scholarly journals Gene similarity between hepatitis C virus and human proteins: A blood transfusion problem

2005 ◽  
Vol 58 (11-12) ◽  
pp. 582-586 ◽  
Author(s):  
Nada Vasiljevic ◽  
Ljiljana Markovic
Keyword(s):  
Hepatitis C ◽  
Growth Factor ◽  
Tyrosine Kinase ◽  
Nitrogen Oxide ◽  
Molecular Mimicry ◽  
Highly Sensitive ◽  
Nitrogen Oxide Synthase ◽  
Human Proteins ◽  
Hepatic Growth Factor ◽  
Oxide Synthase

Introduction Hepatitis C is a post-transfusion hepatitis which causes serious problems in blood transfusion. Blood testing requires highly sensitive and specific assays with high predictive value. Genomic characteristics of hepatitis C virus According to recommendations of International Association for the study of Liver Diseases etiological diagnosis of hepatitis is based on highly sensitive third generation assays: epitopes in the NS5 region comprising noncoding sequence UTR with 324-341 well conserved pair of homologous basis in 92% HCV genomes, therefore appropriate for virus RNA detection. Development of assays for hepatitis virus The first generation of immunoenzyme tests (IET) were based on detection of antibodies on antigen c 100-3, which is a part of the NS4 region of HCV genome. The second generation of tests with two recombinant proteins - c22-3 and c200, achieved higher sensitivity of assays. The third generation included epitopes from NS5 region, and removed the antigen c100-3. Development of autoimmunity Autoimmunity is a pathophysiological mechanism that's leads to chronic inflammatory diseases. Autoimunity is characterized by loss of tolerance towards self-antigens. Viral hepatitis C is associated with development of autoimmune phenomena. Molecular mimicry Molecular mimicry, as a mechanism of autoimmunity, was investigated to establish cross-Reactive immune reactions between HCV antigen and human nitrogen-oxide synthase, Tyrosine kinase Lck, and hepatic growth factor activator. Cross reactivity between HCV proteins and human proteins HCV capsid proteins initiate the autoimmune process in the liver because of cross reaction of antibodies with human Gor protein 19-27, which causes autoimmune chronic hepatitis. However, analysis of human protein from protein basis Swissprot shows homology between NS5 region and 3 human protein nitrogen oxide synthases, tyrosine kinase-Lck, proto-oncogene and hepatic growth factor activator. According to protein data analysis and competitive in vitro experiments, it was concluded that presence of auto-antibodies is probably the consequence of cross reactive immune response. Conclusion Homology of amino acid sequences in the NS5 region of the HCV genome with nitrogen-oxide synthase, tyrosine kinase-Lck, and hepatic growth factor activator, causes auto-immune phenomena in HC, and can be a model for researching autoimmunity and human virus-induced autoimmune diseases.

Actual aspects of sepsis and septic shock

2014 ◽  
Vol 5 (2) ◽  
pp. 81-87
Author(s):  
Danila Viktorovich Strukov ◽  
Yuriy Stanislavovich Alexandrovich ◽  
Andrey Glebovich Vasiliev
Keyword(s):  
Septic Shock ◽  
Nitrogen Oxide ◽  
Shock Therapy ◽  
Infection Process ◽  
Nitrogen Oxide Synthase ◽  
Adults And Children ◽  
Contemporary Medicine ◽  
Sepsis And Septic Shock ◽  
Oxide Synthase

He review presents an analysis of up-to-date views on sepsis and septic shock. Results of consenting conferences are given with classification of sepsis in adults and children. Mortality indexes are presented in patients’ group with sepsis. Basic pathogenesis links are examined i.e. bacteriemia, microbe toxemia, endo(auto)toxicosis, systemic destructive vasculitis, growing hypercoagulation transforming into coagulopathia, consumption trombocytopenia with trombohemorrhagic syndrome and severe immunesuppression. Pathogenesis of septic shock is divided into processes developing in various organs and tissues as well as into intracellular ones: such as oxidative stress and mitochondrial insufficiency. The role of pathogen-associated molecular images - patterns is portrayed in the development of generalized acyclic infection process. A scheme of up-to-date septic shock therapy is presented. An important role of nitrogen oxide in the development of stabile hypotonia resistant to vasopressin therapy is proven. The potency of nitrogen oxide to produce free-radical peroxinitrite inducing lipids peroxide oxidation in membranes is reflected. Its ability to react with non-hem iron- and zink- containing proteins is mentioned. Key factors contributing to activation of genes responsible for inducible nitrogen oxide synthase operation are revealed. Extremely severe sepsis and septic shock are believed to be the most serious problem of contemporary medicine thus necessitating to produce new medicines affecting the most drug-resistant links of its pathogenesis. In many a countries trials are continuing to introduce new medicines like nitrogen oxide synthase inhibitors for the treatment of patients with septic shock.

