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Journal of Virology, February 2008, p. 1505-1517, Vol. 82, No. 3
0022-538X/08/$08.00+0     doi:10.1128/JVI.01331-07
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Cellular Entry of Lymphocytic Choriomeningitis Virus ^,

Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, California 92037,¹ Centro Nacional de Investigaciones Oncológicas, Melchor Fernández Almagro, 3, 28029 Madrid, Spain²

Received 19 June 2007/ Accepted 6 November 2007

In contrast to most enveloped viruses that enter the host cell via clathrin-dependent endocytosis, the Old World arenavirus lymphocytic choriomeningitis virus (LCMV) enters cells via noncoated vesicles that deliver the virus to endosomes, where pH-dependent membrane fusion occurs. Here, we investigated the initial steps of LCMV infection. We found that the attachment of LCMV to its cellular receptor -dystroglycan occurs rapidly and is not dependent on membrane cholesterol. However, subsequent virus internalization is sensitive to cholesterol depletion, indicating the involvement of a cholesterol-dependent pathway. We provide evidence that LCMV entry involves an endocytotic pathway that is independent of clathrin and caveolin and that does not require the GTPase dynamin. In addition, neither the structural integrity nor the dynamics of the actin cytoskeleton are required for infection. These findings indicate that the prototypic Old World arenavirus LCMV uses a mechanism of entry that is different from clathrin-mediated endocytosis, which is used by the New World arenavirus Junin virus, and pathways used by other enveloped viruses.

Published ahead of print on 28 November 2007.

Publication no. 18937 from the Molecular and Integrative Neurosciences Department of the Scripps Research Institute.

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