uu.seUppsala University Publications
Change search
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf
Hijacking of Host Calreticulin Is Required for the White Spot Syndrome Virus Replication Cycle
Show others and affiliations
2014 (English)In: Journal of Virology, ISSN 0022-538X, E-ISSN 1098-5514, Vol. 88, no 14, 8116-8128 p.Article in journal (Refereed) Published
Abstract [en]

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.

IMPORTANCE White spot syndrome virus (WSSV) is a double-stranded DNA virus and the cause of a serious disease in a wide range of crustaceans that often leads to high mortality rates. We have previously shown that the protein calreticulin (CRT), which resides in the endoplasmic reticulum (ER) of the cell, is important in the host response to the virus. In this report, we show that the virus uses this host protein to enter the cell and to make the host produce new viral structural proteins. Through its interaction with two viral proteins, the virus “hijacks” host calreticulin and uses it for its own needs. These findings provide new insight into the interaction between a large DNA virus and the host protein CRT and may help in understanding the viral infection process in general.

Place, publisher, year, edition, pages
2014. Vol. 88, no 14, 8116-8128 p.
National Category
Biological Sciences
Identifiers
URN: urn:nbn:se:uu:diva-229435DOI: 10.1128/JVI.01014-14ISI: 000338442600039OAI: oai:DiVA.org:uu-229435DiVA: diva2:736787
Note

This article has been retracted.

See: Retraction: Hijacking of Host Calreticulin Is Required for the White Spot Syndrome Virus Replication Cycle (vol 88, pg 8116, 2014) DOI: 10.1128/JVI.02629-15

Available from: 2014-08-08 Created: 2014-08-07 Last updated: 2017-12-05

Open Access in DiVA

No full text

Other links

Publisher's full text
In the same journal
Journal of Virology
Biological Sciences

Search outside of DiVA

GoogleGoogle Scholar

doi
urn-nbn

Altmetric score

doi
urn-nbn
Total: 492 hits
CiteExportLink to record
Permanent link

Direct link
Cite
Citation style
  • apa
  • ieee
  • modern-language-association
  • vancouver
  • Other style
More styles
Language
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Other locale
More languages
Output format
  • html
  • text
  • asciidoc
  • rtf