Key result
Overexpression of wild-type and constitutively active Arf6 in HeLa cells decreased CVB3 infection by 2.3- and 3.6-fold, while RNA interference of endogenous Arf6 increased viral titre 3.3-fold.
Population
Non-polarized HeLa cells infected with coxsackievirus type B3 (CVB3)
Comparison
Modulation of Arf6 activity and ERK activation vs Control HeLa cells
Design
Preclinical
Authors
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Arf6 restricts CVB3 infection in vitro; leaves open whether this pathway can be targeted to prevent viral myocarditis.
Arf6-dependent endocytosis, activated by CAR ligation and ERK signaling, redirects coxsackievirus type B3 into non-productive compartments, restricting viral infection.
Marchant et al. (2009) studied Coxsackievirus type B3 (CVB3) infection. Arf6 overexpression or RNA interference was evaluated on CVB3 infection and viral titre. Overexpression of wild-type and constitutively active Arf6 in HeLa cells decreased CVB3 infection by 2.3- and 3.6-fold, while RNA interference of endogenous Arf6 increased viral titre 3.3-fold.
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