Viral ubiquitin ligase WSSV222 is required for efficient white spot syndrome virus replication in shrimp

He, Fang; Syed, Syed Musthaq; Hameed, A.S. Sahul; Kwang, Jimmy

doi:10.1099/vir.0.008912-0

Cited by 31 publications

(17 citation statements)

References 33 publications

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“…Therefore, we performed the ubiquitination assay in vitro and in S2 cells. Both results showed that FcUbc could ubiquitinate WRD2 and WRD3 of WSSV277 and WSSV304, two of the four WSSV RING domain-containing proteins that have been reported to play a great part in WSSV pathogenesis (12,14,31). Although WRD1 and WRD4 of WSSV254 and WSSV462 were not ubiquitinated by FcUbc, FcUbc could possibly interact with them in other ways, and such proteins' interaction in vivo may also contribute to anti-WSSV response.…”

Section: Discussionmentioning

confidence: 80%

“…AAL89330.1), contain the RING-H2 motifs and may function as the E3 ligases (31). The E3 ligase activity of WSSV277 is involved in regulation of antiapoptosis by ubiquitin-mediated degradation of tumor suppressor-like (TSL) protein (12), and it is required for efficient WSSV replication (14). WSSV304 serves as a ubiquitin ligase E3 to sequester a shrimp ubiquitin-conjugating enzyme, Penaeus vannamei Ubc (PvUbc), for viral pathogenesis (31).…”

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confidence: 99%

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Enzyme E2 from Chinese White Shrimp Inhibits Replication of White Spot Syndrome Virus and Ubiquitinates Its RING Domain Proteins

Chen

Wang

Zhao

et al. 2011

J Virol

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Recent studies have shown that the ubiquitin (Ub) proteasome pathway (UPP) is closely related to immune defense. We have identified a ubiquitin-conjugating enzyme, E2, from the Chinese white shrimp, Fenneropenaeus chinensis (FcUbc). Injection of recombinant FcUbc protein (rFcUbc) reduced the mortality of shrimp infected with white spot syndrome virus (WSSV) and inhibited replication of WSSV. rFcUbc, but not a mutant FcUbc (mFcUbc), bound to WSSV RING domains (WRDs) from four potential E3 ligase proteins of WSSV in vitro. Importantly, rFcUbc could ubiquitinate the RING domains (named WRD2 and WRD3) of WSSV277 and WSSV304 proteins in vitro and the two proteins in WSSV-infected Drosophila melanogaster Schneider 2 (S2) cells. Furthermore, overexpression of FcUbc increased ubiquitination of WSSV277 and WSSV304 during WSSV infection. In summary, our study demonstrates that FcUbc from Chinese white shrimp inhibited WSSV replication and could ubiquitinate WSSV RING domain-containing proteins. This is the first report about antiviral function of Ubc E2 in shrimp.

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Section: Discussionmentioning

confidence: 80%

mentioning

confidence: 99%

Enzyme E2 from Chinese White Shrimp Inhibits Replication of White Spot Syndrome Virus and Ubiquitinates Its RING Domain Proteins

Chen

Wang

Zhao

et al. 2011

J Virol

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“…When the titre was measured by quantitative PCR, the viral titre was reduced twofold to 1 log reduction. RNAi targeting the viral ubiquitin ligase WSSV222, an anti-apoptosis protein of WSSV dropped the titre 20 fold from 2.6 9 10 7 to 1.3 9 10 6 [62]. RNAi against the capsid gene of PmergDNV reduced the titre from 3.4 9 10 3 to 3.6 9 10 2 [93].…”

Section: Effects On Viral Titrementioning

confidence: 99%

“…In almost all cases reported, survival increased following the administration of dsRNA, triggering of the RNAi pathway. RNAi has down regulated White Spot Syndrome Virus and allowed a 85 % reduction in mortality when targeting the VP28 envelope gene, suggested to play a role in WSSV infection [114,148]; 78 % reduction in mortality when targeting RR2 ribonucleotide reductase; 70 % reduction in mortality against VP19 envelope gene [154]; 47 % reduction in mortality against viral ubiquitin ligase [62]; 44 % reduction in mortality when antagonistic to the DNA polymerase. Similarly, when yellow head virus was down regulated by attacking its protease gene and a host host Rab7 GTPase, mortality was reduced by 90 % [143].…”

Section: Rnai With Special Reference To Controlling Viruses In Crustaceamentioning

confidence: 99%

RNA Interference with Special Reference to Combating Viruses of Crustacea

Fauce

Owens

2012

Indian J. Virol.

