期刊
VIRUSES-BASEL
卷 14, 期 11, 页码 -出版社
MDPI
DOI: 10.3390/v14112428
关键词
human adenovirus; mRNA biogenesis; mRNA export; next-generation sequencing (NGS); nucleocytoplasmic RNA transport; temporal expression
类别
资金
- Freie und Hansestadt Hamburg
- German Bundesministerium fur Gesundheit (BMG)
- DAAD-CONACYT scholarship program
- CONACyT [A1-S-8696]
- Alexander von Humboldt Foundation
During human adenovirus infection, the late phase of viral replication results in a significant increase in viral late mRNA abundance, which outcompetes cellular mRNA biogenesis rather than selectively exporting viral mRNA.
It is well established that human adenoviruses such as species C, types 2 and 5 (HAdV-C2 and HAdV-C5), induce a nearly complete shutoff of host-cell protein synthesis in the infected cell, simultaneously directing very efficient production of viral proteins. Such preferential expression of viral over cellular genes is thought to be controlled by selective nucleocytoplasmic export and translation of viral mRNA. While detailed knowledge of the regulatory mechanisms responsible for the translation of viral mRNA is available, the viral or cellular mechanisms of mRNA biogenesis are not completely understood. To identify parameters that control the differential export of viral and cellular mRNAs, we performed global transcriptome analyses (RNAseq) and monitored temporal nucleocytoplasmic partitioning of viral and cellular mRNAs during HAdV-C5 infection of A549 cells. Our analyses confirmed previously reported features of the viral mRNA expression program, as a clear shift in viral early to late mRNA accumulation was observed upon transition from the early to the late phase of viral replication. The progression into the late phase of infection, however, did not result in abrogation of cellular mRNA export; rather, viral late mRNAs outnumbered viral early and most cellular mRNAs by several orders of magnitude during the late phase, revealing that viral late mRNAs are not selectively exported but outcompete cellular mRNA biogenesis.
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