Effects of coronary artery disease on expression and microvascular response to VEGF

1998 ◽  
Vol 275 (4) ◽  
pp. H1411-H1418 ◽  
Author(s):  
Caroline Métais ◽  
Jianyi Li ◽  
Jian Li ◽  
Michael Simons ◽  
Frank W. Sellke
Keyword(s):  
Nitric Oxide ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Growth Factor ◽  
Nitric Oxide Synthase ◽  
Substance P ◽  
Tyrosine Kinase ◽  
Northern Analysis ◽  
Artery Disease ◽  
Oxide Synthase

The effects of coronary artery disease (CAD) on human coronary microvascular responses to vascular endothelial growth factor (VEGF) and the alterations of the myocardial expressions of VEGF and its flk-1 and flt-1 receptors were examined in 48 patients. Microvascular studies were performed in vitro with video microscopy. The expressions of VEGF and its receptors were examined using Northern analysis of total mRNA, and the expressions of constitutive nitric oxide synthase (cNOS) and inducible nitric oxide synthase (iNOS) were examined by RT-PCR. VEGF and hepatocyte growth factor (HGF) caused potent relaxations of microvessels. These responses were reduced in the presence of N G-nitro-l-arginine and the tyrosine kinase inhibitor genistein or in microvessels from patients with CAD. Relaxations to substance P and sodium nitroprusside were similar in both groups. The substance P response was abolished in the presence of N G-nitro-l-arginine. The expression of VEGF and its receptors and the expression of cNOS and iNOS were not altered in patients with CAD. In conclusion, VEGF and HGF elicit the release of nitric oxide through activation of tyrosine kinase receptors. CAD is associated with reduced vascular responses to both VEGF and HGF; this is not likely due to a reduced expression of VEGF or flt-1 or flk-1 receptors and not due to a generalized endothelium dysfunction despite the presence of mild hypercholesterolemia in these patients with CAD. These findings may have important implications regarding the efficacy of endogenous and exogenous VEGF in patients with risk factor for CAD.

Hepatitis C Virus Infection: A Brief Review

JMS SKIMS ◽  
2020 ◽  
Vol 23 (1) ◽  
pp. 3-15
Author(s):  
Saleem Kamili ◽  
Hisham Qadri
Keyword(s):  
Hepatitis C Virus ◽  
Hepatitis C ◽  
Basic Research ◽  
World Health ◽  
Hepatitis C Virus Infection ◽  
Poor Countries ◽  
Diagnostic Assays ◽  
Antiviral Therapies ◽  
Highly Sensitive ◽  
Resource Poor

Hepatitis C, caused by hepatitis C virus (HCV) was originally described as parenterally transmitted non-A non-B hepatitis. Since its discovery in 1989, the field of HCV research has become a shining example of successful translation of basic research wherein in a short of span of just 30 years the virus was discovered, highly sensitive and specific diagnostic assays were developed, epidemiology and clinical characteristics of the disease were well defined and now with the availability of highly efficacious antiviral therapies many countries are already on their way to achieving World Health Organization’s (WHO) elimination targets of hepatitis C by 2030.  However, much work needs to be done to eliminate hepatitis C especially in resource poor countries. Most recent data show an estimated 71 million people are currently infected with HCV worldwide and approximately 400,000 people die each year from causes related to HCV. Of these estimates, more than 13 million HCV infected persons are in India and Pakistan (Figure 1). Despite the availability of a cure for hepatitis C, only 20% of those infected patients have been diagnosed (1). In order to achieve the WHO targets of hepatitis C elimination, concerted efforts will have to made to make affordable and reliable diagnostics available worldwide.

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