| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 15173 | Computational Biology and Chemistry | 2012 | 6 Pages |
Parvovirus B19 has an extreme tropism for human erythroid progenitors. Here we propose the hypothesis explaining the tropism of human parvovirus B19. Our speculations are based on experimental results related to the capsid proteins VP1 and VP2. These proteins were not detectable in nonpermissive cells in course of these experiments, although the corresponding mRNAs were synthesized. Our interpretation of these results is an inhibition of translation in nonpermissive cells by human miRNAs. We bring support to our hypothesis and propose detailed experimental procedure to test it.
► We propose a different interpretation of the results of the published experiments. ► We propose the hypothesis explaining the tropism of human parvovirus B19. ► We explain the change in protein production in nonpermissive cells by codon optimization. ► Our explanation is inhibition of translation in nonpermissive cells by human miRNAs. ► We brought support to our hypothesis and proposed experimental procedures to test it.
