White Spot Syndrome

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Feng Yang - One of the best experts on this subject based on the ideXlab platform.

  • VP19 is important for the envelope coating of White Spot Syndrome virus.
    Virus research, 2019
    Co-Authors: Yongcong Hong, Huaina Qiu, Feng Yang
    Abstract:

    Abstract VP19 is a major envelope protein of White Spot Syndrome virus (WSSV), an important pathogen of farmed shrimp. However, the exact function of VP19 in WSSV assembly and infection is unknown. To understand the function of VP19, the gene was knocked down by RNA interference. We found that the dsRNA specific for vp19 gene dramatically reduced the replication of WSSV genomic DNA in infected animals. Further investigation by transmission electron microscopy showed that inhibition of VP19 prevented envelope coating of progeny virions, resulting in a high amount of immature virus particles without outer layer (envelope) in the host cells. This finding was further confirmed by SDS–PAGE analysis, which showed the loss of VP19 and other envelope proteins from the improperly assembled virions. These results suggest that VP19 is essential for WSSV envelope coating.

  • Characterization of White Spot Syndrome virus VP52B and its interaction with VP26.
    Virus genes, 2014
    Co-Authors: Fanyu Lin, Zuliang Jie, Luhong Hou, Feng Yang
    Abstract:

    White Spot Syndrome virus (WSSV) is one of the major pathogens of cultured shrimp. Identification of envelope protein interactions has become a central issue for the understanding of WSSV assembly. In this paper, WSSV envelope protein VP52B was fused with GST-tag and expressed in Escherichia coli BL-21(DE3). Immunogold-electron microscopy revealed that VP52B was located on the outside surface of WSSV virions. Far-Western blotting analysis suggested that VP52B might directly interact with a major viral envelope protein VP26, and their interaction was confirmed by GST pull-down assay. Further investigation showed that the VP52B binding domain was located between residues 135–170 of VP26. These findings will enhance our understanding of the molecular mechanisms of WSSV morphogenesis.

  • Identification of three immediate-early genes of White Spot Syndrome virus.
    Archives of virology, 2011
    Co-Authors: Fanyu Lin, He Huang, Feng Yang
    Abstract:

    Viral immediate-early (IE) genes generally encode regulatory proteins that are critical for viral replication. Their transcription, which is independent of de novo viral protein synthesis, is driven directly by host transcription factors. In this study, we examined promoter activities of 12 predicted regulatory genes of White Spot Syndrome virus (WSSV) belonging to the zinc finger protein family by EGFP-reporter assays in High Five cells. The results showed that the promoters of three genes (wsv056, wsv403 and wsv465) could drive reporter gene expression, and RT-PCR analysis revealed that their expression in WSSV-infected primary crayfish hemocytes was insensitive to the protein synthesis inhibitor cycloheximide (CHX). Therefore, they are IE genes of WSSV.

  • four major envelope proteins of White Spot Syndrome virus bind to form a complex
    Journal of Virology, 2009
    Co-Authors: Qing Zhou, Feng Yang
    Abstract:

    Early events in White Spot Syndrome virus (WSSV) morphogenesis, particularly the formation of viral membranes, are poorly understood. The major envelope proteins of WSSV are VP28, VP26, VP24, and VP19. Our previous results indicated that VP28 interacts with VP26 and VP24. In the present study, we used coimmunoprecipitation assays and pull-down assays to confirm that the four major proteins in the WSSV envelope can form a multiprotein complex. Yeast two-hybrid assays were also used to test for interactions among the four proteins. In summary, three pairwise protein interactions (VP19-VP28, VP19-VP24, and VP24-VP26) and one self-association (VP24-VP24) were identified for the first time.

  • Interaction of White Spot Syndrome virus VP26 protein with actin
    Virology, 2005
    Co-Authors: Xixian Xie, Feng Yang
    Abstract:

    VP26 protein, the product of the WSV311 gene of White Spot Syndrome virus (WSSV), is one of major structural proteins of virus. In this study, when purified virions were treated with Triton X-100 detergent, VP26 protein was present in both the envelope and the nucleocapsid fraction. We have rationalized this finding by suggesting that VP26 protein might be located in the space between the envelope and the nucleocapsid. By using a fluorescent probe method, we have investigated the interaction between VP26 protein and some proteins of host cells. Three major VP26-binding proteins were purified from crayfish hemocytes by affinity-chromatography, in which the protein with an apparent molecular mass of 42 kDa was identified as actin by mass spectrometry (MS). Moreover, the association of VP26 protein with actin microfilaments was confirmed by coimmunoprecipitation.

Jie Huang - One of the best experts on this subject based on the ideXlab platform.

