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This document provides information about Hepatitis C virus (HCV) including its definition, transmission, diagnosis, treatment, and management. Key points include: - HCV is a contagious liver disease caused by the Hepatitis C virus that can range in severity from mild to life-threatening illness. - It is transmitted through blood and body fluids and has an incubation period of 15 days to 6 months. - Diagnosis involves testing for HCV RNA and anti-HCV antibodies in blood. Liver function tests and imaging may also be used. - Treatment involves direct-acting antiviral drugs targeting specific viral proteins, with regimens varying based on factors like cirrhosis and prior treatment experience.
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This document provides an overview of new oral medications for treating hepatitis C virus (HCV) infection, including NS3/4A protease inhibitors telaprevir and boceprevir. It discusses HCV genotypes and lifecycle, focusing on improved understanding of viral targets leading to drug discovery. NS3/4A protease inhibitors and NS5B polymerase inhibitors currently in clinical development are described, targeting polyprotein processing and HCV replication respectively. Nucleoside and non-nucleoside NS5B inhibitors as well as NS5A inhibitors and their mechanisms of action and clinical trial status are summarized.
Hepatitis C:Diagnosis and management.pdf
This document summarizes information about Hepatitis C virus (HCV) including its structure, life cycle, transmission, natural history of infection, pathogenesis, screening recommendations, diagnosis, assessment of fibrosis, and initial evaluation of persons with chronic HCV infection. Key points include that HCV is a spherical RNA virus that causes a spectrum of liver disease, it is primarily transmitted through blood exposure, around 55-85% of infections become chronic, and diagnosis involves antibody testing, RNA detection, genotyping, and noninvasive or biopsy-based staging of fibrosis.
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This document discusses recent advances in the diagnosis of chronic hepatitis. It defines chronic hepatitis as liver inflammation and necrosis that continues for over 6 months. The main causes of chronic hepatitis discussed are viral hepatitis (HBV, HCV, HDV), alcohol, autoimmunity, drugs, and other rare genetic conditions. New diagnostic techniques described include non-invasive tests like FibroTest, ActiTest, and NASHtest which analyze serum biomarkers, as well as proteomics which studies differences in protein expression between healthy and diseased tissue. Invasive techniques like liver biopsy are still the gold standard but these new methods provide alternatives to evaluate liver fibrosis and inflammation.
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This study investigated the role of HCV NS5A protein transcriptional activation in viral replication and the impact of NS5A cleavage and nuclear localization. The researchers analyzed NS5A variants isolated from a chronically infected patient. They found that variants with different transcriptional activities in yeast also demonstrated varying replication efficiencies in a subgenomic replicon system. Further, the C-terminal fragment of NS5A was found to localize to the nucleus, requiring a functional nuclear localization signal and cellular caspase activity. Nuclear localization of NS5A was necessary for efficient viral replication. NS5A in the nucleus bound to host cell promoters of genes important for replication, inducing their transcription - demonstrating a new mechanism by which HCV modulates its cellular environment to
Advances in Management of Hepatitis C
Patients with acute hepatitis C virus (HCV) infection appear to have an excellent chance of responding to 6 months of standard therapy with interferon (IFN). Because spontaneous resolution is common, no definitive timing of therapy initiation can be recommended; however, waiting 2-4 months after the onset of illness seems reasonable.
Treatment for chronic HCV is based on guidelines from the Infectious Diseases Society of America (IDSA) and the American Associations for the Study of Liver Diseases (AASLD), in collaboration with the International Antiviral Society-USA (IAS-USA). These guidelines are constantly being updated. For more information, see HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C.
The guidelines propose that because all patients cannot receive treatment immediately upon the approval of new agents, priority should be given to those with the most urgent need.
The recommendations include the following :
Patients with advanced fibrosis, those with compensated cirrhosis, liver transplant recipients, and those with severe extraheptic hepatitis are to be given the highest priority for treatment
Based on available resources, patients at high risk for liver-related complications and severe extrahepatic hepatitis C complications should be given high priority for treatment
Treatment decisions should balance the anticipated reduction in transmission versus the likelihood of reinfection in patients whose risk of HCV transmission is high and in whom HCV treatment may result in a reduction in transmission (eg, men who have high-risk sex with men, active injection drug users, incarcerated persons, and those on hemodialysis)
Viral Hepatitis
This document summarizes information about viral hepatitis, with a focus on hepatitis C. It discusses the discovery of hepatitis B and hepatitis C viruses, the clinical manifestations of hepatitis C infection, diagnostic tests for hepatitis C including antibody and RNA tests, natural history and progression of hepatitis C disease, and treatment recommendations for chronic hepatitis C. Epidemiological data on hepatitis C prevalence globally and in Thailand is also presented.
Assessment of serum lipid profile in patients with chronic hepatitis c
1. The document discusses a study that assessed the serum lipid profiles of 100 patients diagnosed with chronic hepatitis C.
