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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

Maximum likelihood phylogenetic tree based on the sequences from the 12 subjects who experienced homologous group A reinfections. Reference sequences for genotypes GA1-7 and SAA1-3 were included to assign the strains G genotypes. The GenBank accession numbers of the reference sequences are Aus/A2/1961, M11486; CH57,AF065258 ; NZA_91_05, DQ171722; CH9, AF065254; CH17, AF065255; NZA_89_04, DQ171761, NZA_90_02, DQ171755; and NZA_98_01, DQ171792. The empty triangles represent first infections, and the dark, filled triangles represent the repeat infections.
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JIS570F2: Maximum likelihood phylogenetic tree based on the sequences from the 12 subjects who experienced homologous group A reinfections. Reference sequences for genotypes GA1-7 and SAA1-3 were included to assign the strains G genotypes. The GenBank accession numbers of the reference sequences are Aus/A2/1961, M11486; CH57,AF065258 ; NZA_91_05, DQ171722; CH9, AF065254; CH17, AF065255; NZA_89_04, DQ171761, NZA_90_02, DQ171755; and NZA_98_01, DQ171792. The empty triangles represent first infections, and the dark, filled triangles represent the repeat infections.

Mentions: The evolutionary relationship of the pair viruses from homologous group A reinfections is shown in Figure 2. Four children were reinfected with a heterologous genotype in group A, one of them during the same epidemic (Ken/3919). Two children (Ken/4123 and Ken/3793) were infected and reinfected with the same genotype as in primary infection but in separate epidemics. The reinfecting virus of Ken/4123 had 2 nonsynonymous mutations relative to the primary infecting virus: T113A and N250S. The latter change is predicted to result in a loss of a potential N-glycosylation site (NST→SST). The viruses from Ken/3793 were identical at amino acid sequence level but with the presence of the 4 nucleotide changes.Figure 2.


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)

Maximum likelihood phylogenetic tree based on the sequences from the 12 subjects who experienced homologous group A reinfections. Reference sequences for genotypes GA1-7 and SAA1-3 were included to assign the strains G genotypes. The GenBank accession numbers of the reference sequences are Aus/A2/1961, M11486; CH57,AF065258 ; NZA_91_05, DQ171722; CH9, AF065254; CH17, AF065255; NZA_89_04, DQ171761, NZA_90_02, DQ171755; and NZA_98_01, DQ171792. The empty triangles represent first infections, and the dark, filled triangles represent the repeat infections.
© Copyright Policy - creative-commons
Related In: Results  -  Collection

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

JIS570F2: Maximum likelihood phylogenetic tree based on the sequences from the 12 subjects who experienced homologous group A reinfections. Reference sequences for genotypes GA1-7 and SAA1-3 were included to assign the strains G genotypes. The GenBank accession numbers of the reference sequences are Aus/A2/1961, M11486; CH57,AF065258 ; NZA_91_05, DQ171722; CH9, AF065254; CH17, AF065255; NZA_89_04, DQ171761, NZA_90_02, DQ171755; and NZA_98_01, DQ171792. The empty triangles represent first infections, and the dark, filled triangles represent the repeat infections.
Mentions: The evolutionary relationship of the pair viruses from homologous group A reinfections is shown in Figure 2. Four children were reinfected with a heterologous genotype in group A, one of them during the same epidemic (Ken/3919). Two children (Ken/4123 and Ken/3793) were infected and reinfected with the same genotype as in primary infection but in separate epidemics. The reinfecting virus of Ken/4123 had 2 nonsynonymous mutations relative to the primary infecting virus: T113A and N250S. The latter change is predicted to result in a loss of a potential N-glycosylation site (NST→SST). The viruses from Ken/3793 were identical at amino acid sequence level but with the presence of the 4 nucleotide changes.Figure 2.

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