Abstract
Aim: We aimed to determine the functionality of rotavirus NSP3 dimers. Materials & methods: We expressed rhesus rotavirus NSP3 and determined the kinetics of host cell translation inhibition and the levels of accumulated dimerization intermediates and dimers. Results: We observed a linear kinetics of host cell translation inhibition, which correlated well with the sum of the dimerization intermediates and dimers. Treatment with 17-dimethylaminoethylamino-17-demethoxygeldanamycin reduced the accumulation of NSP3 dimers and potentiated host cell translation inhibition. Conclusion: Our results show that NSP3 dimer formation does not correlate with host cell translation inhibition and suggest that both NSP3 dimers and dimerization intermediates are functional and inhibit host cell translation.
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