Serum paraoxonase and arylesterase activities in various forms of hepatitis B virus infection

Duygu, Fazılet; Koruk, Süda Tekin; Aksoy, Nurten

doi:10.1002/jcla.20473

Cited by 21 publications

(18 citation statements)

References 28 publications

(32 reference statements)

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“…QS factors are secreted by Gram-negative bacteria in particular to regulate biofilm formation [118]. Paraoxonase activity is also decreased upon viral infection (for review, see [111]); this is reported for the hepatitis C virus [119], hepatitis B virus [120] or for the human immunodeficiency virus (HIV) [121]. PON1 was reported to participate in cholesterol efflux from the cell membrane to HDLs [122]; this may contribute to reduce the presence of cholesterol rafts that are necessary for viral infection.…”

Section: Focus On Hdl-bound Paraoxonasementioning

confidence: 97%

High-Density Lipoproteins Are Bug Scavengers

2020

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Lipoproteins were initially defined according to their composition (lipids and proteins) and classified according to their density (from very low- to high-density lipoproteins—HDLs). Whereas their capacity to transport hydrophobic lipids in a hydrophilic environment (plasma) is not questionable, their primitive function of cholesterol transporter could be challenged. All lipoproteins are reported to bind and potentially neutralize bacterial lipopolysaccharides (LPS); this is particularly true for HDL particles. In addition, HDL levels are drastically decreased under infectious conditions such as sepsis, suggesting a potential role in the clearance of bacterial material and, particularly, LPS. Moreover, "omics" technologies have unveiled significant changes in HDL composition in different inflammatory states, ranging from acute inflammation occurring during septic shock to low-grade inflammation associated with moderate endotoxemia such as periodontal disease or obesity. In this review, we will discuss HDL modifications associated with exposure to pathogens including bacteria, viruses and parasites, with a special focus on sepsis and the potential of HDL therapy in this context. Low-grade inflammation associated with atherosclerosis, periodontitis or metabolic syndrome may also highlight the protective role of HDLs in theses pathologies by other mechanisms than the reverse transport of cholesterol.

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Section: Focus On Hdl-bound Paraoxonasementioning

confidence: 97%

High-Density Lipoproteins Are Bug Scavengers

2020

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“…This enzymatic activity is important for the protection of the cells from oxidative damage for the lipid oxidation metabolism and for the innate immunity response. It is reduced during hepatitis virus B infection and correlates with the functional status of the liver [40]. The inhibition of adenosylhomocysteinase activity, obtained by adenosine dialdehyde, has been described as a potent inhibitor of vaccinia virus early protein synthesis and viral mRNA methylation, suggesting that adenosylhomocysteinase activity is important in the translation of viral proteins and virus replication [41].…”

Section: Gene Ontology and Pathway Enrichment Analysismentioning

confidence: 99%

In Silico Discovery of Candidate Drugs against Covid-19

Cava

Bertoli

Castiglioni

2020

Viruses

178

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Previous studies reported that Angiotensin converting enzyme 2 (ACE2) is the main cell receptor of SARS-CoV and SARS-CoV-2. It plays a key role in the access of the virus into the cell to produce the final infection. In the present study we investigated in silico the basic mechanism of ACE2 in the lung and provided evidences for new potentially effective drugs for Covid-19. Specifically, we used the gene expression profiles from public datasets including The Cancer Genome Atlas, Gene Expression Omnibus and Genotype-Tissue Expression, Gene Ontology and pathway enrichment analysis to investigate the main functions of ACE2-correlated genes. We constructed a protein-protein interaction network containing the genes co-expressed with ACE2. Finally, we focused on the genes in the network that are already associated with known drugs and evaluated their role for a potential treatment of Covid-19. Our results demonstrate that the genes correlated with ACE2 are mainly enriched in the sterol biosynthetic process, Aryldialkylphosphatase activity, adenosylhomocysteinase activity, trialkylsulfonium hydrolase activity, acetate-CoA and CoA ligase activity. We identified a network of 193 genes, 222 interactions and 36 potential drugs that could have a crucial role. Among possible interesting drugs for Covid-19 treatment, we found Nimesulide, Fluticasone Propionate, Thiabendazole, Photofrin, Didanosine and Flutamide.While the diagnosis of COVID-19 is based on the amplification of the viral genome in real-time PCR with specific probes, the current treatment of affected individuals is limited to a mixture of a broad-spectrum of antiviral drugs [6]. However, in many cases this pharmacological approach has proven to be totally ineffective.Screening drug studies on pangolin SARS-CoV-2, which is the human-related Coronavirus, demonstrated that three drugs (cepharanthine, selamectin and mefloquine hydrochloride) were effective in inhibiting viral replication, with cepharanthine potently inhibiting coronavirus infection at viral entry and post-entry viral replication [7]. The last drug is an anti-inflammatory and antineoplastic alkaloid approved for leukopenia and it is also proposed to inhibit the human immunodeficiency virus type 1 (HIV) entering in cells by reducing plasma membrane fluidity. In humans, it has a reduced toxicity.Mefloquine is the approved treatment for malaria and has antiviral activity against both MERS-CoV and SARS-CoV [8]. The antiviral mechanism of selamectin is still unknown, as it is used usually as a topical broad-spectrum parasiticide in little animals (e.g., cats and dogs).The entry of the virus in the cells is mediated by spike (S) glycoprotein; in particular, the spike 1 (S1) surface unit allows the attachment of the virus to cellular receptors. To allow the entry of the viral particles, the S protein is cleaved by cellular proteases at the S1/S2 and the S2 site. Then, the viral capside is fused with the cellular membrane, a process driven by the S2 subunit [9]. It has been described that SARS-CoV entrance is ...

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“…22 ROS have been shown to be significant mediators of various inflammatory processes, such as otitis media, maxillary sinusitis, adenotonsillitis, hepatitis, and Behçet's disease. 2,17,18,23,24 In COM patients, chronic inflammation in the middle ear is attributed to various mechanisms, such as the activation of macrophages and T-cells, the production of cytokines, and the presence of bacterial biofilms and endotoxins. 25,26 It is well known that each of these factors increases ROS production and causes tissue damage that should be eliminated by antioxidants.…”

Section: Discussionmentioning

confidence: 99%

“…32,33 Some studies have shown that PON1 prevents the oxidation of cell membrane lipids induced by ROS, which can result in acute and chronic inflammation. 23,24 PON1 activity can be affected by inflammation. Serum PON1 activity is decreased in a series of pathological conditions, including coronary artery disease, hypercholesterolemia, type 2 diabetes, polycystic ovarian syndrome, and renal insufficiency.…”

Section: Discussionmentioning

confidence: 99%