Ebola virus-like particles protect from lethal Ebola virus infection

Warfield, Kelly L.; Bosio, Catharine M.; Welcher, Brent; Deal, Emily M.; Mohamadzadeh, Mansour; Schmaljohn, Alan L.; Aman, M. Javad; Bavari, Sina

doi:10.1073/pnas.2237038100

Cited by 227 publications

(268 citation statements)

References 53 publications

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“…Ebola VLP (eVLP) and Marburg VLP self-assemble and bud from cellular lipid rafts following expression of GP and VP40 in mammalian cells (27)(28)(29)(30)(31)(32). Mice and guinea pigs vaccinated with eVLPs are completely protected from lethal EBOV challenge (28,29,33); therefore, eVLPs represent a promising vaccine candidate for prevention of lethal EBOV infections.…”

mentioning

confidence: 99%

“…Mice and guinea pigs vaccinated with eVLPs are completely protected from lethal EBOV challenge (28,29,33); therefore, eVLPs represent a promising vaccine candidate for prevention of lethal EBOV infections. In this study, the mouse model of EBOV infection was used to examine the components of the immune responses that are required for eVLP-mediated protective immunity, which included humoral, cellular, and cytokine responses.…”

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confidence: 99%

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Induction of Humoral and CD8+ T Cell Responses Are Required for Protection against Lethal Ebola Virus Infection

Warfield

Olinger

Deal

et al. 2005

The Journal of Immunology

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127

142

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Ebola virus (EBOV)-like particles (eVLP), composed of the EBOV glycoprotein and matrix viral protein (VP)40 with a lipid membrane, are a highly efficacious method of immunization against EBOV infection. The exact requirements for immunity against EBOV infection are poorly defined at this time. The goal of this work was to determine the requirements for EBOV immunity following eVLP vaccination. Vaccination of BALB/c or C57BL/6 mice with eVLPs in conjunction with QS-21 adjuvant resulted in mixed IgG subclass responses, a Th1-like memory cytokine response, and protection from lethal EBOV challenge. Further, this vaccination schedule led to the generation of both CD4+ and CD8+ IFN-γ+ T cells recognizing specific peptides within glycoprotein and VP40. The transfer of both serum and splenocytes, but not serum or splenocytes alone, from eVLP-vaccinated mice conferred protection against lethal EBOV infection in these studies. B cells were required for eVLP-mediated immunity to EBOV because B cell-deficient mice vaccinated with eVLPs were not protected from lethal EBOV challenge. We also found that CD8+, but not CD4+, T cells are absolutely required for eVLP-mediated protection against EBOV infection. Further, eVLP-induced protective mechanisms were perforin-independent, but IFN-γ-dependent. Taken together, both EBOV-specific humoral and cytotoxic CD8+ T cell responses are critical to mediate protection against filoviruses following eVLP vaccination.

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confidence: 99%

mentioning

confidence: 99%

Induction of Humoral and CD8+ T Cell Responses Are Required for Protection against Lethal Ebola Virus Infection

Warfield

Olinger

Deal

et al. 2005

The Journal of Immunology

Self Cite

127

142

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“…or i.p. and vaccinated mice were fully protected against challenge with mouse-adapted ZEBOV [57]. Further study in mice suggests that a Th1-type immune response with CD8 + T lymphocytes is critical to the protection against ZEBOV challenge [55].…”

Section: Virus-like Particles (Vlp)mentioning

confidence: 93%

“…inoculation of the virus, the mouse model is not considered ideal for studies of the human disease. Mice have, however, been used as a tool for studying innate immunity, screening vaccine candidates, and elucidating protective epitopes for humoral and cellular immunity to ZEBOV [49][50][51][52][53][54][55][56][57][58].…”

Section: Animal Models Of the Human Diseasementioning

confidence: 99%

Status and challenges of filovirus vaccines

Reed

Mohamadzadeh

2007

Vaccine

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“…It has been reported that Ebola virus-like particles (eVLPs) are immunogenic, in vitro, as they activate mouse bone marrow-derived dendritic cells leading to the upregulation of MHC-I/II and elevated production of IL-6, IL-10, MIP-1a, and TNF-a [140].…”

Section: Altered Mhc Response During Viral Infectionmentioning

confidence: 99%

Immune Regulation and Evasion of Mammalian Host Cell Immunity During Viral Infection

et al. 2013

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The mammalian host immune system has wide array of defence mechanisms against viral infections. Depending on host immunity and the extent of viral persistence, either the host immune cells might clear/restrict the viral load and disease progression or the virus might evade host immunity by down regulating host immune effector response(s). Viral antigen processing and presentation in the host cells through major histocompatibility complex (MHC) elicit subsequent anti-viral effector T cell response(s). However, modulation of such response(s) might generate one of the important viral immune evasion strategies. Viral peptides are mostly generated by proteolytic cleavage in the cytosol of the infected host cells. CD8 ? T lymphocytes play critical role in the detection of viral infection by recognizing these peptides displayed at the plasma membrane by MHC-I molecules. The present review summarises the current knowledge on the regulation of mammalian host innate and adaptive immune components, which are operative in defence mechanisms against viral infections and the variety of strategies that viruses have evolved to escape host cell immunity. The understanding of viral immune evasion strategies is important for designing anti-viral immunotherapies.

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Ebola virus-like particles protect from lethal Ebola virus infection

Cited by 227 publications

References 53 publications

Induction of Humoral and CD8+ T Cell Responses Are Required for Protection against Lethal Ebola Virus Infection

Induction of Humoral and CD8+ T Cell Responses Are Required for Protection against Lethal Ebola Virus Infection

Status and challenges of filovirus vaccines

Immune Regulation and Evasion of Mammalian Host Cell Immunity During Viral Infection

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