๐”– Bobbio Scriptorium
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Baculovirus interaction with host apoptotic pathways

โœ Scribed by Lois K. Miller


Publisher
John Wiley and Sons
Year
1997
Tongue
English
Weight
114 KB
Volume
173
Category
Article
ISSN
0021-9541

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โœฆ Synopsis


During infection, viruses may provoke a cellular which is required for all programmed cell death during nematode development ; Hen-pathway leading to apoptosis, a form of programmed cell death. An apoptotic response by the host cell can gartner & Horvitz, 1994;. The caspase family has expanded rapidly with the discovery result in premature cell death or abortive infection, thereby limiting the spread and/or pathogenesis of in-of numerous homologues in mammals.

In general, members of the caspase family are able fection in the organism (Clem and Miller, 1994). Many viruses, especially the DNA-containing viruses, possess to induce apoptosis when over-expressed in animal cells . Most one or more genes which, if expressed in a timely and efficient manner, can inhibit the apoptotic response of members of the family are synthesized as precursors which must be proteolytically processed, either by auto-the host cell. One of the most thoroughly characterized virus/cell apoptotic interactions is the interaction of ba-catalysis or by other proteases, to achieve a mature, active form. Some caspases may sense an apoptotic sig-culoviruses with the apoptotic pathways of their host insect cells. Baculoviruses induce apoptotic in a tissue nal and participate in a cascade to activate other components of the signal transduction pathway, but some and species-specific manner which can alter viral infectivity and host range (Clem and Miller, 1993; Clem et caspases, especially members of the sub-family which includes CED-3 and CPP32 (also known as YAMA or al., 1994). But baculoviruses possess two classes of antiapoptotic genes, p35 and iaps (inhibitors of apoptotic), caspase 3), are probably the actual executioners of cell death. The executioners would achieve the demise of which can block apoptosis induced by virus infection (Birnbaum et al., 1994; Clem & Miller, 1994a; Clem et the cell (e.g., chromatin fragmentation, cell surface blebbing, and apoptotic body formation) through pro-al.,


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