Article

Human Rhinovirus Species and Season of Infection Determine Illness Severity

Pediatrics, University of Wisconsin, School of Medicine and Public Health, Madison, Wisconsin, United States.
American Journal of Respiratory and Critical Care Medicine (Impact Factor: 11.04). 08/2012; 186(9). DOI: 10.1164/rccm.201202-0330OC
Source: PubMed

ABSTRACT RATIONALE: Human rhinoviruses (HRVs) consist of approximately 160 types that cause a wide range of clinical outcomes including asymptomatic infections, common colds, and severe lower respiratory illnesses. OBJECTIVE: To identify factors which influence the severity of HRV illnesses. METHODS: HRV species and types were determined in 1445 nasal lavages that were prospectively collected from 209 infants participating in a birth cohort who had at least one HRV infection. Questionnaires were used during each illness to identify moderate-to-severe illnesses (MSI). Measurements & MAIN RESULTS: Altogether, 670 HRV infections were identified and 519 of them were solitary infections (only one HRV type). These 519 viruses belonged to 93 different types of 3 species: 49 A, 9 B and 35 C. HRV-A (OR 8.2 [2.7, 25]) and HRV-C (OR 7.6 [2.6, 23]) were more likely to cause MSI compared to HRV-B. In addition, HRV infections were 5-10-fold more likely to cause MSI in the winter months (p<0.0001) compared to summer, in contrast to peak seasonal prevalence in spring and fall. When significant differences in host susceptibility to MSI (p=0.004) were considered, strain-specific rates of HRV MSI ranged from <1% to over 20%. CONCLUSIONS: Factors related to HRV species and type, season, and host susceptibility determine the risk of more severe HRV illness in infancy. These findings suggest that anti-HRV strategies should focus on HRV-A and -C species, and identify the need for additional studies to determine mechanisms for seasonal increases of HRV severity, independent of viral prevalence, in cold weather months.

0 Bookmarks
 · 
243 Views
  • [Show abstract] [Hide abstract]
    ABSTRACT: Human rhinoviruses (RV) are associated with the majority of viral respiratory illnesses in infants, children and adults. Over the last several years, researchers have begun to sequence the many different species and strains of RV in order to determine if certain species were associated with increased disease severity. There are a variety of techniques employed to prepare samples for sequencing. One method utilizes plasmid-cloning, which is expensive and takes several hours to complete. Recently, some investigators have instead used direct sequencing to sequence RV strains, allowing for omission of the time- and labor-intensive cloning step. This study formally compares and contrasts the sequencing results obtained from plasmid-cloning and direct Sanger sequencing of a 500 base pair PCR product covering the VP4/VP2 region of RV. A slightly longer sequence (by 65 base pairs on average) was obtained when specimens were plasmid-cloned, and the sequences were 86% similar. After trimming the extra base pairs from the cloned sequences, the sequences were 99.7% identical. Overall success of directly sequencing samples was similar to that of cloning, 5% on average failed for each technique. Therefore, in many instances, directly sequencing samples may be considered in lieu of the more expensive and time-consuming plasmid-cloning technique.
    Journal of Virological Methods 10/2014; 211. DOI:10.1016/j.jviromet.2014.09.020 · 1.88 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: A first step in primary disease prevention is identifying common, modifiable risk factors that contribute to a significant proportion of disease development. Infant respiratory viral infection and childhood asthma are the two most common acute and chronic diseases of childhood, respectively. Common clinical features and links between these diseases have long been recognized, with early life respiratory syncytial virus (RSV) and rhinovirus (RV) lower respiratory tract infections (LRTI) being strongly associated with increased asthma risk. However, there has long been debate over the role of these respiratory viruses in asthma inception. In this article, we will systematically review the evidence linking early life RSV and RV LRTI with asthma inception and whether they could therefore be targets for primary prevention efforts.
    American Journal of Respiratory and Critical Care Medicine 11/2014; 191(1). DOI:10.1164/rccm.201405-0901PP · 11.04 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Infections with human rhinovirus (HRV) are commonly associated with acute upper and lower respiratory tract disease and asthma exacerbations. The role that HRVs play in these diseases suggests it is important to understand host-specific or virus-specific factors that contribute to pathogenesis. Since species A HRVs are often associated with more serious HRV disease than species B HRVs, differences in immune responses they induce should inform disease pathogenesis. To identify species differences in induced responses, we evaluated 3 species A viruses, HRV 25, 31 and 36 and 3 species B viruses, HRV 4, 35 and 48 by exposing human PBMCs to HRV infected Calu-3 cells. To evaluate the potential effect of memory induced by previous HRV infection on study responses, we tested cord blood mononuclear cells that should be HRV naïve. There were HRV-associated increases (significant increase compared to mock-infected cells) for one or more HRVs for IP-10 and IL-15 that was unaffected by addition of PBMCs, for MIP-1α, MIP-1β, IFN-α, and HGF only with addition of PBMCs, and for ENA-78 only without addition of PBMCs. All three species B HRVs induced higher levels, compared to A HRVs, of MIP-1α and MIP-1β with PBMCs and ENA-78 without PBMCs. In contrast, addition of CBMCs had less effect and did not induce MIP-1α, MIP-1β, or IFN-α nor block ENA-78 production. Addition of CBMCs did, however, increase IP-10 levels for HRV 35 and HRV 36 infection. The presence of an effect with PBMCs and no effect with CBMCs for some responses suggest differences between the two types of cells possibly because of the presence of HRV memory responses in PBMCs and not CBMCs or limited response capacity for the immature CBMCs relative to PBMCs. Thus, our results indicate that different HRV strains can induce different patterns of cytokines and chemokines; some of these differences may be due to differences in memory responses induced by past HRV infections, and other differences related to virus factors that can inform disease pathogenesis.
    PLoS ONE 12/2014; 9(12):e114322. DOI:10.1371/journal.pone.0114322 · 3.53 Impact Factor

Full-text

Download
64 Downloads
Available from
May 29, 2014