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Overcoming drug-resistant herpes simplex virus (HSV) infection by a humanized antibody
Adalbert Krawczyk, Michaela A. E. Arndt, Ludger Grosse-Hovest, Wilko Weichert, Bernd Giebel, Ulf Dittmer, Hartmut Hengel, Dirk Jäger, Karl E. Schneweis, Anna M. Eis-Hübinger, Michael Roggendorf and Jürgen Krauss
Proceedings of the National Academy of Sciences of the United States of America
Vol. 110, No. 17 (April 23, 2013), pp. 6760-6765
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/42590512
Page Count: 6
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Despite the availability of antiviral chemotherapy, herpes simplex virus type 1 (HSV-1) and type 2 (HSV-2) infections remain a severe global health problem. Of particular concern is the growing incidence of drug resistance in immunocompromised patients, which stresses the urgency to develop new effective treatment alternatives. We have developed a humanized monoclonal antibody (mAb hu2c) that completely abrogates viral cell-to-cell spread, a key mechanism by which HSV-1/2 escapes humoral immune surveillance. Moreover, mAb hu2c neutralized HSV fully independent of complement and/or immune effector cell recruitment in a highly efficient manner. Prophylactic and therapeutic administration of mAb hu2c completely prevented infection-related mortality of severely immunodeficient mice being challenged with a lethal dose of HSV-1. The high neutralization capacity of mAb hu2c was fully maintained toward clinical HSV isolates being multiresistant to standard antiviral drugs, and infection was fully resolved in 7/8 nonobese diabetic/SCID mice being infected with a multidrug resistant HSV-1 patient isolate. Immunohistochemical studies revealed no significant cross-reactivity of the antibody toward human tissues. These features warrant further clinical development of mAb hu2c as an immunotherapeutic compound for the management of severe and particularly drugresistant HSV infections.
Proceedings of the National Academy of Sciences of the United States of America © 2013 National Academy of Sciences