eljefe19
Senior Member
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Thanks to @halcyon and @Hip I've been turned onto the Russian atypical antiviral, Arbidol.
I've compiled two relevant studies explicating the immuno-modulatory effects of Arbidiol.
"In vitro, antiviral and immunomodulatory activity of Arbidol and structurally related derivatives in HSV1-infected Human Keratinocytes."
In other beneficial ME/CFS medications such as Cimetidine, a key component is the decreasing of IL-10.
TGF-B is also immunosuppressive according to the above study, so reducing it is most likely beneficial as well. I believe the immuno-modulatory effects are what ultimately make this an effective drug, on paper, for ME/CFS. Case in point, the following study; (props to @halcyon).
CVB4 Arbidol study
I have some low to mid viral titers across the board, tried Valcyte, was a non-responder, and haven't taken any traditional AV's since. Just oxymatrine and others th1 cytokine inducing immune boosters. However, I've purchased Arbidiol and apparently will be the first guinea pig for the community. Wish me luck! Hope some of you found this interesting! Especially....if you have suspected chronic enterovirus infection.
Peace and love yall
I've compiled two relevant studies explicating the immuno-modulatory effects of Arbidiol.
"In vitro, antiviral and immunomodulatory activity of Arbidol and structurally related derivatives in HSV1-infected Human Keratinocytes."
An efficient elimination of the viral infection requires a pro-inflammatory host response and development of T helper (Th)1-type immunity ( Arena et al., 2010 ; Lucey et al., 1996 ; Romagnani, 1997 ). Mogensenet al. (2004) demonstrated that after early induction of the pro-inflammatory host response, HSV-1 down-regulates the pro-inflammatory cytokine production through the accumulation of two VPs, ICP4 and ICP27, whose transcription is induced by the release of tegumental protein VP16. By destabilizing the mRNAs of pro-inflammatory genes, these VPs delay cytokine production to an extent that allows the virus to replicate. Moreover, viral transactivating proteins ICP0 and VP16 induce the expression of the IL-10 and transforming growth factor (TGF)-β immunosuppressive cytokines. The up-regulation in the expression of IL-10 and TGF-β induced by HSV-1 in keratinocytes can be considered part of the viral strategy to avoid local immune defence mechanisms in the skin and to promote the establishment and maintenance of infection ( Zak-Prelich et al., 2001 ).
Cell lysates collected from HaCat cells at 3 and 6 h post-infection ( Figs 3 and 4 , respectively), in the presence or absence of ARB or its analogues, were tested for VP16 and ICP27 viral protein expression. ARB and its derivatives significantly reduced the levels of VP16 protein expression after 3 h of infection compared to HSV-1 alone, and the reduction was more marked after 6 h of treatment. This reduction was more intense with the analogues compared to that obtained with ARB treatment. In addition, the HSV-1-induced ICP27 protein expression was reduced by ARB and the analogues tested only after 6 h of infection. A small amount of constitutive VP16 protein was detected in the mock-infected cells at 3 h compared to untreated cells.
In other beneficial ME/CFS medications such as Cimetidine, a key component is the decreasing of IL-10.
TGF-B is also immunosuppressive according to the above study, so reducing it is most likely beneficial as well. I believe the immuno-modulatory effects are what ultimately make this an effective drug, on paper, for ME/CFS. Case in point, the following study; (props to @halcyon).
CVB4 Arbidol study
Coxsackie virus cannot be completely eliminated due to restrictive replication and impaired immune response, thus causing persistent infection. IL-10 plays a decisive role in the course of persistent viral infection. Umifenovir (Arbidol) is a broad-spectrum antiviral drug, with certain treatment effects on Coxsackie virus infection. Previously, we showed that in addition to inhibiting Coxsackie B4 (CVB4) infection, Umifenovir also down-regulates IL-10 induced by persistent CVB4 virus infection in vitro and in vivo. Here, BALB/c mouse spleen cells infected with CVB4 were used as a model to explore the mechanism by which Umifenovir affects IL-10 expression. We found that subcellular localization of p38 and MAPK-activated protein kinase 2 (MK2) played a very important role in IL-10 secretion, and Umifenovir significantly prevented p38-MK2 complex from exiting the cell nucleus. This in turn blocked the biological functions of the latter pathway, and inhibited the high expression of IL-10 induced by CVB4. These findings suggest that Umifenovir is a potential anti-CVB4 drug; most importantly, Umifenovir could be used to treat IL-10 induced persistent viral infection.
I have some low to mid viral titers across the board, tried Valcyte, was a non-responder, and haven't taken any traditional AV's since. Just oxymatrine and others th1 cytokine inducing immune boosters. However, I've purchased Arbidiol and apparently will be the first guinea pig for the community. Wish me luck! Hope some of you found this interesting! Especially....if you have suspected chronic enterovirus infection.
Peace and love yall