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Apoptosis In Viral Infections.
E. S. Razvi, R. Welsh
Published 1995 · Biology, Medicine
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Publisher Summary Although apoptosis can be induced by a number of stimuli, it has become apparent that there are common connecting themes linking the diverse systems covered in this chapter. Entry into the cell cycle can sensitize cells to apoptosis and abnormal regulation of growth-promoting genes, such as the protooncogenes c-myc and c-fos or of the transcription factor E2F, which can enhance expression of c-myc, results in apoptosis. Lymphocytes responding to viral infection are also more sensitive to apoptosis when in cycle. A second recurring theme is that the tumor suppressor protein p53 will shunt cells into an apoptotic pathway under the conditions of dysregulated expression of growth-promoting genes, and several viruses encode proteins that hind to p53 and interfere with its function. The protective effect of the Bcl-2 protein against apoptosis has been demonstrated repeatedly in viral systems. Apoptosis induced in target cells by either Sindbis or influenza virus infections is greatly inhibited in cells expressing bcl-2. A fourth theme involves the FasITNF receptor system. Activated lymphocytes responding to viral infections express high levels of Fas and are susceptible to apoptosis. Fas is related to the TNF receptor and both are down-regulated when TNF is added to cells. CTL and NK cells encode proteases (granzymes, fragmentins) that induce apoptosis in target cells. It is, therefore, clear that apoptosis plays a major role in viral infections and in the host response to them. Apoptosis is the mechanism, by which many viruses induce cell death and transforming viruses encode proteins that inhibit cellular apoptotic pathways. CTLs, NK cells, and cytotoxic cytokines, all kill virus-infected target cells through apoptotic pathways. In the infected host, T lymphocyte apoptosis plays a role in the natural history of the T cell responses to viral infection.
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