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An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
Genetic and Clinical-epidemiologic Profile of hRSV in Pediatric Patients in Southern Brazil: A Four-year Hospital
Sonia Mara Raboni1,2, Heloisa I G Giamberardino3, Jucelia S Santos1
1From the Molecular Virology Research Laboratory, Universidade Federal do Paraná, Curitiba, Brazil.
Insights
Human respiratory syncytial virus (hRSV) molecular epidemiology in children revealed distinct hRSV-A and hRSV-B genotypes. Certain hRSV-B genotypes (GB5.0.2, GB5.0.4a) were linked to more severe illness in young patients.
Area of Science:
- Virology
- Epidemiology
- Pediatrics
Background:
- Human respiratory syncytial virus (hRSV) is a major cause of acute respiratory illness and hospitalization in children.
- Understanding hRSV molecular epidemiology and its clinical associations is vital for public health.
Purpose of the Study:
- To examine the molecular epidemiology of hRSV in a pediatric cohort over four years.
- To describe the interrelationship between hRSV genotypes and clinical data.
Main Methods:
- A cross-sectional study analyzed respiratory samples from children with acute respiratory illness between 2014 and 2017.
- Respiratory viruses were detected using multiplex real-time polymerase chain reaction, and molecular typing was performed by nucleotide sequencing of the G gene.
Main Results:
- Of 353 children with hRSV, 207 underwent G gene sequencing. hRSV-B was detected in 53% and hRSV-A in 47% of cases.
- hRSV-A sequences were ON1-like (GA2.3.5), while hRSV-B sequences were BA-like with three lineages (GB5.0.2, GB5.0.4a, GB5.0.5a).
- Severe cases were more frequent in younger children and those infected with hRSV-B GB5.0.2 and GB5.0.4a genotypes, with no significant link to comorbidities.
Conclusions:
- Both hRSV subtypes exhibited similar severity, unrelated to comorbidities.
- Younger age and specific hRSV-B genotypes (GB5.0.2, GB5.0.4a) were associated with more severe outcomes.
- Monitoring hRSV molecular evolution is crucial for tracking variants and evaluating the efficacy of vaccines and monoclonal antibodies.
Background:
Respiratory syncytial virus (hRSV) infections primarily cause acute respiratory illness and pediatric hospitalizations. We examined the hRSV molecular epidemiology in a pediatric cohort over a 4-year period and described the interrelationship with clinical data.
Methods:
A cross-sectional study was conducted from 2014 to 2017 on children with acute respiratory illness. Respiratory viruses were detected using a multiplex real-time polymerase chain reaction and molecular typing was performed by nucleotide sequencing.
Results:
Three hundred fifty-three children with hRSV were included; 207 (36%) samples were submitted to partial G gene sequencing. A total of 58.3% (n = 120) were males, the median age was 2.3 months (interquartile range 1-4), and 36.4% (n = 75) of the children required intensive care unit assistance. Coinfection was detected in 27 (5.7%) children, mainly hRSV and rhinovirus (14.2%). A total of 95.6% of patients had no comorbidities, and prematurity (4.4%) was more frequent among those with comorbidities. hRSV-B was detected in 109 patients (53%) and hRSV-A in 98 patients (47%), with changes in incidence over the period. All the hRSV-A sequences were classified as ON1-like, with genetic lineage GA2.3.5 forming distinct clusters. hRSV-B sequences were identified as BA-like, comprising 3 genetic lineages, GB5.0.2, GB5.0.4a and GB5.0.5a, with variation over time, and a higher severity was associated with hRSV type B GB5.0.2 and GB5.0.4a lineages compared with the GB5.0.5a.
Conclusions:
Both hRSV subtypes showed similar severity and were not linked to comorbidities. Severe cases were more common in young patients and those infected with GB5.0.2 and GB5.0.4a genotypes. Understanding hRSV's molecular evolution is crucial for tracking new variants and assessing their impact on the effectiveness of emerging vaccines and monoclonal antibodies.
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