2. It found that 63% of patients had normal lipid levels, 3% were hyperlipidemic, and 34% were hypolipidemic.
3. The study indicates that progression of hepatitis C viral infection can lead to decreased levels of lipids.
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This document summarizes information about Hepatitis C virus (HCV) including its structure, life cycle, transmission, natural history of infection, pathogenesis, screening recommendations, diagnosis, assessment of fibrosis, and initial evaluation of persons with chronic HCV infection. Key points include that HCV is a spherical RNA virus that causes a spectrum of liver disease, it is primarily transmitted through blood exposure, around 55-85% of infections become chronic, and diagnosis involves antibody testing, RNA detection, genotyping, and noninvasive or biopsy-based staging of fibrosis.
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This document discusses recent advances in the diagnosis of chronic hepatitis. It defines chronic hepatitis as liver inflammation and necrosis that continues for over 6 months. The main causes of chronic hepatitis discussed are viral hepatitis (HBV, HCV, HDV), alcohol, autoimmunity, drugs, and other rare genetic conditions. New diagnostic techniques described include non-invasive tests like FibroTest, ActiTest, and NASHtest which analyze serum biomarkers, as well as proteomics which studies differences in protein expression between healthy and diseased tissue. Invasive techniques like liver biopsy are still the gold standard but these new methods provide alternatives to evaluate liver fibrosis and inflammation.
J. Virol.-2013-Maqbool-5523-39
This study investigated the role of HCV NS5A protein transcriptional activation in viral replication and the impact of NS5A cleavage and nuclear localization. The researchers analyzed NS5A variants isolated from a chronically infected patient. They found that variants with different transcriptional activities in yeast also demonstrated varying replication efficiencies in a subgenomic replicon system. Further, the C-terminal fragment of NS5A was found to localize to the nucleus, requiring a functional nuclear localization signal and cellular caspase activity. Nuclear localization of NS5A was necessary for efficient viral replication. NS5A in the nucleus bound to host cell promoters of genes important for replication, inducing their transcription - demonstrating a new mechanism by which HCV modulates its cellular environment to
Advances in Management of Hepatitis C
Patients with acute hepatitis C virus (HCV) infection appear to have an excellent chance of responding to 6 months of standard therapy with interferon (IFN). Because spontaneous resolution is common, no definitive timing of therapy initiation can be recommended; however, waiting 2-4 months after the onset of illness seems reasonable.
Treatment for chronic HCV is based on guidelines from the Infectious Diseases Society of America (IDSA) and the American Associations for the Study of Liver Diseases (AASLD), in collaboration with the International Antiviral Society-USA (IAS-USA). These guidelines are constantly being updated. For more information, see HCV Guidance: Recommendations for Testing, Managing, and Treating Hepatitis C.
The guidelines propose that because all patients cannot receive treatment immediately upon the approval of new agents, priority should be given to those with the most urgent need.
The recommendations include the following :
Patients with advanced fibrosis, those with compensated cirrhosis, liver transplant recipients, and those with severe extraheptic hepatitis are to be given the highest priority for treatment
Based on available resources, patients at high risk for liver-related complications and severe extrahepatic hepatitis C complications should be given high priority for treatment
Treatment decisions should balance the anticipated reduction in transmission versus the likelihood of reinfection in patients whose risk of HCV transmission is high and in whom HCV treatment may result in a reduction in transmission (eg, men who have high-risk sex with men, active injection drug users, incarcerated persons, and those on hemodialysis)
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This document summarizes information about viral hepatitis, with a focus on hepatitis C. It discusses the discovery of hepatitis B and hepatitis C viruses, the clinical manifestations of hepatitis C infection, diagnostic tests for hepatitis C including antibody and RNA tests, natural history and progression of hepatitis C disease, and treatment recommendations for chronic hepatitis C. Epidemiological data on hepatitis C prevalence globally and in Thailand is also presented.
Assessment of serum lipid profile in patients with chronic hepatitis c
1. The document discusses a study that assessed the serum lipid profiles of 100 patients diagnosed with chronic hepatitis C.
