Hijacking of host calreticulin is required for the white spot syndrome virus replication cycle

Apiruck Watthanasurorot, Enen Guo, Sirinit Tharntada, Chu Fang Lo, Kenneth Söderhäll, Irene Söderhäll

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

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. Moreover, CRT was detected in the viral envelope of purified WSSV virions. CRT was also found to be of high importance for proper oligomerization of the viral structural proteins VP26 and VP28, and when CRT glycosylation was blocked with tunicamycin, a significant decrease in both viral replication and assembly was detected. Together, these findings suggest that CRT confers several advantages to WSSV, from the initial steps of WSSV infection to the assembly of virions. Therefore, CRT is required as a "vital factor" and is hijacked by WSSV for its replication cycle.

Original languageEnglish
Pages (from-to)8116-8128
Number of pages13
JournalJournal of Virology
Volume88
Issue number14
DOIs
Publication statusPublished - 2014 Jul

All Science Journal Classification (ASJC) codes

  • Immunology
  • Virology

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    Watthanasurorot, A., Guo, E., Tharntada, S., Lo, C. F., Söderhäll, K., & Söderhäll, I. (2014). Hijacking of host calreticulin is required for the white spot syndrome virus replication cycle. Journal of Virology, 88(14), 8116-8128. https://doi.org/10.1128/JVI.01014-14