Post-Exposure Vaccination Improves Gammaherpesvirus Neutralization 英文参考文献.docVIP

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Post-Exposure Vaccination Improves Gammaherpesvirus Neutralization 英文参考文献.doc

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Post-Exposure Vaccination Improves Gammaherpesvirus Neutralization 英文参考文献

Post-ExposureVaccinationImprovesGammaherpesvirus Neutralization LaurentGillet,JanetS.May,PhilipG.Stevenson* DivisionofVirology,DepartmentofPathology,UniversityofCambridge,AddenbrookesHospital,Cambridge,UnitedKingdom Herpesvirus carriers transmit infection despite making virus-specific antibodies. Thus, their antibody responses are not necessarily optimal. An important question for infection control is whether vaccinating carriers might improve virus neutralization.Theantibodyresponsetomurinegamma-herpesvirus-68(MHV-68)blockscellbinding,butfailstoblockand even enhances an IgG Fc receptor-dependent infection of myeloid cells. Viral membrane fusion therefore remains intact. AlthoughgH/gL-specificmonoclonalantibodiescanblockinfectionatapost-bindingstepclosetomembranefusion,gH/gLis arelativelyminorantibodytargetinviruscarriers.WeshowherethatgH/gL-specificantibodiescanblockbothFcreceptor- independentandFcreceptor-dependentinfections,andthatvaccinatingviruscarrierswithagH/gLfusionproteinimproves their capacity for virus neutralization both in vitro and in vivo. This approach has the potential to reduce herpesvirus transmission. Citation: Gillet L, May JS, Stevenson PG (2007) Post-Exposure Vaccination Improves Gammaherpesvirus Neutralization. PLoS ONE 2(9): e899. doi:10.1371/journal.pone.0000899 INTRODUCTION Persistent viruses have evolved to co-exist with established host immunity. Herpesviruses are among the most successful, and even when it fails to achieve neutralization. It is the need for transmissionratherthanthecapacitytocausediseasethatdrives viralevolution.Adiseasereadoutisthereforenotthebestwayto understandgamma-herpesvirusantibodyevasion. provide an archetype for many of the immune evasion The MHV-68 glycoprotein-specific antibody response pre- dominantly targets gp150,and gp150-specific antibodies account formostoftheFcR-dependentinfectionthatisdrivenbyimmune sera[21].Monoclonalantibodies(mAbs)directedagainstgH/gL block infection at a post-binding step cl