Key result
Adenovirus infection induces viral-host RNA trans-splicing that inhibits cell proliferation when overexpressed.
Heterologous trans-splicing occurs naturally during adenovirus infection and may contribute to the disruption of host cell function by inhibiting cell proliferation.
May suggest antiviral targets via trans-splicing modulation; leaves open relevance to human infections and clinical translation.
The impact of viral infection on normal host RNA processing remains largely unexplored. We postulated that the high abundance of virally derived nuclear RNA in infected cells could impact host cell RNA splicing and viability. To test for aberrant RNA splicing we examined trans-splicing following infection with the replication-competent adenovirus mutant d11520 that lacks E1B 55 kDa protein. Trans-splicing was observed between viral RNA and several cellular precursor mRNAs, including beta-actin and glyceraldehyde-3-phosphate dehydrogenase. Using a tetracycline-inducible model system simulating viral trans-splicing activity we observed that overexpression of a trans-splicing RNA specifically inhibited cell proliferation. These results demonstrate that heterologous trans-splicing occurs naturally during adenovirus infection and suggest that trans-splicing may contribute to disruption of cell function.
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Kikumori et al. (2002) studied Adenovirus infection. Adenovirus mutant d11520 infection and trans-splicing RNA overexpression was evaluated on Trans-splicing occurrence and cell proliferation. Adenovirus infection causes heterologous trans-splicing with host cellular transcripts, and overexpression of a trans-splicing RNA specifically inhibited cell proliferation.
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