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Published on: October 7, 2011
Update on BK virus entry and intracellular trafficking
A S Dugan1, S Eash, W J Atwood
1Graduate Program in Pathobiology, Brown University, Providence, RI 02903, USA.
Summary
BK virus (BKV), a polyomavirus, invades host cells using sialic acid receptors and caveolae-mediated endocytosis. Understanding BKV entry is key to combating polyomavirus-associated nephropathy.
Area of Science:
- Virology
- Cell Biology
- Molecular Biology
Background:
- BK virus (BKV) is a double-stranded DNA virus in the Polyomaviridae family.
- BKV is recognized as the cause of polyomavirus-associated nephropathy.
- Understanding BKV's host cell invasion is crucial for studying its pathogenesis.
Purpose of the Study:
- To elucidate the early steps of BK virus (BKV) host cell entry and intracellular trafficking.
- To identify the specific mechanisms and cellular components involved in BKV infection.
Main Methods:
- Utilized cell culture models to observe BKV-host interactions.
- Investigated viral attachment, entry pathways, and intracellular transport.
Main Results:
- BKV utilizes an N-linked glycoprotein with alpha(2,3)-linked sialic acid as its cellular receptor.
- Viral entry occurs via caveolae-mediated endocytosis, a cholesterol-dependent process.
- Intracellular trafficking involves the cellular cytoskeleton, preceding nuclear localization.
Conclusions:
- The early viral lifecycle of BKV involves specific receptor binding and endocytic entry.
- Elucidating these early events provides insights into BKV's infectious spread and associated pathology.
- Further research into BKV's mechanism of infection can inform strategies against polyomavirus-associated nephropathy.
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