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The adenovirus life cycle is separated by the DNA replication process into two phases: an early and a late phase. [2] In both phases, a primary transcript that is alternatively spliced to generate monocistronic mRNAs compatible with the host's ribosome is generated, allowing for the products to be translated. [citation needed]
Adenovirus DNA replication begins at each end of the viral DNA, using the TP protein (rather than RNA) as a primer, so the viral DNA polymerase replicates every base of the genome. Membrane protein E3 RID-alpha and membrane protein E3 RID-beta performs a variety of molecular functions that contribute to inhibiting apoptosis.
Adenovirus early region 1A (E1A) is a gene expressed during adenovirus replication to produce a variety of E1A proteins. [1] It is expressed during the early phase of the viral life span. E1A encodes two major proteins in Ad5, translated after alternative splicing of the viral DNA transcript, that are able to cause a variety of different ...
Replication of the virus can also vary in one cell type, depending on the cell's current cell cycle phase. [110] The characteristic feature of the adeno-associated virus is a deficiency in replication and thus its inability to multiply in unaffected cells. Adeno-associated virus spreads by co-infecting a cell with a helper virus.
For adenovirus replication to occur, the host cell must be induced into S phase by viral proteins interfering with cell cycle proteins. The adenoviral E1A gene is responsible for inactivation of several proteins, including retinoblastoma, allowing entry into S-phase.
The fourth step in the viral cycle is replication, which is defined by the rapid production of the viral genome. How a virus undergoes replication relies on the type of genetic material the virus possesses. Based on their genetic material, viruses will hijack the corresponding cellular machinery for said genetic material.
E1B-19k blocks a p53-independent apoptosis mechanism. Without E1B-19k, degradation of both cellular and viral DNA occurs, in addition to premature host cell death during the lytic cycle, thus limiting viral replication. [3] E1B-19k mimics MCL1, which is a cellular antiapoptotic protein. [4]
To enter the cells, proteins on the surface of the virus interact with proteins of the cell. Attachment, or adsorption, occurs between the viral particle and the host cell membrane. A hole forms in the cell membrane, then the virus particle or its genetic contents are released into the host cell, where replication of the viral genome may commence.