HRV2 vs. HRV16 – variation in the nuclear effects of Group-A rhinovirus infection (#329)
Human rhinovirus (HRV) is a positive sense RNA virus that is a major cause of upper respiratory tract infections and contributes significantly to virus-induced asthma exacerbations. Despite replicating in the cytoplasm, HRV has a significant impact on nuclear transport and nuclear localisation of host proteins. A number of studies have identified differences between HRV serotypes, with respect to host response, protease activity and replicative ability.
Here we report the sero-specific effects of two group A human rhinovirus serotypes, the minor group HRV2 and the major group HRV16, on nuclear transport and nuclear protein localisation. Using Western analysis, immunofluorescence and real time PCR of infected cell samples, we show that HRV2 replicates at a faster rate than HRV16, which correlates with earlier production of viral proteases and disruption of host nuclear transport. In addition, we show the mislocalisation of the host protein SC35 and Sam68 occur at similar time points after infection with HRV2 or HRV16. Interestingly, the mislocalisation of hnRNP-C1/C2 is delayed in HRV16 infection, and appears to correlate with more complete disruption of nuclear pore components. It therefore appears that mislocalisation of select host nuclear proteins occurs irrespective of the extent of nuclear pore degradation.