Key result
Coxsackievirus B3 nonstructural proteins 2B, 2BC, and 3A inhibit intracellular protein trafficking and secretion by targeting and disrupting the Golgi complex.
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Coxsackievirus B3 relies on multiple viral proteins (2B, 2BC, 3A) targeting the Golgi complex to block host protein secretion, which may explain its ability to evade strong CD8 T-cell responses.
Despite replicating to very high titers, coxsackieviruses do not elicit strong CD8 T-cell responses, perhaps because antigen presentation is inhibited by virus-induced disruption of host protein trafficking. Herein, we evaluated the effects of three viral nonstructural proteins (2B, 2BC, and 3A) on intracellular trafficking. All three of these proteins inhibited secretion, to various degrees, and directly associated with the Golgi complex, causing trafficking proteins to accumulate in this compartment. The 3A protein almost completely ablated trafficking and secretion, by moving rapidly to the Golgi, and causing its disruption. Using an alanine-scanning 3A mutant, we show that Golgi targeting and disruption can be uncoupled. Thus, coxsackieviruses rely on the combined effects of several gene products that target a single cellular organelle to successfully block protein secretion during an infection. These findings have implications for viral pathogenesis.
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Cornell et al. (2006) studied Coxsackievirus B3 infection. Viral nonstructural proteins (2B, 2BC, and 3A) was evaluated on Intracellular trafficking and secretion. Coxsackievirus B3 nonstructural proteins 2B, 2BC, and 3A inhibit intracellular protein trafficking and secretion by targeting and disrupting the Golgi complex.
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