scholarly journals WSV056 Inhibits Shrimp Nitric Oxide Synthase Activity by Downregulating Litopenaeus vannamei Sepiapterin Reductase to Promote White Spot Syndrome Virus Replication

2021 ◽  
Vol 12 ◽  
Author(s):  
Wei Wang ◽  
Qin Zheng ◽  
Chen Yu ◽  
Changkun Pan ◽  
Peng Luo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Litopenaeus Vannamei ◽  
White Spot Syndrome Virus ◽  
White Spot ◽  
No Production ◽  
Sepiapterin Reductase ◽  
Copy Numbers ◽  
White Spot Syndrome ◽  
Oxide Synthase

Sepiapterin reductase (Spr) plays an essential role in the biosynthesis of tetrahydrobiopterin (BH4), a key cofactor of multiple enzymes involved in various physiological and immune processes. Suppression of Spr could result in BH4 deficiency-caused diseases in human and murine models. However, information on the biological function of Spr in invertebrates is limited. In this study, two Sprs (CG12116 and Sptr) from Drosophila melanogaster were found to be downregulated in transgenic flies overexpressing white spot syndrome virus (WSSV) immediate-early protein WSV056. CG12116 and Sptr exerted an inhibitory effect on the replication of the Drosophila C virus. A Litopenaeus vannamei Spr (LvSpr) exhibiting similarity of 64.1–67.5% and 57.3–62.2% to that of invertebrate and vertebrate Sprs, respectively, were cloned. L. vannamei challenged with WSSV revealed a significant decrease in LvSpr transcription and Spr activity in hemocytes. In addition, the BH4 co-factored nitric oxide synthase (Nos) activity in shrimp hemocytes was reduced in WSSV-infected and LvSpr knockdown shrimp, suggesting WSSV probably inhibits the LvNos activity through LvSpr downregulation to limit the production of nitric oxide (NO). Knockdown of LvSpr and LvNos caused the reduction in NO level in hemocytes and the increase of viral copy numbers in WSSV-infected shrimp. Supplementation of NO donor DETA/NO or double gene knockdown of WSV056 + LvSpr and WSV056 + LvNos recovered the NO production, whereas the WSSV copy numbers were decreased. Altogether, the findings demonstrated that LvSpr and LvNos could potentially inhibit WSSV. In turn, the virus has evolved to attenuate NO production via LvSpr suppression by WSV056, allowing evasion of host antiviral response to ensure efficient replication.

scholarly journals Small Molecule Inhibitors of White Spot Syndrome Virus: Promise in Shrimp Seedling Culture

2021 ◽  
Vol 22 (7) ◽  
pp. 3450
Author(s):  
Lei Liu ◽  
Li-Peng Shan ◽  
Yan Zhou ◽  
Jiong Chen
Keyword(s):  
Litopenaeus Vannamei ◽  
White Spot Syndrome Virus ◽  
Environmental Issues ◽  
Therapeutic Strategies ◽  
Effective Concentration ◽  
White Spot ◽  
Rapid Production ◽  
White Spot Syndrome ◽  
Median Effective Concentration ◽  
Artificial Pressure

Rapid production of prawn (Litopenaeus vannamei) under artificial pressure can result in a series of obvious challenges and is vulnerable to serious losses related to aquatic environmental issues and the unrestrained outbreak of white spot syndrome (WSS). However, to date, there are no therapeutic strategies to contain the spread of the virus. Here, we synthesized 27 coumarin deriv-atives and evaluated their anti-white spot syndrome virus (WSSV) activity in L. vannamei larvae. We demonstrated that electron-withdrawing and electron-giving substituent groups play an im-portant role in reducing toxicity and WSSV replication, respectively. Two coumarin C2 (2-amino-5-oxo-4-(p-tolyl)-4H,5H-pyrano[3,2-c]chromene-3-carbonitrile) and C7 (2-amino-4-(4-chlorophenyl)-5-oxo-4H,5H-pyrano[3,2-c]chromene-3-carbonitrile) were regarded as the most promising anti-WSSV compounds with maximum antiviral response <5% and median effective concentration <10 mg/L. The mortality of WSSV-infected larvae decreased by more than 60% after exposure to C2 and C7. With continuous immersion of C2 and C7 exchange, the mortality further decreased to 40% at 120 h.Additionally, C2 and C7 are the relatively stable in aquacultural water, making these agents

scholarly journals Draft Genome Sequence of White Spot Syndrome Virus Isolated from Cultured Litopenaeus vannamei in Mexico

2016 ◽  
Vol 4 (2) ◽  
Author(s):  
Libia Zulema Rodriguez-Anaya ◽  
Jose Reyes Gonzalez-Galaviz ◽  
Ramón Casillas-Hernandez ◽  
Fernando Lares-Villa ◽  
Karel Estrada ◽  
...  
Keyword(s):  
Disease Prevention ◽  
Genome Sequence ◽  
Litopenaeus Vannamei ◽  
White Spot Syndrome Virus ◽  
Draft Genome ◽  
Epidemiological Studies ◽  
Shrimp Farming ◽  
White Spot ◽  
Molecular Diagnostic ◽  
White Spot Syndrome

