Journal
VIROLOGY
Volume 369, Issue 1, Pages 1-11Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2007.07.014
Keywords
Pichinde virus; lassa virus; arenavirus; cholesterol; viral entry; hemorrhagic fever; clathrin
Categories
Funding
- NIAID NIH HHS [R01 AI063513, T32 AI007536-08, T32 AI07536, 1R01AI063513-01A2, U54 AI057156, T32 AI007536] Funding Source: Medline
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Arenaviruses are important causes of viral hemorrhagic fevers in humans. Arenavirus infection of cells occurs via a pH-dependent endocytic route, but detailed studies of entry pathways have not been done. We investigated the role of cell membrane cholesterol, caveolae, and clathrin coated pits in infection by Lassa virus (LASV), which utilizes alpha-dystroglycan (alpha-DG) as a receptor, and Pichinde virus (PICV), which does not. Depletion of cellular cholesterol by treatment with methyl betacyclodextrin (M beta CD) or nystatin/progesterone inhibited PICV replication and transfer of packaged marker gene by LASV or PICV pseudotyped retroviral particles. In cells lacking caveolae due to silencing of the caveolin-1 gene, no inhibition of PICV infection or LASV pseudotype transduction was observed. However, PICV infection and LASV and PICV pseudotype transduction was inhibited when an Eps15 dominant negative mutant was used to inhibit clathrin-mediated endocytosis. Altogether, the results indicate that diverse arenaviruses have a common requirement for cell membrane cholesterol and clathrin mediated endocytosis in establishing infection.
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