAB1-3 and the BA. Their GenBank accession numbers are CH10b, AF065250; CH93-9B,AF065251; CH93-53B, AF065253; BE/400/91, AY751275; BE/12252/96, AY751241; BE/1054/98,DQ985156; Uru/41605; AF251557; and Arg//3997/1999, DQ227366. The empty triangles represent first infections, and the dark, filled triangles represent the second infections.
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JIS570F3: A maximum likelihood tree showing the evolutionary relationship of strains from subjects who experienced homologous group B reinfections. The tree is based on sequences from 11 subjects and reference sequences representing genotypes GB1-4, SAB1-3 and the BA. Their GenBank accession numbers are CH10b, AF065250; CH93-9B,AF065251; CH93-53B, AF065253; BE/400/91, AY751275; BE/12252/96, AY751241; BE/1054/98,DQ985156; Uru/41605; AF251557; and Arg//3997/1999, DQ227366. The empty triangles represent first infections, and the dark, filled triangles represent the second infections.

Mentions: The phylogenetic relationship of the G-gene sequences from the children with homologous group B reinfection is shown in Figure 3. The sequences fell into 2 clusters: one that included virus strains that have the 60-nucleotide duplication (BA genotype) and another of virus strains that lack the duplication (SAB1 genotype). Eleven children with an initial infection with SAB1 genotype virus strains were reinfected with BA genotype virus strains during a subsequent epidemic. Two children (Ken/3757 and Ken/3912) were infected and reinfected in consecutive epidemics with SAB1 genotype virus strains that had amino acid changes. In these 2, the reinfecting strain from Ken/3757 possessed 2 nonsynonymous changes (N66H and S297L), and in Ken/3912, the reinfecting strain possessed 11 nonsynonymous changes occurring together with a mutation at a stop codon site that resulted in a changed predicted protein length (Table 2).Figure 3.


Genetic relatedness of infecting and reinfecting respiratory syncytial virus strains identified in a birth cohort from rural Kenya.

Agoti CN, Mwihuri AG, Sande CJ, Onyango CO, Medley GF, Cane PA, Nokes DJ - J. Infect. Dis. (2012)

A maximum likelihood tree showing the evolutionary relationship of strains from subjects who experienced homologous group B reinfections. The tree is based on sequences from 11 subjects and reference sequences representing genotypes GB1-4, SAB1-3 and the BA. Their GenBank accession numbers are CH10b, AF065250; CH93-9B,AF065251; CH93-53B, AF065253; BE/400/91, AY751275; BE/12252/96, AY751241; BE/1054/98,DQ985156; Uru/41605; AF251557; and Arg//3997/1999, DQ227366. The empty triangles represent first infections, and the dark, filled triangles represent the second infections.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3475639&req=5

JIS570F3: A maximum likelihood tree showing the evolutionary relationship of strains from subjects who experienced homologous group B reinfections. The tree is based on sequences from 11 subjects and reference sequences representing genotypes GB1-4, SAB1-3 and the BA. Their GenBank accession numbers are CH10b, AF065250; CH93-9B,AF065251; CH93-53B, AF065253; BE/400/91, AY751275; BE/12252/96, AY751241; BE/1054/98,DQ985156; Uru/41605; AF251557; and Arg//3997/1999, DQ227366. The empty triangles represent first infections, and the dark, filled triangles represent the second infections.
Mentions: The phylogenetic relationship of the G-gene sequences from the children with homologous group B reinfection is shown in Figure 3. The sequences fell into 2 clusters: one that included virus strains that have the 60-nucleotide duplication (BA genotype) and another of virus strains that lack the duplication (SAB1 genotype). Eleven children with an initial infection with SAB1 genotype virus strains were reinfected with BA genotype virus strains during a subsequent epidemic. Two children (Ken/3757 and Ken/3912) were infected and reinfected in consecutive epidemics with SAB1 genotype virus strains that had amino acid changes. In these 2, the reinfecting strain from Ken/3757 possessed 2 nonsynonymous changes (N66H and S297L), and in Ken/3912, the reinfecting strain possessed 11 nonsynonymous changes occurring together with a mutation at a stop codon site that resulted in a changed predicted protein length (Table 2).Figure 3.

Bottom Line: The extent to which this is a consequence of RSV antigenic diversity is unclear.A positive sample separated from a previous positive by ≥14 days was defined as a reinfection a priori.Heterologous group reinfections were observed in 28 episodes, and homologous group reinfections were observed in 25 episodes; 10 involved homologous genotypes, 5 showed no amino acid changes, and 3 were separated by 21-24 days and were potentially persistent infections.

View Article: PubMed Central - PubMed

Affiliation: Kenya Medical Research Institute, Centre for Geographic Medicine Research, Coast, Kenya. cnyaigoti@kilifi.kemri-wellcome.org

ABSTRACT

Background: Respiratory syncytial virus (RSV) reinfects individuals repeatedly. The extent to which this is a consequence of RSV antigenic diversity is unclear.

Methods: Six-hundred thirty-five children from rural Kenya were closely monitored for RSV infection from birth through 3 consecutive RSV epidemics. RSV infections were identified by immunofluorescence testing of nasal washing samples collected during acute respiratory illnesses, typed into group A and B, and sequenced in the attachment (G) protein. A positive sample separated from a previous positive by ≥14 days was defined as a reinfection a priori.

Results: Phylogenetic analysis was undertaken for 325 (80%) of 409 identified infections, including 53 (64%) of 83 reinfections. Heterologous group reinfections were observed in 28 episodes, and homologous group reinfections were observed in 25 episodes; 10 involved homologous genotypes, 5 showed no amino acid changes, and 3 were separated by 21-24 days and were potentially persistent infections. The temporal distribution of genotypes among reinfections did not differ from that of single infections.

Conclusions: The vast majority of infection and reinfection pairs differed by group, genotype, or G amino acid sequence (ie, comprised distinct viruses). The extent to which this is a consequence of immune memory of infection history or prevalent diversity remains unclear.

Show MeSH
Related in: MedlinePlus