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RNA interference has evolved from being a nuisance biological phenomenon to a valuable research tool to determine gene function and as a therapeutic agent. Since pioneering observations regarding RNA interference were first reported in the 1990s from the nematode worm, plants and Drosophila, the RNAi phenomenon has since been reported in all eukaryotic organisms investigated from protozoans, plants, arthropods, fish and mammals. The design of RNAi therapeutics has progressed rapidly to designing dsRNA that can specifically and effectively silence disease related genes. Such technology has demonstrated the effective use of short interfering as therapeutics. In the absence of a B cell lineage in arthropods, and hence no long term vaccination strategy being available, the introduction of using RNA interference in crustacea may serve as an effective control and preventative measure for viral diseases for application in aquaculture.

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“…For example, adenovirus cannot replicate its genome if proteasome activity is inhibited (8). It has already been shown that WSSV encodes ubiquitin ligase (E3) and that this is required for WSSV pathogenesis and replication (14,38). This suggests that proteasome ␣4 might also be required for WSSV replication, and if so, then the dsRNA suppression of proteasome ␣4 at 25°C would account for the observed reduction in WSSV copy number.…”

Section: Discussionmentioning

confidence: 99%

The Role of Aldehyde Dehydrogenase and Hsp70 in Suppression of White Spot Syndrome Virus Replication at High Temperature

Lin

Hung

Leu

et al. 2011

J Virol

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High temperature (32 to 33°C) has been shown to reduce mortality in white spot syndrome virus (WSSV)-infected shrimps, but the mechanism still remains unclear. Here we show that in WSSV-infected shrimps cultured at 32°C, transcriptional levels of representative immediate-early, early, and late genes were initially higher than those at 25°C. However, neither the IE1 nor VP28 protein was detected at 32°C, suggesting that high temperature might inhibit WSSV protein synthesis. Two-dimensional gel electrophoresis analysis revealed two proteins, NAD-dependent aldehyde dehydrogenase (ALDH) and the proteasome alpha 4 subunit (proteasome ␣4), that were markedly upregulated in WSSV-infected shrimps at 32°C. Reverse transcription-PCR (RT-PCR) analysis of members of the heat shock protein family also showed that hsp70 was upregulated at 32°C. When aldh, proteasome ␣4, and hsp70 were knocked down by double-stranded RNA interference and shrimps were challenged with WSSV, the aldh and hsp70 knockdown shrimps became severely infected at 32°C, while the proteasome ␣4 knockdown shrimps remained uninfected. Our results therefore suggest that ALDH and Hsp70 both play an important role in the inhibition of WSSV replication at high temperature.White spot syndrome virus (WSSV) is a notorious pathogen in shrimp aquaculture. It has caused huge economic losses since it was first reported in 1992 in East Asia (6), and the virus is presently endemic in many parts of the world. WSSV is an ovoid to rod-shaped, enveloped, double-stranded DNA virus which belongs to the genus "Whispovirus" of the family Nimaviridae (35). The destructiveness of WSSV is partly due to its wide host range, which includes shrimp, crayfish, crabs, lobsters, and copepods (2, 9). In shrimps, mortality can reach 100% in 3 to 10 days after WSSV infection (20).Shrimps are exothermic animals, and unlike the case for endotherms, the body temperature of exotherms is directly susceptible to change depending on environmental conditions. Shrimp culture records show that outbreaks of WSSV are less likely to occur during warm seasons (29, 39), and there is other evidence suggesting that high temperature might protect shrimps from WSSV. Vidal et al. (34) reported that temperatures of 32 to 33°C can significantly reduce mortality in WSSVinfected shrimps. Other research has suggested that the water temperature needs to be maintained at 33°C for only 12 or 18 h per day in order to delay or reduce mortality in WSSV-infected shrimps (26). However, even though the use of warm water for shrimp cultivation has generally been accepted as beneficial by the shrimp culture industry and is already applied in some commercial shrimp farms, the exact mechanisms that underlie this phenomenon are still unknown. Granja et al. (12) proposed that high temperature might increase cell apoptosis and that this would help to prevent the replication of WSSV. However, apoptosis is no longer thought to be a principal protective factor against WSSV in shrimps (10, 40). Others have suggested that high tempera...

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Viral ubiquitin ligase WSSV222 is required for efficient white spot syndrome virus replication in shrimp

Cited by 31 publications

References 33 publications

Enzyme E2 from Chinese White Shrimp Inhibits Replication of White Spot Syndrome Virus and Ubiquitinates Its RING Domain Proteins

Enzyme E2 from Chinese White Shrimp Inhibits Replication of White Spot Syndrome Virus and Ubiquitinates Its RING Domain Proteins

RNA Interference with Special Reference to Combating Viruses of Crustacea

The Role of Aldehyde Dehydrogenase and Hsp70 in Suppression of White Spot Syndrome Virus Replication at High Temperature

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