Nosocomial outbreak of respiratory syncytial virus subgroup B variants with the 60 nucleotides-duplicated G protein gene

2004 ◽  
Vol 74 (1) ◽  
pp. 161-165 ◽  
Author(s):  
Kazushige Nagai ◽  
Hotaka Kamasaki ◽  
Yuki Kuroiwa ◽  
Lisa Okita ◽  
Hiroyuki Tsutsumi
2009 ◽  
Vol 5 (1) ◽  
pp. e1000254 ◽  
Author(s):  
Viviane F. Botosso ◽  
Paolo M. de A. Zanotto ◽  
Mirthes Ueda ◽  
Eurico Arruda ◽  
Alfredo E. Gilio ◽  
...  

2010 ◽  
Vol 84 (19) ◽  
pp. 10425-10428 ◽  
Author(s):  
Charles N. Agoti ◽  
Jean L. Mbisa ◽  
Ann Bett ◽  
Graham F. Medley ◽  
D. James Nokes ◽  
...  

ABSTRACT Intrapatient variability of the attachment (G) protein gene of respiratory syncytial virus (RSV) was examined using both population and single-genome sequencing. Samples from three patients infected with a group B virus variant which has a 60-nucleotide duplication in the G protein gene were examined. These samples were chosen because occasional mixed sequence bases were observed. In a minority of RSV genomes from these patients considerable variability was found, including point mutations, insertions, and deletions. Of particular note, the deletion of the exact portion of the gene which had been duplicated in some isolates was observed in viral RNAs from two patients.


2008 ◽  
Vol 80 (9) ◽  
pp. 1653-1660 ◽  
Author(s):  
Luciana Helena Antoniassi da Silva ◽  
Fernando Rosado Spilki ◽  
Adriana Gut Lopes Riccetto ◽  
Renata Servan de Almeida ◽  
Emílio Carlos Elias Baracat ◽  
...  

2010 ◽  
Vol 84 (15) ◽  
pp. 7500-7512 ◽  
Author(s):  
Alfonsina Trento ◽  
Inmaculada Casas ◽  
Ana Calderón ◽  
Maria L. Garcia-Garcia ◽  
Cristina Calvo ◽  
...  

ABSTRACT The emergence of natural isolates of human respiratory syncytial virus group B (HRSV-B) with a 60-nucleotide (nt) duplication in the G protein gene in Buenos Aires, Argentina, in 1999 (A. Trento et al., J. Gen. Virol. 84:3115-3120, 2003) and their dissemination worldwide allowed us to use the duplicated segment as a natural tag to examine in detail the evolution of HRSV during propagation in its natural host. Viruses with the duplicated segment were all clustered in a new genotype, named BA (A. Trento et al., J. Virol. 80:975-984, 2006). To obtain information about the prevalence of these viruses in Spain, we tested for the presence of the duplicated segment in positive HRSV-B clinical samples collected at the Severo Ochoa Hospital (Madrid) during 12 consecutive epidemics (1996-1997 to 2007-2008). Viruses with the 60-nt duplication were found in 61 samples, with a high prevalence relative to the rest of B genotypes in the most recent seasons. Global phylogenetic and demographic analysis of all G sequences containing the duplication, collected across five continents up until April 2009, revealed that the prevalence of the BA genotype increased gradually until 2004-2005, despite its rapid dissemination worldwide. After that date and coinciding with a bottleneck effect on the population size, a relatively new BA lineage (BA-IV) replaced all other group B viruses, suggesting further adaptation of the BA genotype to its natural host.


PLoS ONE ◽  
2021 ◽  
Vol 16 (2) ◽  
pp. e0246770
Author(s):  
Margaret E. Martinez ◽  
Cristina Capella Gonzalez ◽  
Devra Huey ◽  
Mark E. Peeples ◽  
Douglas McCarty ◽  
...  

Human respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infection in infants and young children worldwide. The attachment (G) protein of RSV is synthesized by infected cells in both a membrane bound (mG) and secreted form (sG) and uses a CX3C motif for binding to its cellular receptor. Cell culture and mouse studies suggest that the G protein mimics the cytokine CX3CL1 by binding to CX3CR1 on immune cells, which is thought to cause increased pulmonary inflammation in vivo. However, because these studies have used RSV lacking its G protein gene or blockade of the G protein with a G protein specific monoclonal antibody, the observed reduction in inflammation may be due to reduced virus replication and spread, and not to a direct role for G protein as a viral chemokine. In order to more directly determine the influence of the soluble and the membrane-bound forms of G protein on the immune system independent of its attachment function for the virion, we expressed the G protein in cotton rat lungs using adeno-associated virus (AAV), a vector system which does not itself induce inflammation. We found no increase in pulmonary inflammation as determined by histology and bronchoalveolar lavage after inoculation of AAVs expressing the membrane bound G protein, the secreted G protein or the complete G protein gene which expresses both forms. The long-term low-level expression of AAV-G did, however, result in the induction of non-neutralizing antibodies, CD8 T cells and partial protection from challenge with RSV. Complete protection was accomplished through co-immunization with AAV-G and an AAV expressing cotton rat interferon α.


2006 ◽  
Vol 80 (2) ◽  
pp. 975-984 ◽  
Author(s):  
Alfonsina Trento ◽  
Mariana Viegas ◽  
Mónica Galiano ◽  
Cristina Videla ◽  
Guadalupe Carballal ◽  
...  

ABSTRACT A total of 47 clinical samples were identified during an active surveillance program of respiratory infections in Buenos Aires (BA) (1999 to 2004) that contained sequences of human respiratory syncytial virus (HRSV) with a 60-nucleotide duplication in the attachment (G) protein gene. This duplication was analogous to that previously described for other three viruses also isolated in Buenos Aires in 1999 (A. Trento et al., J. Gen. Virol. 84:3115-3120, 2003). Phylogenetic analysis indicated that BA sequences with that duplication shared a common ancestor (dated about 1998) with other HRSV G sequences reported worldwide after 1999. The duplicated nucleotide sequence was an exact copy of the preceding 60 nucleotides in early viruses, but both copies of the duplicated segment accumulated nucleotide substitutions in more recent viruses at a rate apparently higher than in other regions of the G protein gene. The evolution of the viruses with the duplicated G segment apparently followed the overall evolutionary pattern previously described for HRSV, and this genotype has replaced other prevailing antigenic group B genotypes in Buenos Aires and other places. Thus, the duplicated segment represents a natural tag that can be used to track the dissemination and evolution of HRSV in an unprecedented setting. We have taken advantage of this situation to reexamine the molecular epidemiology of HRSV and to explore the natural history of this important human pathogen.


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