Abstract
There is currently no effective treatment for the Ebola virus (EBOV) thus far. Most drugs and vaccines developed to date have not yet been approved for human trials. Two FDA-approved c-AbI1 tyrosine kinase inhibitors Gleevec and Tasigna block the release of viral particles; however, their clinical dosages are much lower than the dosages required for effective EBOV suppression. An α-1,2-glucosidase inhibitor Miglustat has been shown to inhibit EBOV particle assembly and secretion. Additionally, the estrogen receptor modulators Clomiphene and Toremifene prevent membrane fusion of EBOV and 50-90% of treated mice survived after Clomiphene/Toremifene treatments. However, the uptake efficiency of Clomiphene by oral administration is very low. Thus, I propose a hypothetical treatment protocol to treat Ebola virus infection with a cumulative use of both Miglustat and Toremifene to inhibit the virus effectively and synergistically. EBOV infection induces massive apoptosis of peripheral lymphocytes. Also, cytolysis of endothelial cells triggers disseminated intravascular coagulation (DIC) and subsequent multiple organ failures. Therefore, blood transfusions and active treatments with FDA-approved drugs to treat DIC are also recommended.Electronic supplementary materialThe online version of this article (doi:10.1186/s40249-015-0055-z) contains supplementary material, which is available to authorized users.
Highlights
There is currently no effective treatment for the Ebola virus (EBOV) far
Receptor Niemann-Pick C1 (NPC1) which may limit viral spread and force the virus to be exposed under the monitoring of the host immune system; (b) Blood transfusion which may control EBOV-induced acute disseminated intravascular coagulation (DIC), an excessive immune response
Current drugs and treatments Antiserum transfer Levels of neutralizing antibodies are always low in EBOV-infected patients, likely because of glycosylation of the viral surface glycoprotein GP [8,9]
Summary
There is currently no effective treatment for the Ebola virus (EBOV) far. Most drugs and vaccines developed to date have not yet been approved for human trials. I propose a hypothetical treatment protocol to treat Ebola virus infection with a cumulative use of both Miglustat and Toremifene to inhibit the virus effectively and synergistically. Viral infection often leads to excessive host immune responses, which may cause death. In this case, the body attacks itself [7]. I put forward a similar treatment protocol for Ebola virus infection, which includes two suggestions: (a) Combined inhibition of glycosylation of viral GP protein (by Miglustat, presumably) and EBOV intracellular. Receptor NPC1 (by Toremifene, presumably) which may limit viral spread and force the virus to be exposed under the monitoring of the host immune system; (b) Blood transfusion which may control EBOV-induced acute DIC, an excessive immune response
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