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Title | Immunization with Components of the Viral Fusion Apparatus Elicits Antibodies That Neutralize Epstein-Barr Virus in B Cells and Epithelial Cells. |
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Journal, issue, pages | Immunity, Vol. 50, Issue 5, Page 1305-11316.e6, Year 2019 |
Publish date | May 21, 2019 |
Authors | Wei Bu / M Gordon Joyce / Hanh Nguyen / Dalton V Banh / Fiona Aguilar / Zeshan Tariq / Moh Lan Yap / Yusuke Tsujimura / Rebecca A Gillespie / Yaroslav Tsybovsky / Sarah F Andrews / Sandeep R Narpala / Adrian B McDermott / Michael G Rossmann / Yasuhiro Yasutomi / Gary J Nabel / Masaru Kanekiyo / Jeffrey I Cohen / |
PubMed Abstract | Epstein-Barr virus (EBV) causes infectious mononucleosis and is associated with epithelial-cell cancers and B cell lymphomas. An effective EBV vaccine is not available. We found that antibodies to ...Epstein-Barr virus (EBV) causes infectious mononucleosis and is associated with epithelial-cell cancers and B cell lymphomas. An effective EBV vaccine is not available. We found that antibodies to the EBV glycoprotein gH/gL complex were the principal components in human plasma that neutralized infection of epithelial cells and that antibodies to gH/gL and gp42 contributed to B cell neutralization. Immunization of mice and nonhuman primates with nanoparticle vaccines that displayed components of the viral-fusion machinery EBV gH/gL or gH/gL/gp42 elicited antibodies that potently neutralized both epithelial-cell and B cell infection. Immune serum from nonhuman primates inhibited EBV-glycoprotein-mediated fusion of epithelial cells and B cells and targeted an epitope critical for virus-cell fusion. Therefore, unlike the leading EBV gp350 vaccine candidate, which only protects B cells from infection, these EBV nanoparticle vaccines elicit antibodies that inhibit the virus-fusion apparatus and provide cell-type-independent protection from virus infection. |
External links | Immunity / PubMed:30979688 / PubMed Central |
Methods | EM (single particle) |
Resolution | 20.0 - 23.0 Å |
Structure data | EMDB-7798: EMDB-7799: |
Source |
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