Abstract
Binding of viruses to cell surface molecules is an essential step in viral infection. In vitro studies suggested that the αvβ3 integrin receptor is the epithelial cell receptor for Hantaan virus (HTNV). Whether β3 is in vivo the only or central cellular receptor for HTNV infection is not known. To investigate the role of β3 integrin for cellular entry of HTNV, we established an HTNV infection model in newborn murine pups. Infected pups died at an average age of 14.2 ± 1.1 days with high levels of viral antigen detected in their brain, lung, and kidney. Pre-injection of blocking monoclonal antibodies (mAb) specific for either β3 or av prolonged survival significantly to a maximal average survival of 19.7 ± 1.5 days (P<0.01) and 18.4 ± 0.9 days (P<0.01), respectively. XT-199, a chemical blocker of the αvβ3 receptor also prolonged survival to 19.5 ± 1.3 days (P<0.01). In contrast to these receptor blockades, anti-HTNV antibody was not only able to prolong survival, but 20% of infected pups achieved long-term survival. An anti-murine β1 antibody comparatively prolonged survival (19.0 ± 1.2 days), suggesting that HTNV infection is partly mediated through integrin β1 receptors as well as through β3 receptors in vivo. Our data demonstrate that the β3 receptor is important for HTNV infection in vivo, but also suggest that HTNV may utilize additional receptors beyond β3 for cellular entry within an organism.
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Song, JW., Song, KJ., Baek, LJ. et al. In vivo characterization of the integrin β3 as a receptor for Hantaan virus cellular entry. Exp Mol Med 37, 121–127 (2005). https://doi.org/10.1038/emm.2005.16
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DOI: https://doi.org/10.1038/emm.2005.16
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