Respiratory syncytial virus (RSV) is

Both TTDC and SRRIAT showed excellent outcomes and cosmetic appearance for suitable VSD candidates. Although its costs were higher, TTDC had the advantages over SRRIAT of a short operation duration and intensive care unit stay and fewer days in the hospital.

Respiratory syncytial virus (RSV) causes respiratory tract infection, particularly acute lower respiratory tract infection (ALRTI), in early childhood. The RSV fusion protein (F protein) is an important surface protein, and it is the target of both cytotoxic T lymphocytes (CTL) and neutralizing antibodies; thus, it may be useful as a candidate for vaccine research. This study investigated the genetic diversity of the RSV F protein. To this end, a total of 1800 nasopharyngeal aspirates from hospitalized children with ALRTI were collected for virus isolation between June 2009 and March 2012. There were 333 RSV-positive cases (277 cases of RSV A, 55 of RSV B, and 1 with both RSV A and RSV B), accounting for 18.5 % of the total cases. Next, 130 clinical strains (107 of RSV A, 23 of RSV B) were selected for F gene sequencing. Phylogenetic analysis revealed that the F gene sequence is highly conserved, with significant amino acid changes at residues 16, 25, 45, 102, 122, 124, 209, and 447. Mutations in human histocompatibility leukocyte antigen (HLA)-restricted CTL epitopes were also observed. Variations in RSV A F protein at the palivizumab binding site 276 (N→S) increased between 2009 and 2012 and became predominant. Western blot analysis and microneutralization data showed a substitution at residue 276 (N→S) in RSV A that did not cause resistance to palivizumab. In conclusion, the RSV F gene is geographically and temporally conserved, but limited genetic variations were still observed. These data could be helpful for the development of vaccines against RSV infection.

The human bocavirus 1 (HBoV1) parvovirus causes respiratory disease and primarily affects children. Despite its worldwide prevalence, the mechanisms of HBoV1 replication and pathogenesis remain largely undefined. In this study of 846 children hospitalized at the Children's Hospital of Chongqing Medical University in China for respiratory tract infection between June 2009 and May 2011, HBoV1 was detected in 112 (13.2%) by real-time quantitative PCR. The median age of HBoV1-positive patients was 10 months old. Forty-five (40.2%) of the HBoV1 cases were monoinfections, and 67 (59.8%) were viral co-infections. Genotyping of all 112 HBoV1-positive cases yielded 27 full HBoV1 sequences, as well as two NS1 gene sequences, 15 NP1 gene sequences and 10 VP1/VP2 gene sequences harbouring 24, 10 and 43 mutations, respectively. Statistical analysis revealed no relationship between genetic mutations and clinical manifestations of HBoV1-positive patients. However, the viral loads were significantly lower in samples with mutations G236A or A447G in NP1, or G1461A in VP1/VP2, than in samples with wild-type HBoV1. Future studies should investigate whether these mutations in the HBoV1 gene may represent useful markers of disease pathogenesis.