  • The establishment and application of isothermal cross-priming amplification techniques in detecting penaeid shrimp White Spot Syndrome virus.
    Letters in applied microbiology, 2014
    Co-Authors: H.‐l. Yang, Jie Huang, B. Yang, Feng Liu, Qing-li Zhang
    Abstract:

    Significance and Impact of the Study: White Spot Syndrome, caused by White Spot Syndrome virus (WSSV), is the major disease threatening the shrimp aquaculture industry and leads to tens of billion dollars of economic losses in the world each year. This study established a CPA-based method for detecting WSSV, which is rapid, sensitive and specific. It is anticipated that this novel assay will be instrumental for diagnosis and surveillance of WSSV.

  • Multiple proteins of White Spot Syndrome virus involved in recognition of β-integrin
    Journal of biosciences, 2014
    Co-Authors: Jing-yan Zhang, Qing-hui Liu, Jie Huang
    Abstract:

    The recognition and attachment of virus to its host cell surface is a critical step for viral infection. Recent research revealed that β-integrin was involved in White Spot Syndrome virus (WSSV) infection. In this study, the interaction of β-integrin with structure proteins of WSSV and motifs involved in WSSV infection was examined. The results showed that envelope proteins VP26, VP31, VP37, VP90 and nucleocapsid protein VP136 interacted with LvInt. RGD-, YGL- and LDV-related peptide functioned as motifs of WSSV proteins binding with β-integrin. The β-integrin ligand of RGDT had better blocking effect compared with that of YGL- and LDV-related peptides. In vivo assay indicated that RGD-, LDV- and YGL-related peptides could partially block WSSV infection. These data collectively indicate that multiple proteins were involved in recognition of β-integrin. Identification of proteins in WSSV that are associated with β-integrin will assist development of new agents for effective control of the White Spot Syndrome.

  • Arginine kinase of Litopenaeus vannamei involved in White Spot Syndrome virus infection
    Gene, 2014
    Co-Authors: Qing-hui Liu, Guang-kuo Guan, Jie Huang
    Abstract:

    Abstract Virus–host interaction is important for virus infection. White Spot Syndrome virus VP14 contains transmembrane and signal peptides domain, which is considered to be important for virus infection. Until now, the function of this protein remains undefined. In this study, we explored the interaction of VP14 with host cell. A new shrimp protein (arginine kinase of Litopenaeus vannamei , LvAK) is selected and its localization in shrimp cells is also confirmed. Cellular localization of LvAK protein in shrimp hemocytes showed that LvAK was primarily located at the periphery of hemocytes and was scarcely detectable in the nucleus. Tissue distribution indicated that arginine kinase gene was spread commonly in the tissues and was highly present in shrimp muscle tissue. The expression of LvAK mRNA in muscle was significantly up-regulated after WSSV stimulation. Indirect immunofluorescence assay showed that LvAK interacted with VP14 in WSSV-infected shrimp. Injection of LvAK protein enhanced the mortality of shrimp infected with White Spot Syndrome virus (WSSV). These results showed that LvAK is involved in WSSV infection. Future research on this topic will help to reveal the molecular mechanism of WSSV infection.

  • VP292 of White Spot Syndrome virus Interacts with VP26.
    Indian journal of virology : an official organ of Indian Virological Society, 2012
    Co-Authors: Qing-hui Liu, Jie Huang
    Abstract:

    Interactions between virus structural proteins are suggested to be crucial for virus assembly. Many steps in the process of White Spot Syndrome virus (WSSV) assembly and maturation remain unclear. In this paper, we discovered a new interaction of WSSV VP292. Temporal-transcription analysis showed that VP292 is expressed in the late stage of WSSV infection. Western blot and matrix-assisted laser desorption ionization MS assays showed that VP292 interacts with VP26, a major envelope protein. Far-western blot provided further evidence for interaction between VP292 and VP26. These results collectively demonstrated that VP292 anchors to the envelope through interaction with VP26.

  • Rotifer cellular membranes bind to White Spot Syndrome virus (WSSV)
    Aquaculture, 2007
    Co-Authors: Dong-chun Yan, Shu-ying Feng, Jie Huang, Shuanglin Dong
    Abstract:

    Cell membranes from the rotifer, Brachionus urceus, were obtained by centrifugation and found to specifically bind White Spot Syndrome virus (WSSV) in vitro. This finding suggests that there is likely a WSSV receptor on the rotifer cell membrane and provides evidence that rotifers may be a host for WSSV.

Takeshi Kawarabata - One of the best experts on this subject based on the ideXlab platform.

