To: Mark Bartlett who wrote (8314 ) 12/29/2001 4:47:23 PM From: axial Read Replies (3) | Respond to Hi, Mark - sfaf.org "...Yet research has shown that none of the currently available therapies appears likely to eliminate completely HIV replication in most people with HIV. In part, this observation relates to (non-)adherence ." "...WF10 is designed to counteract abnormal macrophage activity. WF10 works by promoting phagocytosis and by reducing macrophages' production of TNF-alpha. The idea is that WF10 will help slow disease progression by inducing a more optimal immune response. Furthermore, WF10 may help decrease the likelihood of developing an OI by increasing the ability of macrophages to destroy opportunistic pathogens including fungi and mycobacteria. "specifically understood. Since that time, R+D on WF10 has continued. The question is, IYO, can you see WF10 being "fine-tuned" (and improved) as it is better understood?generalized modulation of the immune response, and does not breed resistance, do you see a possible path to more widespread antiviral use? (I'm aware of the Hep C trials). Where I'm going is: I'm trying to understand why WF10 would not be used as an adjunct to all viral infections, especially to limit the possible development of coincidental opportunistic infections (especially in severe or life-threatening cases).specific mechanism underlying WF10's success so far is still undiscovered; and if so, does the recent decision by DMX to acquire the rest of Oxo indicate promising R+D, ie., the possiblity of finding, and being able to generate, more specific immune-activators/modulators based on WF10? Or is it more likely a commercial transaction founded on the simple promise of WF10 "as is"?
