Endocytic pathway is indicated for white spot syndrome virus (WSSV) entry in shrimp

Huang, Zih-Jhan; Kang, Shih-Ting; Leu, Jiann-Horng; Chen, Lili

doi:10.1016/j.fsi.2013.05.028

Cited by 33 publications

(23 citation statements)

References 41 publications

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“…PmRab7 has a high homology to the small GTP-binding protein Pab7, which represents a family of w30 proteins that are localized on the surfaces of distinct membrane-enclosed compartments of exocytic and endocytic pathways (Chavrier et al, 1990;Feng et al, 1995). Huang et al (2013) previously reported that endocytosis was involved in the entry of WSSV into shrimp haemocytes. More work needs to be performed to determine the different viral and cellular proteins involved in this endocytic pathway.…”

Section: Discussionmentioning

confidence: 99%

Virus replication cycle of white spot syndrome virus in secondary cell cultures from the lymphoid organ of Litopenaeus vannamei

Desmarets

Gryse

et al. 2015

Journal of General Virology

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The replication cycle of white spot syndrome virus (WSSV) was investigated in secondary cell cultures from the lymphoid organ of Litopenaeus vannamei. The secondary cells formed a confluent monolayer at 24 h post-reseeding, and this monolayer could be maintained for 10 days with a viability of 90 %. Binding of WSSV to cells reached a maximum (73¡3 % of cells and 4.84¡0.2 virus particles per virus-binding cell) at 120 min at 4 8C. WSSV entered cells by endocytosis. The co-localization of WSSV and early endosomes was observed starting from 30 min post-inoculation (p.i.). Double indirect immunofluorescence staining showed that all cell-bound WSSV particles entered these cells in the period between 0 and 60 min p.i. and that the uncoating of WSSV occurred in the same period. After 1 h inoculation at 27 8C, the WSSV nucleocapsid protein VP664 and envelope protein VP28 started to be synthesized in the cytoplasm from 1 and 3 h p.i., and were transported into nuclei from 3 and 6 h p.i., respectively. The percentage of cells that were VP664-and VP28-positive in their nuclei peaked (50¡4 %) at 12 h p.i. Quantitative PCR showed that WSSV DNA started to be synthesized from 6 h p.i. In vivo titration of the supernatants showed that the progeny WSSV were released from 12 h p.i. and peaked at 18 h p.i. In conclusion, the secondary cell cultures from the lymphoid organ were proven to be ideal for examination of the replication cycle of WSSV.

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Section: Discussionmentioning

confidence: 99%

Virus replication cycle of white spot syndrome virus in secondary cell cultures from the lymphoid organ of Litopenaeus vannamei

Desmarets

Gryse

et al. 2015

Journal of General Virology

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“…Cholesterol is important for generating and maintaining the structure of caveolae, the critical endocytic vesicle used by many viruses, such as SV40 and tiger frog virus, to enter host cells via endocytosis (50,51). By using MbCD to block infection and showing the colocalization of virions with early endosomes, a recent study claimed that WSSV also adopts caveolae-mediated endocytosis to break through the membrane barrier (8). Although our present findings did not definitively determine whether the MjsvCL-CRT-mediated viral entry occurs through caveolae-mediated endocytosis, our observations by depleting and restoring membrane cholesterol supported the possibility of such a mechanism.…”

Section: Discussionmentioning

confidence: 99%

“…Because ie1 is an immediate early gene, its expression can be used to monitor viral entry into host cells. A previous study had shown that WSSV enters shrimp cells through caveolae-mediated endocytosis by treating shrimp cells with MbCD, which effectively inhibits this process by removal of cholesterol in the cell membrane (8). To determine whether MjsvCL-CRT-mediated viral entry is dependent on cholesterol, we used MbCD in this study to treat shrimp hemocytes (Fig.…”

Section: Mjsvcl-crt Enhancement Of Virus Infection Is Dependent On Chmentioning

confidence: 99%

“…The transmission of WSSV in the natural environment is mainly through oral ingestion (i.e., by healthy shrimp consuming dead or sick shrimp infected by the virus) (6,7). Recently, caveolae-mediated endocytosis was found to be likely critical for viral entry into shrimp cells (8). The principle envelope proteins of WSSV, viral protein 28 (VP28) and VP19, play important roles in virus entry and systemic infection (9,10).…”

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confidence: 99%

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Collaboration between a Soluble C-Type Lectin and Calreticulin Facilitates White Spot Syndrome Virus Infection in Shrimp

Wang

et al. 2014

The Journal of Immunology

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White spot syndrome virus (WSSV) mainly infects crustaceans through the digestive tract. Whether C-type lectins (CLs), which are important receptors for many viruses, participate in WSSV infection in the shrimp stomach remains unknown. In this study, we orally infected kuruma shrimp Marsupenaeus japonicus to model the natural transmission of WSSV and identified a CL (designated as M. japonicus stomach virus–associated CL [MjsvCL]) that was significantly induced by virus infection in the stomach. Knockdown of MjsvCL expression by RNA interference suppressed the virus replication, whereas exogenous MjsvCL enhanced it. Further analysis by GST pull-down and coimmunoprecipitation showed that MjsvCL could bind to viral protein 28, the most abundant and functionally relevant envelope protein of WSSV. Furthermore, cell-surface calreticulin was identified as a receptor of MjsvCL, and the interaction between these proteins was a determinant for the viral infection–promoting activity of MjsvCL. The MjsvCL–calreticulin pathway facilitated virus entry likely in a cholesterol-dependent manner. This study provides insights into a mechanism by which soluble CLs capture and present virions to the cell-surface receptor to facilitate viral infection.

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“…For the purpose of finding feasible approaches against this virus, more and more studies have focused on the entry process, especially on the recognition and attachment of the virus to its host cell surface (Huang et al, 2013;Huang et al, 2014;Zhang et al, 2014;Huang et al, 2015). Since entry into the cell is the first step for the initiation, dissemination, and maintenance of virus infection, blocking this process will have a significant inhibitory effect.…”

Section: Introductionmentioning

confidence: 99%

Computational identification of self-inhibitory peptides from white spot syndrome virus envelope protein VP28

Qiu

et al. 2019

Aquaculture Reports

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Since effective chemotherapeutics or preventive measures are still unavailable, finding feasible approaches against white spot syndrome virus (WSSV) has always been the vital subject in shrimp farming field. Envelope proteins are the ideal targets for antiviral strategies development due to their indispensable roles in virus entry, and inhibitory peptides targeting them have been proved to be promising in blocking virus infection. In this study, the Wimley-White interfacial hydrophobicity scale (WWIHS) in combination with known structural data was applied to identify potential inhibitory peptides that targeted the envelope protein VP28 of WSSV. Results showed that two potential inhibitory peptides were identified, one of which exhibited not only obvious antiviral activity, but also broad-spectrum antimicrobial activity. The inhibitory peptide identified here can serve as a lead compound for anti-WSSV strategies development.

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Endocytic pathway is indicated for white spot syndrome virus (WSSV) entry in shrimp

Cited by 33 publications

References 41 publications

Virus replication cycle of white spot syndrome virus in secondary cell cultures from the lymphoid organ of Litopenaeus vannamei

Virus replication cycle of white spot syndrome virus in secondary cell cultures from the lymphoid organ of Litopenaeus vannamei

Collaboration between a Soluble C-Type Lectin and Calreticulin Facilitates White Spot Syndrome Virus Infection in Shrimp

Computational identification of self-inhibitory peptides from white spot syndrome virus envelope protein VP28

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