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this cohort study was approved by the centre hospitalier universitaire de qubec research ethics board .
participants were <3 years of age and either received medical attention at an outpatient pediatric clinic or were hospitalized at a pediatric center for acute rti during 4 winter seasons ( 20062010 ) , in qubec city , qubec , canada .
clinical data were prospectively collected at study entry and after 1-month follow - up . for all patients , at the first visit a nasopharyngeal aspirate was collected .
the aspirate was frozen at 80c until subsequent testing by a multiplex pcr / dna hybridization assay that detects rsv genotype - a ( rsv - a ) , rsv - b , and 22 other respiratory viruses ( infiniti rvp assay ; autogenomics , carlsbad , ca , usa ) ( 14 ) .
rsv infection was identified in aspirates from 467 ( 63.6% ) of 734 hospitalized children ( 257 rsv - a , 210 rsv - b ) and from 147 ( 48.2% ) of 305 outpatient children ( 85 rsv - a , 62 rsv - b ) . during 20062010 ,
a total of 724 children received palivizumab in the qubec city region ( l. cliche , pers .
rsv - positive samples from all 12 study participants receiving palivizumab and from 100 not receiving palivizumab underwent rsv - f sequencing .
additionally , f - gene analysis was performed on 11 rsv - positive clinical samples from palivizumab recipients retrospectively identified by using neonatal clinic registries at mcmaster children s hospital ( hamilton , ontario , canada ) and montral children s hospital ( montral , qubec , canada ) during 20092010 .
rna was extracted directly from nasopharyngeal samples by using a qiamp viral rna mini kit ( qiagen , mississauga , ontario , canada ) .
random primers ( amersham , piscataway , nj , usa ) and superscript ii rt kit ( invitrogen , carlsbad , ca , usa ) were used for reverse transcription .
pcr amplification was performed with quantifast probe pcr+rox vial kit ( qiagen ) ; primers and thermocycling conditions are available from g.b . upon request .
rsv - f amplicons were sequenced by using an automated sequencer ( applied biosystems , foster city , ca , usa ) . along with the newly generated nucleotide sequences from the 123 children ( 23 palivizumab recipients ; 100 nonrecipients )
, we analyzed 92 clinical rsv - f sequences provided by other investigators ( 10,11 ) or available from genbank .
we also included 10 unpublished rsv - f sequences from a 20042005 study of palivizumab recipients in canada ( 15 ) .
a 1,524-bp region ( positions 791602 in the prototype a2 and b1 rsv - f genes ) was translated into amino acid sequences , and the palivizumab binding site ( residues 262276 ) was assessed for variations .
the final dataset comprised 170 unique sequences , including 89 that were newly generated in this study ( genbank accession nos .
however , this segregation likely reflects temporal evolution rather than geographic influence because all rsv - f sequences originating from other countries were collected > 10 years ago .
previous rsv - g studies have demonstrated concurrent circulation of related lineages in distant areas ( 13 ) .
. this difference may reflect sampling bias because more rsv - a sequences originating from diverse locations and years were available ; however , the greater genetic diversity of rsv - a compared with rsv - b has also been observed in a study conducted in south korea ( 10 ) .
phylogenetic analysis of 170 near  full - length unique respiratory syncitial virus fusion ( rsv - f ) gene sequences ( nt 791602 ) .
panels a and b are detailed phylograms of the rsv - a and rsv - b taxa analyzed , respectively . one bovine rsv - f sequence was added to the dataset ( genbank accession no .
af295543.1 ) as the outgroup ( not shown ) and used for rooting the phylograms .
topology was inferred by using the neighbor - joining method , and evolutionary distances were computed by using the maximum - composite likelihood method in mega5 software ( www.megasoftware.net ) .
only bootstrap values > 50% are shown . blue text and triangles represent rsv strains isolated in canada and sequenced at the centre de recherche du centre hospitalier universitaire de qubec ; red branches indicates a sublineage of rsv - a with a n276s mutation ; underlining indicates prototypical rsv a2 and rsv b1 strains .
the clinical origin of strains from canada ( prospective study hospitalized patient [ h ] or clinic patient [ c ] ; 20042005 palivizumab study patient [ s ] ; retrospectively identified patient from the montral children s hospital [ mch ] or mcmaster children s hospital [ mac ] ) is indicated , followed by the year collected , the specimen identifier , and the result of rsv genogroup testing ( rsv - a [ a ] , rsv - b [ b ] ) by multiplex pcr / dna hybridization assay ( 14 ) .
specimens with a nonsilent mutation at codon 272 have the amino acid substitution identified in brackets .
when a taxon represents > 1 identical sequences , the number of patients that it represents and the number of palivizumab recipients ( pzb ) among these patients are noted in parentheses .
sa , south africa ; chn , people s republic of china ; uk , united kingdom , jpn , japan ; aus , australia ; usa , united states ; cdc , us centers for disease control and prevention ; ny , new york ; sl , st .
louis ; wv , west virginia ; mn , minnesota ; md , maryland ; wa , washington ; sel , seoul , south korea .
