Lysis, cell virion release

Once the mature virion has been assembled, it is ready for release from the cell. The release of certain viruses (c.g. poliovirus) is accompanied by lysis of the ho.st cell membrane and cell death. Some of the enveloped viruses, however. are released by budding m exocyloyis. a process involving fusion between the viral envelope and the cell mcmbiaiK This process is nearly a reversal nf the entry process the host cell membrane remains intact under these cxinditioos and the cell may survive. 

If this altered ganglioside metabolism is related to some viral function, is it a function involved in transformation, productive infection, or both Mouse cells are permissive for polyoma virus and are rarely transformed by it (cf. Eckhart, 1969). Upon viral infection, the cells undergo a series of discrete events which result in cell lysis and release of new virions (cf. Weil and Kara, 1970). These include the appearance of viral-specific T-antigen, induction of cellular and viral DNA synthesis which is maximum at 25-30 hr postinfection, synthesis of viral coat proteins and new virions (present at 50 hr.), and, finally, cell lysis and virus release (5-7 days after infection). Swiss 3T3 and TAL/N cells were treated with sufficient polyoma virus to ensure infection of all cells. Hematoside UDP-GalN AcA-acetylgalactosaminyl-transferase was then determined at two key times after infection (Table V). The activity of this enzyme was similar to that seen in mock-infected cells. The results indicate that the reduced aminosugar transferase activity in virally transformed cells is specifically related to some transforming function of the viruses and is not a consequence of lytic infection of the cell. 

Ultimately, assembly occurs and release of virions from die cell occurs as a result of cell lysis. The features of replication of these simple RNA viruses are themselves fairly simple. The viral RNA itself functions as an mRNA and regulation occurs primarily by way of controlling access of ribosomes to the appropriate start sites on the viral RNA. 

There is an important immunological distinction between apoptosis and cell lysis . For example, lysis of a virus-infected cell will only release virions to spread infection, whereas apoptosis leads to the death of the cell and the contained pathogen. 

Reiease—Infected cell either ruptures suddenly (lysis), releasing all the newly formed virions at once, or disintegrates gradually, with slow release of virions. 

Figure 4-40 Illustrates the lytic cycle for T4 bacteriophage, a nonenveloped DNA virus that Infects E. coii. Viral capsid proteins generally are made In large amounts because many copies of them are required for the assembly of each progeny virion. In each Infected cell, about 100-200 T4 progeny virions are produced and released by lysis.

Most antivirals target one of five major viral processes (1) attachment of the virus to the host cell, (2) penetration and/or uncoating of the virus to release the viral nucleic acid into the host cell, (3) replication of the viral genome, (4) viral gene expression to produce viral proteins, and (5) assembly and maturation of the virus structure and the release of the progeny virions with or without lysis of the host cell. 

Each genus differs in morphology and phy-siochemical details. In general, virions are naked, polyhedral, dsRNA (10-12 segments). Synthesis and maturation take place in the host cell cytoplasm. Viruses are released via cell lysis. Virions contain ribosomes. 

Lytie and latent life cycles are two distinctive phases of AAV replication and persistence, respectively. Productive infection occurs in the presence of helper virus (such as adenovims, herpes virus, vaccinia virus) or genotoxic stimuli (such as ultraviolet [UV] irradiation, chemical carcinogens) (29). The propagation of both helper and AAV vimses leads to cell lysis and release of mature infectious virions. Up to 10 infectious AAV particles can be produced fiom a single cell (79). 

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