ANTIVIRAL STRATEGIES FOR EBOLA VIRUS in .NET

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ANTIVIRAL STRATEGIES FOR EBOLA VIRUS
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Recombinant Vaccines
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Researchers have also examined the potential of heterologous live viral vectors in effectively preventing Ebola virus infection. Vesicular stomatitis virus (VSV)-based vectors are ne contenders, as VSV is known to elicit strong antibody and cellular immune responses.139 Rose and colleagues previously demonstrated that vaccination of mice with a recombinant VSV containing the glycoprotein of HIV-1 elicited high antibody titers as well as robust long-term memory and cellular immune responses.140,141 Based on this strategy, Feldmann and colleagues have generated a recombinant VSV vector expressing the Ebola virus GP. Protection against lethal challenge was conferred within a month and animals required only a single administration.30 7.7.4 Ebola Virus VLPs
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There is precedent in the literature for the use of VLPs as vaccines. Indeed, VLPs have been shown to generate humoral and cell-mediated immunity toward the viral components they are engineered to express.142 146 Because coexpression of the Ebola virus proteins GP and VP40 have been shown to induce ef cient formation of Ebola virus VLPs (eVLPs), and since both of these viral proteins are known to be immunogenic in animals, the use eVLPs as a vaccine is an important new area of investigation. The eVLPs generated by VP40 and GP coexpression are the most recently examined vaccine strategy being tested by researchers. For example, a study by War eld and co-workers demonstrated the ability of eVLPs to activate dendritic cells in vitro, induce a transient activation (days 1 5 postadministration) of B and T cells in vaccinated BALB/c mice, and elicit a dose-dependent antibody response.147 In a lethal challenge experiment, BALB/c mice vaccinated with 10 mg of eVLPs and subsequently infected with a high dose of Ebola virus (300 pfu) were 100% protected and showed no signs of morbidity for up to 28 days postchallenge.147 These preliminary results are promising, although examination of the protective ability of these eVLPs in primates is necessary. Notably, a VLP vaccine developed for the treatment of papillomavirus infection has recently entered Phase III human trials, suggesting precedent for the ef cacy of such a vaccine strategy.137 This vaccine approach may be improved upon by incorporating other viral proteins, such as NP, into the delivered VLP to enhance CTL responses, or by incorporating viral genes from various strains of Ebola virus to generate a more comprehensive vaccine. 7.7.5 Cell-Mediated Immunity
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For some time, development of a vaccine for Ebola virus had focused on the use of immune serum and elicitation of humoral responses as a defense. Because these therapies never proved to be completely successful in disease prevention, the need for robust cellular immune mechanisms was likely critical for ef cient protection. Thus, several investigations into the role of cell-mediated immunity for protection
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against Ebola virus infections have been initiated. For example, adoptive transfer of CTLs from mice vaccinated with a VEE replicon encoding viral NP into na ve mice protected the recipients from lethal challenge with Ebola virus.148 These ndings provided de nitive proof for a role of cell-mediated immunity in combating Ebola virus infection. With this knowledge, improvements to the aforementioned vaccine strategies have been attempted, focusing on induction of cellular immune responses. For example, immunization of mice with irradiated Ebola virus in liposomes (L) containing lipid A elicited CTL responses toward GP peptides.149 Liposomes serve as vehicles for the transfer of viral antigens, and, upon delivery, these peptides enter the major histocompatibility complex (MHC) I pathway, thereby eliciting CTL responses.150 Vaccination of mice with L-encapsidated irradiated Ebola virus protected mice from a 300-LD50 Ebola virus challenge, prevented the development of viremia, and generated CTLs to two GP peptides. Elicitation of GP CTLs appears to be due to the presence of the liposome, as immunization with unencapsidated virus did not generate CTLs.151
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