Circulating Strains of Human Respiratory Syncytial Virus in Central and South America

Sovero, Merly; Garcia, Josefina; Kochel, Tadeusz J.; Laguna-Torres, V. Alberto; Gómez, Jorge; Chicaiza, Wilson; Barrantes, Melvin; Sanchez, Felix; Jimenez, Mirna; Comach, Guillermo; Lorenzana, Ivette; Arango, Ana E.; Agudo, Roberto; Halsey, Eric S.

doi:10.1371/journal.pone.0022111

Cited by 12 publications

(17 citation statements)

References 46 publications

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“…In Fortaleza, during the five epidemic periods, genotypes GA2 and GA5 of HRSV‐A occur in varying proportions. Brazilian and international studies have shown a high diversity of genotypes of HRSV with GA2 and GA5 as the predominant circulating genotypes . The small number of strains analyzed should not be the only reason for the low diversity of genotypes of HRSV‐A detected in Fortaleza.…”

Section: Discussionmentioning

confidence: 93%

“…This genotype, named BA, has a duplication of 60 nucleotides . Since 1999, the BA genotype has spread globally and in some places now predominates or has replaced genotypes that circulated for several years . In Fortaleza, BA strains were detected in 2004 but in 2005, when there was a predominance of HRSV‐A, all five strains of HRSV‐B corresponded to genotype GB3.…”

Section: Discussionmentioning

confidence: 99%

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Respiratory syncytial virus epidemic periods in an equatorial city of Brazil

Moura

Perdigão

Ribeiro

et al. 2013

Influenza Resp Viruses

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BackgroundCharacterization of the human respiratory syncytial virus (HRSV) season at the local level has important implications for appropriate decisions on the time period for administration of specific prophylaxis.Objectives(1) To describe five consecutive epidemic periods of HRSV in an equatorial city of Brazil and (2) to show preliminary data on genomic diversity of circulating HRSV.Patients/MethodsNasopharyngeal aspirates of 2885 children attending the emergency room and wards of a public hospital were collected and screened by indirect immunofluorescence for HRSV infections during five consecutive years (from January 2004 to December 2008). In addition, the genetic and antigenic variability of the HRSV strains isolated was evaluated by partial nucleotide sequencing of the protein G gene.Results HRSV was detected in 15·8% of the analyzed samples. HRSV seasons occurred in a restricted period of each year. The onset of each HRSV season was variable (February to May), but the end always occurred in July. From the 456 HRSV infections found, 86 cases with bronchiolitis were genotyped. Both HRSV subgroups (A and B) cocirculated during the five epidemic periods. The 58 HRSV‐A strains grouped into two clades, GA2 and GA5. In respect of the HRSV‐B strains, the 28 samples grouped into two clades: GB3 and BA.Conclusions HRSV accounts for a substantial proportion of ARI in the study population. As in temperate countries, HRSV infections in this equatorial area of Brazil also cause seasonal yearly epidemics, and this has implications for prophylaxis strategies. The city of Fortaleza follows the same worldwide trend of circulation of genotypes of HRSV.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Respiratory syncytial virus epidemic periods in an equatorial city of Brazil

Moura

Perdigão

Ribeiro

et al. 2013

Influenza Resp Viruses

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“…GA2 and GA5 circulate worldwide and are recognized as stable genotypes [24], [25], [28], [35]–[40]. The select dominance of GA2 has also been observed in South Western China during epidemic seasons 2006–2009 [40] and Central and South America [36], Ireland in 2008/2009 [25] and South Africa in 2007–2008 [28]. The efficient circulation of these genotypes could not be explained by high genetic variability of the carboxy-terminal hypervariable region, since this region was remarkably conserved comparing strains isolated over several years [41].…”

Section: Discussionmentioning

confidence: 99%

Circulation of HRSV in Belgium: From Multiple Genotype Circulation to Prolonged Circulation of Predominant Genotypes

Houspie¹,

Lemey²,

Keyaerts³

et al. 2013

PLoS ONE

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Molecular surveillance of HRSV in Belgium for 15 consecutive seasons (1996–2011) revealed a shift from a regular 3-yearly cyclic pattern, into a yearly alternating periodicity where HRSV-B is replaced by HRSV-A. Phylogenetic analysis for HRSV-A demonstrated the stable circulation of GA2 and GA5, with GA2 being dominant over GA5 during 5 consecutive seasons (2006–2011). We also identified 2 new genotype specific amino acid mutations of the GA2 genotype (A122 and Q156) and 7 new GA5 genotype specific amino acid mutations (F102, I108, T111, I125, D161, S191 and L217). Several amino acid positions, all located in the second hypervariable region of HRSV-A were found to be under positive selection. Phylogenetic analysis of HRSV-B showed the circulation of GB12 and GB13, where GB13 represented 100% of the isolated strains in 4 out of 5 consecutive seasons (2007–2011). Amino acids under positive selection were all located in the aminoterminal hypervariable region of HRSV-B, except one amino acid located in the conserved region. The genotype distribution within the HRSV-B subgroup has evolved from a co-circulation of multiple genotypes to the circulation of a single predominant genotype. The Belgian GB13 strains circulating since 2006, all clustered under the BAIV branch and contained several branch specific amino acid substitutions. The demographic history of genotypes GA2, GA5 and GB13 demonstrated a decrease in the total GA2 and GA5 population size, coinciding with the global expansion of the GB13 population. The emergence of the GB13 genotype resulted in a newly established balance between the predominant genotypes.

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“…Another Rho family protein, Cdc42 along with WASP and neuronal N-WASP induces Arp2/3-mediated actin branching to form filopodia and granule secretion [343-346]. In the absence of pre-existing actin filaments, IRSp53 initiates this process via its I-BAR domain by bending the membrane outward and binding Cdc42 along with its target proteins.…”

Section: Cdc42-induced Filopodiamentioning

confidence: 99%

Platelets and cancer: a casual or causal relationship: revisited

Menter

Tucker

Kopetz

et al. 2014

Cancer Metastasis Rev

279

256

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Human platelets arise as subcellular fragments of megakaryocytes in bone marrow. The physiologic demand, presence of disease such as cancer, or drug effects can regulate the production circulating platelets. Platelet biology is essential to hemostasis, vascular integrity, angiogenesis, inflammation, innate immunity, wound healing, and cancer biology. The most critical biological platelet response is serving as “First Responders” during the wounding process. The exposure of extracellular matrix proteins and intracellular components occurs after wounding. Numerous platelet receptors recognize matrix proteins that trigger platelet activation, adhesion, aggregation, and stabilization. Once activated, platelets change shape and degranulate to release growth factors and bioactive lipids into the blood stream. This cyclic process recruits and aggregates platelets along with thrombogenesis. This process facilitates wound closure or can recognize circulating pathologic bodies. Cancer cell entry into the blood stream triggers platelet-mediated recognition and is amplified by cell surface receptors, cellular products, extracellular factors, and immune cells. In some cases, these interactions suppress immune recognition and elimination of cancer cells or promote arrest at the endothelium, or entrapment in the microvasculature, and survival. This supports survival and spread of cancer cells and the establishment of secondary lesions to serve as important targets for prevention and therapy.

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Circulating Strains of Human Respiratory Syncytial Virus in Central and South America

Cited by 12 publications

References 46 publications

Respiratory syncytial virus epidemic periods in an equatorial city of Brazil

Respiratory syncytial virus epidemic periods in an equatorial city of Brazil

Circulation of HRSV in Belgium: From Multiple Genotype Circulation to Prolonged Circulation of Predominant Genotypes

Platelets and cancer: a casual or causal relationship: revisited

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