The Adenovirus E3-10.4K/14.5K Complex Mediates Loss of Cell Surface Fas (CD95) and Resistance to Fas-induced Apoptosis

Overview

Journal J Virol

Publisher American Society for Microbiology

Date 1997 Oct 29

PMID 9343182

Citations 57

Authors

J Shisler

C Yang

B Walter

C F Ware

L R Gooding

Affiliations

Soon will be listed here.

Abstract

Cytotoxic T cells use Fas (CD95), a member of the tumor necrosis factor (TNF) receptor superfamily, to eliminate virus-infected cells by activation of the apoptotic pathway for cell death. The adenovirus E3 region encodes several proteins that modify immune defenses, including TNF-dependent cell death, which may allow this virus to establish a persistent infection. Here we show that, as an early event during infection, the adenovirus E3-10.4K/14.5K complex selectively induces loss of Fas surface expression and blocks Fas-induced apoptosis of virus-infected cells. Loss of surface Fas occurs within the first 4 h postinfection and is not due to decreased production of Fas protein. The decrease in surface Fas is distinct from the 10.4K/14.5K-mediated loss of the epidermal growth factor receptor on the same cells, because intracellular stores of Fas are not affected. Further, 10.4K/14.5K, which was previously shown to protect against TNF cytolysis, does not induce a loss of TNF receptor, indicating that this complex mediates more than one function to block host defense mechanisms. These results suggest yet another mechanism by which adenovirus modulates host cytotoxic responses that may contribute to persistent infection by human adenoviruses.

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References

Chiou S, Rao L, White E . Bcl-2 blocks p53-dependent apoptosis. Mol Cell Biol. 1994; 14(4):2556-63. PMC: 358623. DOI: 10.1128/mcb.14.4.2556-2563.1994. View

Ju S, Cui H, Panka D, Ettinger R, Marshak-Rothstein A . Participation of target Fas protein in apoptosis pathway induced by CD4+ Th1 and CD8+ cytotoxic T cells. Proc Natl Acad Sci U S A. 1994; 91(10):4185-9. PMC: 43749. DOI: 10.1073/pnas.91.10.4185. View

Hoffman P, Carlin C . Adenovirus E3 protein causes constitutively internalized epidermal growth factor receptors to accumulate in a prelysosomal compartment, resulting in enhanced degradation. Mol Cell Biol. 1994; 14(6):3695-706. PMC: 358737. DOI: 10.1128/mcb.14.6.3695-3706.1994. View

Chiou S, Tseng C, Rao L, White E . Functional complementation of the adenovirus E1B 19-kilodalton protein with Bcl-2 in the inhibition of apoptosis in infected cells. J Virol. 1994; 68(10):6553-66. PMC: 237076. DOI: 10.1128/JVI.68.10.6553-6566.1994. View

Stewart A, Tollefson A, Krajcsi P, Yei S, Wold W . The adenovirus E3 10.4K and 14.5K proteins, which function to prevent cytolysis by tumor necrosis factor and to down-regulate the epidermal growth factor receptor, are localized in the plasma membrane. J Virol. 1995; 69(1):172-81. PMC: 188561. DOI: 10.1128/JVI.69.1.172-181.1995. View

Alderson M, Tough T, Braddy S, Falk B, Schooley K, Goodwin R . Fas ligand mediates activation-induced cell death in human T lymphocytes. J Exp Med. 1995; 181(1):71-7. PMC: 2191813. DOI: 10.1084/jem.181.1.71. View

Vignaux F, Vivier E, Malissen B, Depraetere V, Nagata S, Golstein P . TCR/CD3 coupling to Fas-based cytotoxicity. J Exp Med. 1995; 181(2):781-6. PMC: 2191883. DOI: 10.1084/jem.181.2.781. View

Tewari M, Dixit V . Fas- and tumor necrosis factor-induced apoptosis is inhibited by the poxvirus crmA gene product. J Biol Chem. 1995; 270(7):3255-60. DOI: 10.1074/jbc.270.7.3255. View

Nagata S, Golstein P . The Fas death factor. Science. 1995; 267(5203):1449-56. DOI: 10.1126/science.7533326. View

10.

Cleveland J, Ihle J . Contenders in FasL/TNF death signaling. Cell. 1995; 81(4):479-82. DOI: 10.1016/0092-8674(95)90068-3. View

11.

Beidler D, Tewari M, Friesen P, Poirier G, Dixit V . The baculovirus p35 protein inhibits Fas- and tumor necrosis factor-induced apoptosis. J Biol Chem. 1995; 270(28):16526-8. DOI: 10.1074/jbc.270.28.16526. View

12.

Kolesnick R, Haimovitz-Friedman A, Fuks Z . The sphingomyelin signal transduction pathway mediates apoptosis for tumor necrosis factor, Fas, and ionizing radiation. Biochem Cell Biol. 1994; 72(11-12):471-4. DOI: 10.1139/o94-063. View

13.

Griffith T, Brunner T, Fletcher S, Green D, Ferguson T . Fas ligand-induced apoptosis as a mechanism of immune privilege. Science. 1995; 270(5239):1189-92. DOI: 10.1126/science.270.5239.1189. View

14.

White E . Life, death, and the pursuit of apoptosis. Genes Dev. 1996; 10(1):1-15. DOI: 10.1101/gad.10.1.1. View

15.

Chinnaiyan A, Tepper C, Seldin M, ORourke K, Kischkel F, Hellbardt S . FADD/MORT1 is a common mediator of CD95 (Fas/APO-1) and tumor necrosis factor receptor-induced apoptosis. J Biol Chem. 1996; 271(9):4961-5. DOI: 10.1074/jbc.271.9.4961. View

16.

Browning J, Miatkowski K, Sizing I, Griffiths D, Zafari M, Benjamin C . Signaling through the lymphotoxin beta receptor induces the death of some adenocarcinoma tumor lines. J Exp Med. 1996; 183(3):867-78. PMC: 2192357. DOI: 10.1084/jem.183.3.867. View

17.

Datta R, Kojima H, Banach D, Bump N, Talanian R, Alnemri E . Activation of a CrmA-insensitive, p35-sensitive pathway in ionizing radiation-induced apoptosis. J Biol Chem. 1997; 272(3):1965-9. DOI: 10.1074/jbc.272.3.1965. View

18.

Rao L, White E . Bcl-2 and the ICE family of apoptotic regulators: making a connection. Curr Opin Genet Dev. 1997; 7(1):52-8. DOI: 10.1016/s0959-437x(97)80109-8. View

19.

Yang J, Liu X, Bhalla K, Kim C, Ibrado A, Cai J . Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked. Science. 1997; 275(5303):1129-32. DOI: 10.1126/science.275.5303.1129. View

20.

Kluck R, Bossy-Wetzel E, Green D, Newmeyer D . The release of cytochrome c from mitochondria: a primary site for Bcl-2 regulation of apoptosis. Science. 1997; 275(5303):1132-6. DOI: 10.1126/science.275.5303.1132. View