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reported today a new peer reviewed publication entitled, "The Quest for Effective Ebola Treatment; Ebola VP35 is an Evidence-Based Target for dsRNA Drugs" in the Nature Group's current issue of Emerging Microbes and Infections (October 29, 2014). This publication was authored by affiliates of Hemispherx. The publication provides an illustration of the crystallographic coordinates of a truncated VP35 complex with dsRNA.
Death from Ebola virus (EBOV) infection is associated with markedly impaired coagulation and innate immunity cascades, increased production of pro-inflammatory cytokines, profound immune suppression resulting in peripheral T lymphocyte apoptosis, and a lack of adaptive immunity (Fields Virology 923-956, 2013). By contrast, survivors of infection by EBOV develop an effective immune response with the production of EBOV neutralizing antibodies. Early events in EBOV infection influence the patient's ability to develop an effective immune response. The success of EBOV replication is dependent on viral inhibition of initial innate immune responses to infection. Disarming innate immune responses is a common mechanism employed by highly pathogenic human viruses, including those of the influenza and coronavirus families (Antiviral Res 100:615, 2013). EBOV is one of the more successful of the emerging highly pathogenic viruses in evasion of innate immune mechanisms.
VP35 is a multifunctional major virulence protein that is indispensable for EBOV replication. Double-stranded RNA (dsRNA) is a necessary component of viral replication, which initiates systemic signaling cascades that normally activate interferon (IFN) regulatory factors leading to the production of IFN-a/(type I IFNs). VP35 inhibition of dsRNA effectively disarms essential components of the innate immune response.