Epidemiological analysis and follow-up of human rhinovirus infection in children with asthma exacerbation

Abstract

To determine the prevalence of human rhinovirus (HRV) infection in children with acute asthma exacerbations, investigation of HRV viral load and severity of asthma exacerbations is also required. Nasopharyngeal aspirates and swabs were collected and assessed for respiratory viruses. HRV-positive samples were sequenced to identify types and determine viral load. Outpatients with asthma exacerbations underwent follow-up evaluations, their swabs were collected and clinical outcomes were recorded at their next clinic visit 4 weeks later. One hundred forty-three inpatients and 131 outpatients, including 88 patients with asthma exacerbations and 43 controls with stable asthma were recruited. HRV-A was mainly detected in September and February (45.5% and 33.3%, respectively), while HRV-C was mainly detected in November and April (70.0% and 55.6%, respectively). HRV-C was the primary type and was primarily found in inpatients with severe asthma exacerbations. HRV-A viral load in the group of inpatients with severe exacerbations was higher than in the mild and moderate groups (P < 0.001 and P = 0.022). The HRV-A viral load of both inpatients and outpatients was higher than that of HRV-C (P < 0.001 and P = 0.036). The main genotypes were HRV-C53 and HRV-A20 among inpatients, and this genotype caused more severe clinical manifestations. HRV persisted for no more than 4 weeks, and their symptoms or signs of disease were well-controlled well. HRV-C was most frequently detected in asthma exacerbations. HRV-A with high viral load led to severe asthma exacerbations.

Keywords: asthma exacerbations; children; human rhinoviruses; type; viral load.

Figure 1

Seasonal incidence (rate of positive samples) by month of HRV‐A, HRV‐B, and HRV‐C. Data was combined from 3 years and bar graph represents the detection rate of the three HRV types

Figure 2

Relationship between HRV viral load and severity of asthma exacerbations among inpatients. A: HRV total viral load among the three groups shows no significant difference. B: HRV‐A viral load in severe group was significantly higher than in the mild and moderate groups (P < 0.001 and P = 0.022). C: HRV‐C viral load the among three groups shows no significant difference. D: HRV‐A and HRV‐B viral load were significantly higher than HRV‐C regardless of the severity (P < 0.001 and P = 0.014). E: In the severe group, HRV‐A viral load was significantly higher than HRV‐C (P < 0.0001). The comparison of viral load was conducted by nonparametric Mann‐Whitney U‐test

Figure 3

Phylogenetic analysis of the HRV VP4/VP2 coding region from inpatients using the neighbour‐joining method with 1000 bootstrap replicates with MEGA5.05; branches showing >70% bootstrap support are indicated. The strains in this study are marked with CQ (Chongqing) and HRV‐A labeled ♦, HRV‐B labeled ●, and HRV‐C labeled ▴

Figure 4

Phylogenetic analysis of the HRV 5′‐NCR region in outpatients using the neighbor‐joining method with 1000 bootstrap replicates with MEGA5.05; branches showing >70% bootstrap support are indicated. The strains in this study are marked with CQ (Chongqing), F (follow‐up samples) and C (control group samples) and HRV‐A labeled ♦, HRV‐B labeled, ● and HRV‐C labeled ▴