  • Red swamp crawfish (Procambarus clarkii): An alternative experimental host in the study of White Spot Syndrome virus
    Acta Virologica, 2000
    Co-Authors: Minoru Maeda, Eiichi Mizuki, Y. Yoshizu, Chisa Yasunaga-aoki, Yukinori Takahashi, Toshiaki Itami, R. Tanaka, Takeshi Kawarabata
    Abstract:

    : The pathogenicity of White Spot Syndrome virus (WSSV) for the red swamp crawfish (Procambarus clarkii) was investigated after infection by intramuscular (i.m.) injection and oral route. The cumulative mortality of crawfish injected i.m. with WSSV reached 100% in 5 days. After oral feeding WSSV-infected kuruma shrimp (Penaeus japonicus) muscle tissues to the crawfish the cumulative mortality of this host reached 100% in 11 days. On reinfection trials, all the crawfish fed WSSV-infected crawfish muscle tissues died in 9 days. All the shrimp injected with a filtrate of infected crawfish heart tissues died in 12 days with typical signs of White Spot Syndrome (WSS). Electron microscopy clearly demonstrated that WSSV propagated in the cells of the crawfish midgut. This study showed that the red swamp crawfish can be used as alternative experimental host in the study of WSSV.

  • Red swamp crawfish (Procambarus clarkii): An alternative experimental host in the study of White Spot Syndrome virus
    Acta Virologica, 2000
    Co-Authors: Minoru Maeda, Eiichi Mizuki, Y. Yoshizu, Chisa Yasunaga-aoki, Yukinori Takahashi, Toshiaki Itami, R. Tanaka, Takeshi Kawarabata
    Abstract:

    : The pathogenicity of White Spot Syndrome virus (WSSV) for the red swamp crawfish (Procambarus clarkii) was investigated after infection by intramuscular (i.m.) injection and oral route. The cumulative mortality of crawfish injected i.m. with WSSV reached 100% in 5 days. After oral feeding WSSV-infected kuruma shrimp (Penaeus japonicus) muscle tissues to the crawfish the cumulative mortality of this host reached 100% in 11 days. On reinfection trials, all the crawfish fed WSSV-infected crawfish muscle tissues died in 9 days. All the shrimp injected with a filtrate of infected crawfish heart tissues died in 12 days with typical signs of White Spot Syndrome (WSS). Electron microscopy clearly demonstrated that WSSV propagated in the cells of the crawfish midgut. This study showed that the red swamp crawfish can be used as alternative experimental host in the study of WSSV.

Xufeng Jian - One of the best experts on this subject based on the ideXlab platform.

  • the effect of acute salinity change on White Spot Syndrome wss outbreaks in fenneropenaeus chinensis
    Aquaculture, 2006
    Co-Authors: Bo Liu, Yueqiang Guan, Xiuxian Song, Xufeng Jian
    Abstract:

    In order to observe the effect of salinity on disease resistance and White Spot Syndrome virus (WSSV) proliferation in Fenneropenaeus chinensis, shrimps with latent WSSV were subjected to two acute salinity changes from the original salinity of 22 ppt to 18 and 14 ppt in an hour, respectively. The total haemocyte count (THC) of the challenged group showed no evident change under salinity adjustments, but the phenoloxidase (PO) index declined significantly (P<0.05) corresponding to continuing acute salinity changes from the 24th to the 72nd hour. According to the WSSV load detected by quantitative real-time PCR method, it was found that WSSV carried by the challenged group and control group were significantly different (P<0.05); acute salinity change from 22 to 14 ppt led to the WSSV carried in the challenged group being significantly higher (P<0.05) than that of those surviving in 22 ppt, but salinity change from 22 to 18 ppt had no such effect. At the end of the 72-h experiment, the challenged group subjected to salinity change from 22 to 14 ppt had nearly 3 times the WSSV load as the control group with no salinity change. Therefore, salinity changes over a particular range could result in a decrease of immunocompetence and obvious WSSV proliferation in the shrimps, leading to White Spot Syndrome developing from a latent infection to an acute outbreak. (C) 2005 Elsevier B.V All rights reserved.

  • The effect of acute salinity change on White Spot Syndrome (WSS) outbreaks in Fenneropenaeus chinensis
    Aquaculture, 2005
    Co-Authors: Bo Liu, Yueqiang Guan, Xiuxian Song, Xufeng Jian
    Abstract:

    In order to observe the effect of salinity on disease resistance and White Spot Syndrome virus (WSSV) proliferation in Fenneropenaeus chinensis, shrimps with latent WSSV were subjected to two acute salinity changes from the original salinity of 22 ppt to 18 and 14 ppt in an hour, respectively. The total haemocyte count (THC) of the challenged group showed no evident change under salinity adjustments, but the phenoloxidase (PO) index declined significantly (P

Haizhi Quan - One of the best experts on this subject based on the ideXlab platform.

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