* mean nucleotide and amino acid identities were estimated by calculating pairwise distances in mega5 software ( www.megasoftware.net ) and using the maximum - composite likelihood and poisson correction models , respectively .
rsv , respiratory syncytial virus . of the 23 rsv - f amino acid sequences from patients who received palivizumab ( table 2 )
, 2 exhibited a mutation at residue 272 ( k272q , k272 m ) , whereas no such mutations were identified in the other 100 strains obtained from those who did not receive palivizumab ( 8.7% versus 0% ; p = 0.03 , by fisher exact test ) .
a sublineage of rsv - a , noteworthy for an n276s substitution in the palivizumab binding site , emerged during 20082009 ( 8 [ 44% ] of 18 rsv - a strains ) and became the predominant rsv - a clade during 20092010 ( 25 [ 100% ] of 25 strains ) in palivizumab recipients and nonrecipients .
no sequences from genbank or other studies ( 10,11 ) harbored any palivizumab binding site mutation . * patient identification ( i d ) nomenclature : hospitalized ( h ) or clinic ( c ) prospective study participant , montral children s hospital ( mch ) or mcmaster children s hospital ( mac ) patient .
ga , gestational age ; pzb , palivizumab ; multiplex pcr / dna , hybridization assay ; mutation , mutation in respiratory syncytial virus fusion protein pzb binding site ( residues 262276 ) ; rsv , respiratory syncytial virus ; lbw , low birthweight ( 1,5002,500 g ) ; nf , no mutation found in pzb binding site ; vlbw , very low birthweight ( 1,0001,499 g ) ; elbw , extremely low birthweight ( < 1,000 g ) ; rti , respiratory tract infection ; bpd , bronchopulmonary dysplasia ; iugr , intrauterine growth restriction .  median patient age 6.0 mo ( range 124 mo ) . 
 median interval between last palivizumab dose and symptom onset : 15.0 d ( range 327 d ) . 
retrospectively identified participants from montral children s hospital or mcmaster children s hospital were rsv - positive by direct immunofluorescence assay ( chemicon international , temecula , ca , usa ) and were not tested by the multiplex pcr / dna hybridization assay ( 14 ) .
rsv was incubated ( for 2 h at 37c ) with serially diluted palivizumab , then cultured in vero cells ( for 5 d ) .
rsv replication and 50% inhibitory concentrations ( ic50 ) were subsequently determined by f protein quantification by using elisa .
the mean  sd ic50 of c09101006a , a n276s strain , was 0.33  0.04 g / ml , similar to that of rsv - a2 wild type ( ic50 0.46  0.04 g / ml ) and therefore was considered susceptible .
we report the prevalence of resistance - conferring mutations in rsv - f among children receiving or not receiving palivizumab .
although infrequent ( 8.7% of infections in palivizumab recipients ) , residue 272 mutations were significantly associated with palivizumab exposure and not observed at all in nonexposed patients .
we identified 2 new clinical specimens with position 272 mutations ( k272q and k272 m ) .
we can not exclude the possibility that additional specimens contained mixed viral populations with minor proportions of position-272 mutants not detectable by conventional sequencing methods .
changes at this position ( from lysine to asparagine , glutamine , glutamic acid , methionine , or threonine ) have produced palivizumab resistance in vitro ( 9 ) and in a cotton rat model ( 7 ) . as previously reported , 1 ( 10.0% ) of 10 sequences from our 20042005 study of palivizumab patients carried a 272 mutation ( k272e ) ( 15 ) .
the k272e substitution is the only substitution also demonstrated to confer resistance to motavizumab , an enhanced - potency monoclonal antibody developed by affinity maturation of palivizumab ( 9 ) .
we could not perform neutralization assays on position-272 variants because they did not grow in culture .
phylogenetic analysis demonstrated that mutations in the palivizumab binding site occur in diverse genetic backgrounds ; all 3 strains with substitutions at residue 272 grouped to different clades ( figure ) .
furthermore , these mutant strains caused mild disease treatable in an outpatient clinic and severe illness requiring hospitalization .
from 3 canadian communities we detected a lineage harboring an n276s mutation in 44.4% of rsv - a sequences from 20082009 and 100% from 20092010 , unrelated to palivizumab exposure .
adams et al . have proposed that n276s led to palivizumab resistance in a clinical specimen ( 8) . however , that sample also comprised a k272e subpopulation .
our microneutralization assay results and unpublished neutralization data using recombinant viruses and clinical isolates ( q. zhu , pers . comm . ) suggest that n276s does not confer resistance .
although serious rsv rtis during palivizumab prophylaxis remain uncommon , we observed an 8.7% prevalence of known resistance mutations among 23 medically attended patients receiving palivizumab .
to assess molecular evolution of the respiratory syncytial virus ( rsv ) fusion gene , we analyzed rsv - positive specimens from 123 children in canada who did or did not receive rsv immunoprophylaxis ( palivizumab ) during 20062010 . 
 resistance - conferring mutations within the palivizumab binding site occurred in 8.7% of palivizumab recipients and none of the nonrecipients .