Cellmediated maintenance of the intra and intercellular environment

As discussed above, long periods of passage of cells in culture as well as mutations in the genetic information carried by cells can alter their growth properties. Such changes can take place within the animal leading to formation of a tumor, but usually this does not happen. This is because the vertebrate body and the cells comprising it have a number of "check points" that respond to genetic alterations of individual cells. This is a major function of MHC-I mediated antigen presentation. When an abnormal epitope from a genetically damaged protein, which would normally not be expressed, is presented at the surface of the cell it triggers the destruction of the cell by a cytotoxic T lymphocyte. This interaction leads to the death of the cell by the apoptotic pathway. As noted in Chapter 8, Part II, apoptosis is a consequence of the action of specific cellular genes that lead to a phased shutdown of cellular functions and cell death. The process has a protective function in the body by inducing the death and elimination of highly differentiated cells no longer needed (such as effector cells of the immune system), aged cells, as well as cells with mutations in genes that normally function to limit cell division. It is important to understand that the apoptotic pathway leads to cell death without release of cellular contents to the immune system and resulting inflammation and potential pathology, rather it is a highly regulated process designed only to eliminate those cells that are no longer of value in the tissue in question. The apoptotic pathway should be contrasted with the other major route of cell death, necrosis, where the swelling and bursting of the cell targeted for death leads to inflammation in order to stimulate the immune response. The two processes are schematically outlined and contrasted in Fig. 10.3.

Obviously, it is of value for a virus replicating in a cell to ensure that the cell is maintained for a sufficient length of time to ensure an appropriate yield of virus, while at the same time limiting immune responses to the infection. Conversely, it is to the benefit of the cell and the organism composed of such cells to mount a controlled immune response as rapidly as possible as well as to eliminate infected tissue. It is the tension between these two processes that leads

Apoptosis

Mild convolution Chromatin compaction and segregation Condensation of cytoplasm

Nuclear fragmentation Blebbing Apoptotic bodies

Phagocytosis

Uninfected cell

Mild convolution Chromatin compaction and segregation Condensation of cytoplasm

Nuclear fragmentation Blebbing Apoptotic bodies

Phagocytosis

Apoptotic body

Uninfected cell

Phagocytic cell

Phagocytic cell

Apoptotic body

Necrosis

Chromatin clumping Swollen organelles Flocculent mitochondria

Disintegration

Uninfected cell

Uninfected cell

Disintegration

Release of

■>• intracelluar ->■ Inflammation contents

Fig. 10.3 Apoptosis vs necrosis in cell death to evolutionary change in both virus and host, and the manifestations of both processes lead to macroscopic and microscopic changes in virus-infected cells that defines cytopathology.

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