AI Article Synopsis
- The study examines the role of the poly(A) tail in the replication of hepatitis A virus (HAV) RNA genomes, revealing its importance for stability and replication.
- A tailless HAV genome was found to have a shorter lifespan and could not replicate in non-dividing (quiescent) cells, while a poly(A)-containing genome thrived.
- The results indicate that the poly(A) tail can be restored in dividing cells, and the amount of infectious virus produced varies with the cell cycle stages, suggesting regulation by cellular factors.
Article Abstract
The precise role of the poly(A) tail at the 3' end of the picornavirus RNA genome and the cellular factors that control its homeostasis are unknown. To assess the importance of the poly(A) tail for virus replication, the genome of the slowly replicating hepatitis A virus (HAV) with and without a poly(A) tail was studied after transfection into cells maintained under various conditions. A tailless HAV genome had a shorter half-life than a poly(A)-containing genome and was unable to replicate in quiescent cells. In dividing cells, the tailless RNA gave rise to infectious virus with a restored poly(A) tail of up to 60 residues. Cells arrested at the G(0) and the G(2)/M phase produced lower amounts of infectious HAV than cells in the G(1) phase. These data suggest that the 3' poly(A) tail of HAV can be restored with the help of a cellular and/or viral function that is regulated during the cell cycle.
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| http://dx.doi.org/10.1099/vir.0.80644-0 | DOI Listing |
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