Antibody-based immunotherapy of aciclovir resistant ocular herpes simplex virus infections

The increasing incidence of aciclovir- (ACV) resistant strains in patients with ocular herpes simplex virus (HSV) infections is a major health problem in industrialized countries. In the present study, the humanized monoclonal antibody (mAb) hu2c targeting the HSV-1/2 glycoprotein B was examined for...

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Veröffentlicht in:Virology (New York, N.Y.) N.Y.), 2017-12, Vol.512, p.194-200
Hauptverfasser: Bauer, Dirk, Keller, Jessica, Alt, Mira, Schubert, Axel, Aufderhorst, Ulrich Wilhelm, Palapys, Vivien, Kasper, Maren, Heilingloh, Christiane Silke, Dittmer, Ulf, Laffer, Björn, Eis-Hübinger, Anna Maria, Verjans, Georges M., Heiligenhaus, Arnd, Roggendorf, Michael, Krawczyk, Adalbert
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Sprache:eng
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Zusammenfassung:The increasing incidence of aciclovir- (ACV) resistant strains in patients with ocular herpes simplex virus (HSV) infections is a major health problem in industrialized countries. In the present study, the humanized monoclonal antibody (mAb) hu2c targeting the HSV-1/2 glycoprotein B was examined for its efficacy towards ACV-resistant infections of the eye in the mouse model of acute retinal necrosis (ARN). BALB/c mice were infected by microinjection of an ACV-resistant clinical isolate into the anterior eye chamber to induce ARN and systemically treated with mAb hu2c at 24h prior (pre-exposure prophylaxis) or at 24, 40, and 56h after infection (post-exposure immunotherapy). Mock treated controls and ACV-treated mice showed pronounced retinal damage. Mice treated with mAb hu2c were almost completely protected from developing ARN. In conclusion, mAb hu2c may become a reliable therapeutic option for drug/ACV-resistant ocular HSV infections in humans in order to prevent blindness. •Efficacy of an antibody-based immunotherapy in the ARN mouse model.•Mice were infected with an ACV resistant HSV-1 isolate to induce ARN.•Mice treated with the humanized antibody mAb hu2c were protected from ocular disease.
ISSN:0042-6822
1096-0341
DOI:10.1016/j.virol.2017.09.021