Natural presence of substitution R155K within hepatitis C virus NS3 protease from a treatment-naïve chronically infected patient
✍ Scribed by Philippe Colson; Nabil Brouk; Frédérique Lembo; Paul Castellani; Catherine Tamalet; René Gérolami
- Publisher
- John Wiley and Sons
- Year
- 2008
- Tongue
- English
- Weight
- 51 KB
- Volume
- 47
- Category
- Article
- ISSN
- 0270-9139
No coin nor oath required. For personal study only.
✦ Synopsis
mediated hepatitis and inhibition of hepatocellular regeneration is novel and most interesting.
There is copious evidence in the literature to suggest a connection between lipid accumulation within hepatocytes and their decreased propensity or ability for proliferation. 3 Likewise, there is evidence to suggest that key proinflammatory cytokines including tumor necrosis factor ␣ and others may modulate the development and progression of hepatosteatosis. [4][5][6] The ability of T cells to either directly or indirectly modify lipid accumulation within hepatocytes has not been investigated, though very recent preliminary studies by our laboratory would suggest that T cells themselves may indeed contribute to the progression of hepatosteatosis.
Together, the findings by Drs. Feng and Xu and our recent preliminary data provide an important and exciting connection between concanavalin A-induced, T cell-mediated liver injury and hepatocellular lipid accumulation. Future investigation into the direct mechanisms by which this occurs will provide the experimental and clinical community with important information regarding the impact of lymphocyte-mediated liver injury on the initiation or enhancement of secondary pathologies including hepatosteatosis.