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February 27, 2014Journal of VirologyOpen Access

Coxsackievirus A9 Infects Cells via Nonacidic Multivesicular Bodies

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Population

Cells infected with Coxsackievirus A9 (CVA9)

Design

Preclinical

Authors

MHMoona HuttunenUniversity of JyväskyläMWMatti WarisResearch Council of FinlandRKRitva KajanderUniversity of Turku

Discussion

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Overview

Identifies MVB-dependent CVA9 entry as a potential target; leaves open whether PLC or Rac1 inhibition yields clinical antivirals.

Structured PICO

P
Population
Cells infected with Coxsackievirus A9 (CVA9)
I
Intervention
Inhibitors of phospholipase C (PLC), Rac1, and Na+/H+ exchanger; wild-type form of Hrs; dominant negative form of VPS4; Bafilomycin A1
O
Outcome
Viral internalization, uncoating, and infection mechanisms

CVA9 uses a nonclathrin, nonacidic pathway involving neutral multivesicular bodies for cellular infection.

Cite This Study

Huttunen et al. (2014) studied this question.

synapsesocial.com/papers/6a87cd750112b7b407bb50d2https://doi.org/10.1128/jvi.03275-13
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Structural and Functional Analysis of Coxsackievirus A9 Integrin α v β 6 Binding and Uncoating2013 · 52 citations
  2. 2Dynamin- and Lipid Raft-Dependent Entry of Decay-Accelerating Factor (DAF)-Binding and Non-DAF-Binding Coxsackieviruses into Nonpolarized Cells2009 · 73 citations
  3. 3Involvement of β2-microglobulin and integrin αvβ3 molecules in the coxsackievirus A9 infectious cycle1999 · 54 citations
  4. 4Internalization of Echovirus 1 in Caveolae2002 · 219 citations
  5. 5Characterization of the early endosome and putative endocytic carrier vesicles in vivo and with an assay of vesicle fusion in vitro.1989 · 588 citations