The fight of viruses against apoptosis

Institut für Klinische und Molekulare Virologie, Schlossgarten 4, D-91054 Erlangen, Germany
Current Opinion in Genetics & Development (Impact Factor: 8.57). 02/1998; DOI: 10.1016/S0959-437X(98)80066-X

ABSTRACT The induction of apoptosis of virus-infected cells is an important host defense mechanism against invading pathogens. Some viruses express anti-apoptotic proteins that efficiently block apoptosis induced by death receptors or in response to stress signaled through mitochondria. Viral interference with host cell apoptosis leads to enhanced viral replication and may promote cancer.

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    ABSTRACT: Herpes simplex virus type 1 (HSV-1) is a cytolytic alpha-herpesvirus which profoundly impacts its host cells. It is now widely rec-ognized that consequences of HSV-1 infec-tion include the induction of programmed cell death, also known as apoptosis, and the concomitant synthesis of proteins which act to block this process. While our current un-derstanding of the precise mechanism by which apoptosis induction occurs remains elusive, several breakthrough studies have re-vealed much about how HSV-1 modulates the apoptotic process. In this chapter, we will review recent data focusing on the triggering of apoptosis by HSV-1, as well as evidence showing how this important human patho-gen interferes with the fundamental cell death process.
  • Frontiers in Bioscience 01/2004; 9(1-3):2106. DOI:10.2741/1320 · 4.25 Impact Factor
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    ABSTRACT: Apoptosis is a host defense mechanism that the cell uses to limit production of infectious pathogens. Although many bacteria, viruses and parasites can induce apoptosis in infected cells, some pathogens usually exhibit the ability to suppress the induction of apoptosis in the infected cells. Sophisticated evasion strategies of obligate intracellular parasites, in particular prevention of host cell apoptosis, are necessary to ensure successful replication. To study the ability of Eimeria tenella in this regard, in vitro experiments were performed applying Madin-Darby bovine kidney (MDBK) cells as host cell. We have demonstrated that productive infection of adherent cell lines by E. tenella resulted in an anti-apototic effect. This phenomenon was confirmed using in situ terminal deoxynucleotidyl transferase-mediated (TdT) deoxyuridine triphosphates (dUTP)-fluorescein nick end labeling (TUNEL) assay to detect apoptosis. Therefore, E. tenella could complete its cycle of productive infection while inducing anti-apoptosis in the infected cells. This finding might have implications for the pathobiology of E. tenella and other Eimeria species.
    06/2012; 35(2). DOI:10.7853/kjvs.2012.35.2.105