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. 1999 Aug;58(8):454–461. doi: 10.1136/ard.58.8.454

Mechanisms of viral pathogenesis in rheumatic disease

A PERL 1
PMCID: PMC1752929  PMID: 10419862

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Regulation of apoptosis pathways by viral proteins. Oxidants, ultra violet light, and corticosteroids trigger apoptosis by mitochondrial damage, which, in turn, leads to the release of caspase activating factors.112 This process is inhibited by bcl-2 and its viral homologues. Release of reactive oxygen intermediates causes increased production of FasL and DNA fragmentation. Fas ligand (FasL) crosslinks the Fas receptor (Fas/Apo1/CD95), which recruits an adapter protein with a Fas associated death domain (FADD). Viral FLIPs (vFLIPs) possess a death effector domain similar to those of FADD and caspase 8 and, thus, interrupt Fas signalling. While not shown, vFLIPs may also block TNF receptor mediated signalling through FADD shared by both the Fas and TNF pathways.113 Upon recruitment of caspase 8, its oligomerisation causes self cleavage and activation of downstream effector caspases.113 A caspase activated DN-ase cleaves chromosomal DNA. Oxidants and ultra violet light as well as ROI released from damaged mitochondria cause DNA fragmentation, which in turn activates p53. p53 induces oxidative stress and augments surface expression of the Fas receptor. HIV-1 tat increases mitochondrial ROI production thus increasing apoptosis. By contrast HBV pX protein interferes with the proapoptotic effects of p53.

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