Question

Cell death (apoptosis) is a structured and organized process. Describe why the process of shrinking and fragmenting virally infected cells, as opposed to breaking open the cell membrane to cause death, is beneficial to the rest of the body. Predict reactions to the arrest of apoptosis within in an organism. Justify your answers with examples.

Answer 1

Apoptosis is a form of programmed cell death, .Apoptosis is referred to as “programmed” cell death because it happens due to biochemical instructions in the cell’s DNA. It is very complex cellular processes which is triggered by signal molecules that tell the cell to commit cellular 'suicide'

Their are two major types of apoptosis pathways are -

“intrinsic pathways,” in which a cell receives a signal to destroy itself from its own genes or proteins due to detection of DNA damage; and in “extrinsic pathways,” where a cell receives signal to undergo apoptosis from other cells in the organism. The extrinsic pathway may be triggered when a organism recognises that a cell has is no longer a good investment for the organism to support.

Apoptosis is an very important evolutionary adaptation as it allows organisms to destroy their own cells. It is important because cells with damaged DNA that could become cancerous.

When a cell is compelled to commit suicide or triggers for apoptosis, proteins called caspases go into action. They break down the important cellular components needed for survival, and they initiate the production of enzymes known as DNases, which destroy the DNA in the nucleus of the cell.. The cell undergoes shrinking process due distress signals and then the shrunken cells cleaned away macrophages, leaving no trace, so these cells does not cause the damage to nearby cells that necrotic cells do.

One example of modulation of apoptosis in adenoviruses. Infection with strains of adenovirus that lacked a functional EIB 19 kDa gene was observed to produce an entirely different phenotype than infection with wild-type viruses This phenotype was characterized by a dramatically enhanced cytopathic effect, together with degradation of host cell chromosomal DNA and viral DNA typical of apoptosis. The inability of EIB 19K loss-of-function mutants to prevent apoptosis resulted in the premature host cell death and reduction in the production of progeny virus. Further, the capacity of the adenovirus E1A oncogene to transform the host cell, dependent on the coexpression of the E1B 19K protein. The E1B 19K protein could be complemented by over-expression of Bcl-2, and comparison of amino acid sequence of viral protein and Bcl-2 identified the region of limited sequence homology (i.e. the BH domain) which proved to be essential for function. These observations is the example of adenoviruses to delay apoptosis of the host cell in order to proliferate efficiently and the capacity of the adenoviruses to ‘hijack’ host cell's apoptotic machinery.