Molecular and Biological Aspects of Apoptosis - Role of apoptosis in viral infections
7 important questions on Molecular and Biological Aspects of Apoptosis - Role of apoptosis in viral infections
Intracellular viral antigen presentation
- Viral antigen presentation by MHC I to activate immune cells
- Virus is cleaved by immuno-proteasome (LMP2), resulting in antigenic peptides.
- These peptides are transported to the ER, where they are loaded onto the groove of the MHC I complex.
- MHC I complexes are presented on cell surface, and recognized by CD8+ T cells
Extracellular viral antigen presentation
- Endolysosomal enzymes process the virus into peptides.
- The peptides bind to the groove of MHC II by displacing CLIP.
- The antigen loading process is mediated by HLA-DO and HLA-DM
- MHC II complexes are presented on cell surface, and recognized by CD4+ T cells
Viral inhibition of CTL-mediated killing
- Interfering with expression of cell-surface MHC I molecules, through: (i) endocytosis of MHC I, (ii) retention and degradation of MHC I in ER, (iii) modulation of the transporter for antigen processing necessary for the transport of viral peptides into ER
- Virus-encoded caspase inhibitors, inhibit apotosis by blocking caspase activity
- Virus encoded BCL2-like proteins inhibit apoptosis by blocking the release of cytochrome C from the mitochondria.
- Inhibition of granzyme B
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Viral regulation of extrinsic apoptotic pathway
- Block signaling via TNF by producing soluble decoy receptors
- vFLIPs contain two DEDs that interact with homologous DED of FADD and pro-caspase-8/10, blocking caspase activity and blocking death receptor-induced apoptosis
- vlCA binds and inhibits pro-caspase-8, lacks DED
- LMP1 self-aggregates and engages TRAF and TRADD molecules, activating NF-kB and NJK-dependent pathways
- Adenovirus E3 comples facilitates the removal of the death receptors Fas, TRAILR1 and TRIALR2 from infected cells. The receptors accumulate in late endocytic compartments, celss are desensitized to killing.
Inhibition of caspases by virus
- Viral IAPs inhibit active caspases by blocking the catalytic part of the enzyme or by E3 ubiquitin ligase activity targeting the caspase for degradation via proteasome
- Crma targets cysteine proteases
Inhibition of host apoptosis by viral BCL2-like protein
- Can prevent cell death, but often escape cellular regulatory mechanism that govern their cellular counterpart.
- Are shorter and often devoid of a membrane-anchored domain
Activation of host caspases by virus
- Facillitates virion release after host cell death
- Since the content of the cell will be packed into membrane-bound apoptotic bodies which are taken up by surrounding cells, the inflammatory response is limited allowing the virus to spread without detection.
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