Rhinovirus load and disease severity in children with lower respiratory tract infections

Takeyama, Aya; Hashimoto, Koichi; Sato, Masatoki; Sato, Toshiko; Kanno, Shuto; Takano, Kei; Ito, Masaki; Katayose, Masahiko; Nishimura, Hidekazu; Kawasaki, Yukihiko

doi:10.1002/jmv.23306

Cited by 40 publications

(31 citation statements)

References 41 publications

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“…In our previous study, we found that HRV infection was associated with asthma in our region . Some authors have demonstrated a close correlation between the HRV viral load and the disease severity in children with lower respiratory tract infections . However, there have been no reports on the correlation of the viral load of different HRV species with the severity of asthma exacerbations.…”

Section: Introductionmentioning

confidence: 54%

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

Zheng

Wang

Luo

et al. 2017

Journal of Medical Virology

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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.

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Section: Introductionmentioning

confidence: 54%

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

Zheng

Wang

Luo

et al. 2017

Journal of Medical Virology

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“…There is a positive, albeit loose, relationship between RV virus load and clinical symptoms, 40, 41 and virus-induced cytokines, chemokines, and interferons may also contribute to respiratory symptoms. 42–45 We demonstrated that RV-B types induce lower quantities of pro-inflammatory cytokines, which also could lead to milder illness.…”

Section: Discussionmentioning

confidence: 99%

Effects of rhinovirus species on viral replication and cytokine production

Nakagome¹,

Bochkov²,

Ashraf³

et al. 2014

Journal of Allergy and Clinical Immunology

101

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Background Epidemiological studies provide evidence of differential virulence of rhinovirus (RV) species. We recently reported that RV-A and RV-C induced more severe illnesses than RV-B, suggesting that the biology of RV-B might be different from RV-A or RV-C. Objective To test the hypothesis that RV-B has lower replication and induces lesser cytokine responses than RV-A or RV-C. Methods We cloned full-length cDNA of RV-A16, A36, B52, B72, C2, C15 and C41 from clinical samples, and grew clinical isolates of RV-A7 and B6 in cultured cells. Sinus epithelial cells were differentiated at air-liquid interface. We tested for differences in viral replication in epithelial cells after infection with purified viruses (108 RNA copies) and measured virus load by quantitative RT-PCR. We measured lactate dehydrogenase (LDH) concentration as a marker of cellular cytotoxicity, and cytokine/chemokine secretion by multiplex ELISA. Results At 24 hours post infection, virus load of RV-B (RV-B52, B72, or B6) in adherent cells was lower than that of RV-A or RV-C. The growth kinetics of infection indicated that RV-B types replicate more slowly. Furthermore, RV-B released less LDH than RV-A or RV-C, and induced lower levels of cytokines and chemokines such as CXCL10, even after correction for viral replication. RV-B replicates to lower levels also in primary bronchial epithelial cells. Conclusions Our results indicate that RV-B types have lower and slower replication, and lower cellular cytotoxicity and cytokine/chemokine production compared to RV-A or RV-C. These characteristics may contribute to reduced severity of illnesses that has been observed with RV-B infections. Clinical implications RV-B types replicate at a lower rate and produce less cytokine/chemokine compared to RV-A or RV-C, which may contribute to the clinical observation that RV-B causes less severe illnesses. Capsule summary RV-B types replicate more slowly and to lower levels, and less cytokine/chemokine production compared to RV-A or RV-C. These characteristics may contribute to reduced severity of illnesses that has been observed with RV-B infections.

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“…The literature on the relation between disease severity and viral load is conflicting. Some investigators suggest a positive relationship [6][7][8][9][10][11][12][13][14][15], although others cannot confirm these results [16][17][18][19][20]. Multiple viruses are detected rather frequently in children with respiratory infections and in these cases it is almost impossible to determine the causative pathogen and the relation between viral load and disease severity [21][22][23].…”

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confidence: 99%

Pitfalls in interpretation of CT-values of RT-PCR in children with acute respiratory tract infections

Wishaupt

Ploeg²,

Smeets³

et al. 2017

Journal of Clinical Virology

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Although correlations between CT values and clinical parameters in patients with single and multiple viral infection were found, the clinical importance of these findings is limited because individual differences in host-, viral and laboratory factors complicate the interpretation of statistically significant findings. In multiple infections, viral load cannot be used to differentiate between disease causing virus and innocent bystanders.

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Rhinovirus load and disease severity in children with lower respiratory tract infections

Cited by 40 publications

References 41 publications

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

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

Effects of rhinovirus species on viral replication and cytokine production

Pitfalls in interpretation of CT-values of RT-PCR in children with acute respiratory tract infections

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