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| http://dx.doi.org/10.1128/JVI.02629-15 | DOI Listing |
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Retraction for Watthanasurorot et al., Hijacking of Host Calreticulin Is Required for the White Spot Syndrome Virus Replication Cycle.
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Department of Comparative Physiology, Uppsala University, Uppsala, Sweden
Retraction for Watthanasurorot et al., A gC1qR Prevents White Spot Syndrome Virus Replication in the Freshwater Crayfish Pacifastacus leniusculus.
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Department of Comparative Physiology, Uppsala University, Uppsala, Sweden
Hijacking of host calreticulin is required for the white spot syndrome virus replication cycle.
J Virol
July 2014
Department of Comparative Physiology, Uppsala University, Uppsala, Sweden
We have previously shown that multifunctional calreticulin (CRT), which resides in the endoplasmic reticulum (ER) and is involved in ER-associated protein processing, responds to infection with white spot syndrome virus (WSSV) by increasing mRNA and protein expression and by forming a complex with gC1qR and thereby delaying apoptosis. Here, we show that CRT can directly interact with WSSV structural proteins, including VP15 and VP28, during an early stage of virus infection. The binding of VP28 with CRT does not promote WSSV entry, and CRT-VP15 interaction was detected in the viral genome in virally infected host cells and thus may have an effect on WSSV replication.
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