The first genome sequence of a Mexican white spot syndrome virus is presented here. White spot syndrome is a shrimp pandemic virus that has devastated production in Mexico for more than 10 years. The availability of this genome will greatly aid epidemiological studies worldwide, contributing to the molecular diagnostic and disease prevention in shrimp farming.

scholarly journals Protein kinase Cδ regulates endothelial nitric oxide synthase expression via Akt activation and nitric oxide generation

2008 ◽  
Vol 294 (3) ◽  
pp. L582-L591 ◽  
Author(s):  
Neetu Sud ◽  
Stephen Wedgwood ◽  
Stephen M. Black
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Promoter Activity ◽  
Dominant Negative ◽  
No Production ◽  
Enos Expression ◽  
Akt Activation ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

In this study, we explore the roles of the delta isoform of PKC (PKCδ) in the regulation of endothelial nitric oxide synthase (eNOS) activity in pulmonary arterial endothelial cells isolated from fetal lambs (FPAECs). Pharmacological inhibition of PKCδ with either rottlerin or with the peptide, δV1-1, acutely attenuated NO production, and this was associated with a decrease in phosphorylation of eNOS at Ser1177 (S1177). The chronic effects of PKCδ inhibition using either rottlerin or the overexpression of a dominant negative PKCδ mutant included the downregulation of eNOS gene expression that was manifested by a decrease in both eNOS promoter activity and protein expression after 24 h of treatment. We also found that PKCδ inhibition blunted Akt activation as observed by a reduction in phosphorylated Akt at position Ser473. Thus, we conclude that PKCδ is actively involved in the activation of Akt. To determine the effect of Akt on eNOS signaling, we overexpressed a dominant negative mutant of Akt and determined its effect of NO generation, eNOS expression, and phosphorylation of eNOS at S1177. Our results demonstrated that Akt inhibition was associated with decreased NO production that correlated with reduced phosphorylation of eNOS at S1177, and decreased eNOS promoter activity. We next evaluated the effect of endogenously produced NO on eNOS expression by incubating FPAECs with the eNOS inhibitor 2-ethyl-2-thiopseudourea (ETU). ETU significantly inhibited NO production, eNOS promoter activity, and eNOS protein levels. Together, our data indicate involvement of PKCδ-mediated Akt activation and NO generation in maintaining eNOS expression.

scholarly journals Induction of nitric oxide synthesis in J774 cells lowers intracellular glutathione: effect of modulated glutathione redox status on nitric oxide synthase induction

1997 ◽  
Vol 322 (2) ◽  
pp. 477-481 ◽  
Author(s):  
John S. HOTHERSALL ◽  
Fernando Q. CUNHA ◽  
Guy H. NEILD ◽  
Alberto A. NOROHNA-DUTRA
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
De Novo ◽  
Redox Status ◽  
No Production ◽  
Duration Of Treatment ◽  
Intracellular Glutathione ◽  
J774 Cells ◽  
Oxide Synthase ◽  
Glutathione Redox

Under pathological conditions, the induction of nitric oxide synthase (NOS) in macrophages is responsible for NO production to a cytotoxic concentration. We have investigated changes to, and the role of, intracellular glutathione in NO production by the activated murine macrophage cell line J774. Total glutathione concentrations (reduced, GSH, plus the disulphide, GSSG) were decreased to 45% of the control 48 h after cells were activated with bacterial lipopolysaccharide plus interferon γ. This was accompanied by a decrease in the GSH/GSSG ratio from 12:1 to 2:1. The intracellular decrease was not accounted for by either GSH or GSSG efflux; on the contrary, rapid export of glutathione in control cells was abrogated during activation. The loss of intra- and extracellular glutathione indicates either a decrease in synthesis de novo, or an increase in utilization, rather than competition for available NADPH. All changes in activated cells were prevented by pretreatment with the NOS inhibitor l-N-(1-iminoethyl)ornithine. Basal glutathione levels in J774 cells were manipulated by pretreatment with (1) buthionine sulphoximine (glutathione synthase inhibitor), (2) acivicin (γ-glutamyltranspeptidase inhibitor), (3) bromo-octane (glutathione S-transferase substrate) and (4) diamide/zinc (thiol oxidant and glutathione reductase inhibitor). All treatments significantly decreased the output of NO following activation. The degree of inhibition was dependent on (i) duration of treatment prior to activation, (ii) rate of depletion or subsequent recovery and (iii) thiol end product. The level of GSH did not significantly affect the production of NO, after induction of NOS. Thus, glutathione redox status appears to plays an important role in NOS induction during macrophage activation.

Transcriptome analysis reveals differential gene expression associated with white spot syndrome virus resistance in the shrimp Litopenaeus vannamei fed on functional diets

Aquaculture ◽  
2022 ◽  
Vol 547 ◽  
pp. 737434
Author(s):  
Monica Janeth Cabrera-Stevens ◽  
Arturo Sánchez-Paz ◽  
Fernando Mendoza-Cano ◽  
Cristina Escobedo-Fregoso ◽  
Trinidad Encinas-García ◽  
...  
Keyword(s):  
Gene Expression ◽  
Differential Gene Expression ◽  
Transcriptome Analysis ◽  
Litopenaeus Vannamei ◽  
Virus Resistance ◽  
White Spot Syndrome Virus ◽  
White Spot ◽  
Differential Gene ◽  
White Spot Syndrome
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