Background:
HRVs infect the epithelial cells in both upper and lower respiratory tract. VP1 protein from capsid is responsible for virus entry to cells by attachment to ICAM-1, LDL, or CDHR3 cell-surface receptors. In this study, we investigated the spectrum of HRV serotypes in circulation, their genetic variability and immune responses of interferons plus inflammatory cytokines to determine the consequences for genetic variability.
Methods:
The study specimens were obtained from the pediatric patients presenting with cough and fever(n=374), attending OPD or those admitted to the ICU.Extracted viral RNA was reverse transcribed using random hexamers. Rhinovirus samples (n=102) were tested by conventional nested reverse transcription PCR (RT-PCR). Genetic sequencing was performed on 77 PCR +ve isolates on VP4/VP2 region
Results:
Nested RT-PCR based testing showed that 102 children were positive for HRV; of these 48 cases were HRV-A +ve, 29 cases were HRV-C +ve and 25 cases were untyped rhinoviruses.We observed a very low level (n=9) of co-infecting respiratory pathogens in the study population.Th1/Th2 profiling showed up regulation of 29 genes in HRV-A101 and HRV-C8 phenotypes. Th1 profiling revealed high IFN-? and IL-18 in HRV-A101 compared to HRV-C8.
Conclusions
We observed mutations among HRV-A serotypes- Serine- at position 18, 20, 21 and 23 at amino(N) terminal of VP4. This could affect the cross neutralizing capacity of the conserved epitopes thus having implications for their antiviral application. Robust Th1 response and a subdued Th2 response in HRV-A101 infected individuals could be responsible for the severity of disease.