ANTIVIRAL STRATEGIES FOR EBOLA VIRUS in .NET framework

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ANTIVIRAL STRATEGIES FOR EBOLA VIRUS
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replication in primary cells.79 Unfortunately, similar approaches using antisense RNA have thus far been unsuccessful when applied to Ebola virus replication.80 While the potential use of antisense RNA and siRNA as antiviral therapies is intriguing, much work remains to be done in both identifying appropriate, accessible genomic targets of these RNAs, and in optimizing the stability and delivery81 of these molecules to infected patients. 7.4 ANTIVIRAL RESPONSE TO INFECTION
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Filoviruses initially infect cells of the monocyte lineage such as macrophages. The virus subsequently spreads in a pantropic manner to many other cell types, including endothelial cells.82 While endothelial cells are not believed to represent an early target of viral replication, Ebola virus does appear to induce damage to these cells by indirect mechanisms, perhaps involving the secretion of host factors.83 It is noteworthy that endothelial cells are a viral target, as they are known to play an important role in mediating the host antiviral response by appropriating expression of immunomodulatory genes.84 Induction of the antiviral state in the host is attributed to the presence of double-stranded RNA (dsRNA) as well as other infection indicators. The presence of these indicators results in the synthesis and secretion of type 1 interferon (IFN), including variants of IFN-a and IFN-b.85 Numerous viruses have developed strategies to evade the type 1 IFN antiviral response,86 including Ebola virus.87 90 7.4.1 VP35 Protein and the IFN Response
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In addition to its vital role in viral RNA synthesis and assembly, VP35 has been shown to potentiate an inhibitory effect on the cellular IFN response to Ebola virus infection. A role for VP35 as an IFN antagonist came from an initial study by Basler and colleagues, which demonstrated that VP35 was able to complement an in uenza A virus lacking the NS1 protein, a well-documented IFN antagonist.89 A preliminary mechanism of action for this suppressive effect of VP35 appears to be the ability of VP35 to inhibit phosphorylation, and therefore activation of interferon regulatory factor (IRF)-3,91 a transcription factor. IRF-3 plays a central role in host cell IFN response to viral infection and has been shown to activate IFN-b and a subset of IFN-a genes (as reviewed92). Elucidation of the precise mechanism of VP35-mediated suppression of the IFN response is an active area of investigation, and a better understanding of the IFN antagonist activity associated with Ebola virus would clearly be important for future development of both antivirals and vaccines.89 7.4.2 Adenosine Analogues Revisited
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The surprisingly robust inhibition of Ebola virus-induced death conveyed by only a single dose of adenosine analogues C-c3 Ado and c3-Npc A77 prompted two
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ANTIVIRAL RESPONSE TO INFECTION
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follow-up studies to explore further the mechanisms of action of these analogues. Findings from the rst study indicated that the ef cacy of adenosine analogue administration was diminished when coadministered with antibodies targeting both IFN-a and IFN-b in a murine model of Ebola virus infection,93 suggesting a role for the type 1 IFN response in the effectiveness of this treatment. Results from the second study indicated that delivery of the analogue c3-NpcA resulted in a massive production of IFN-a by virus-infected cells. IFN-a levels were not elevated in the serum of drug-treated mice that were not infected with Ebola virus.94 However, the authors do point out that enhancement of IFN-a production was not observed in Ebola virus-infected primates treated with c3-NpcA, suggesting that rodent and nonhuman primate models of infection differ greatly in regard to immune induction.94 In addition to potentially enhancing type 1 IFN responses to viral infection, adenosine homologues may affect immune response to infection in a variety of other manners. Notably, two adenosine homologues were shown to impair proper functioning of murine macrophages,95 and C-c3 Ado was shown to block the release of interleukin-1 from activated human monocytes.96 Therefore, in addition to their ability to inhibit viral replication, it is intriguing to speculate that treatment with these drugs may additionally affect normal macrophage functioning, thereby rendering these cells poor hosts for supporting initial infection by Ebola virus.77
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