2. It found that 63% of patients had normal lipid levels, 3% were hyperlipidemic, and 34% were hypolipidemic.
3. The study indicates that progression of hepatitis C viral infection can lead to decreased levels of lipids.
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The Impacts of Viral Hepatitis on Liver Enzymes and Bilrubin
Viral hepatitis is an infection that causes liver inflammation and damage. Several different viruses cause hepatitis, including hepatitis A, B, C, D, and E. The hepatitis A and E viruses typically cause acute infections. The hepatitis B, C, and D viruses can cause acute and chronic infections. Hepatitis A causes only acute infection and typically gets better without treatment after a few weeks. The hepatitis A virus spreads through contact with an infected person’s stool. Protection by getting the hepatitis A vaccine. Hepatitis E is typically an acute infection that gets better without treatment after several weeks. Some types of hepatitis E virus are spread by drinking water contaminated by an infected person’s stool. Other types are spread by eating undercooked pork or wild game. Hepatitis B can cause acute or chronic infection. Recommendation for screening for hepatitis B in pregnant women or in those with a high chance of being infected. Protection from hepatitis B by getting the hepatitis B vaccine. Hepatitis C can cause acute or chronic infection. Doctors usually recommend one-time screening of all adults ages 18 to 79 for hepatitis C. Early diagnosis and treatment can prevent liver damage. The hepatitis D virus is unusual because it can only infect those who have a hepatitis B virus infection. A coinfection occurs when both hepatitis D and hepatitis B infections at the same time. A superinfection occurs already have chronic hepatitis B and then become infected with hepatitis D. The aim of this study is to find the effect of each type of viral hepatitis on the bilirubin (TB , DSB) , and liver enzymes; AST, ALT, ALP,GGT among viral hepatitis patients. 200 patients were selected from the viral hepatitis units in the central public health laboratory in Baghdad city, all the chosen cases were confirmed as a positive samples , they are classified into four equal group each with fifty individual and with a single serological viral hepatitis type either; anti-HAV( IgM ) , HBs Ag , anti-HCV ,or anti-HEV(IgM ). All patients were tested for; serum bilirubin ( TB ,D.SB ) , AST , ALT , ALP , GGT. Another fifty quite healthy and normal person was selected as a control group for comparison. . Liver enzymes and bilirubin changes are more pronounced in HAV, HEV than HCV and HBVAST and ALT lack some sensitivity in detecting HCV ,HBV and mild elevations of ALT or AST in asymptomatic patients can be evaluated efficiently by considering ,hepatitis B, hepatitis C. ALT is generally a more sensitive indicator of acute liver cell damage than AST, It is relatively specific for hepatocyte necrosis with a marked elevations in viral hepatitis. Liver enzymes and bilirubin changes are more pronounced in HAV, HEV than HCV and HBV.AST and ALT lack some sensitivity in detecting HCV ,HBV and mild elevations of ALT or AST in asymptomatic patients can be evaluated efficiently by considering ,hepatitis B, hepatitis C. ALT is generally a more sensitive indicator of acute liver
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1) Hepatitis C virus (HCV) was identified in 1989 and is a leading cause of liver disease. Egypt has the largest HCV epidemic in the world with a prevalence of 14.7% based on antibody testing.
2) HCV is a small enveloped RNA virus that is classified into 6 major genotypes. Genotypes 1 and 4 typically require longer treatment than genotypes 2, 3, 5 and 6.
3) HCV infection may be acute or chronic. About 60-70% of infections become chronic and 20% of chronic carriers may develop cirrhosis or liver cancer over time if left untreated.
A Review Paper of Hepatitis C virus (HCV) Include Risk Factors, Diagnostic Te...
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Every year universal expiries after viral hepatitis are 1.4 million. The organization has known a method to treat 80% of HCV patients by 2030. In Pakistan, HCV occurrence is 1%. There is no correct indication about the real occurrence of HCV chronic infection, though current meta-analyses approximation that currently, about 130-150 million people live with chronic hepatitis C and that HCV reasons about 500,000 deaths each year The purpose of this review article to describes the introduction of HCV, risk factors of HCV, Early treatment option sand result of sofosbuvir plus Ribavirin on the treatment of HCV.Hcv
Hepatitis C is a global problem caused by the hepatitis C virus (HCV). HCV is a blood-borne virus that infects approximately 200 million people worldwide. Laboratory testing plays an important role in diagnosing HCV, evaluating patients for treatment, monitoring patients during treatment, and following up after treatment. There are 6 major genotypes of HCV with genotypes 1 and 4 being more difficult to treat and less responsive to interferon-based therapy.
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This document outlines a proposed collaborative project between researchers at NUST in Pakistan and UCSD in the US to study Hepatitis B virus (HBV) genotypes and their association with Hepatocellular Carcinoma (HCC) in Pakistan. The objectives are to characterize HBV genotypes, identify virus mutations that increase risk of HCC, and study the role of cellular editing enzymes and HBx protein. The project will involve sample collection from hospitals, genotyping, sequencing, and in vitro studies over 3 years. The researchers have facilities and expertise to conduct molecular and clinical analyses of HBV in Pakistan where genotype D is prevalent and HBV infection is a major health problem.
In vitro transcription and transfection of HCV genomic replicon
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In vitro transcription and transfection of HCV genomic replicon
ABSTRACT:
Introduction: Hepatitis C virus (HCV) is a positive stranded RNA virus that causes acute and chronic hepatitis and hepatocellular carcinoma. Aims & Objectives: The study was conducted to establish the transfection of Huh 7.5 derived cell lines with In-vitro transcript of HCV pF6/JFH-1 for production of infectious virus particles in naïve Huh 7.5 cells, its detection by RT-PCR. Materials and Method: Huh 7.5 cells, a highly permissive cell lines for HCV replication, were grown in Dulbecco’s Modified Eagle’s Medium and pFL-J6/JFH plasmid was linearized with XbaI and subjected to in-vitro transcription using MEGAscript Kit (Ambion, USA) Huh-7.5 cells were transfected with 2.5 μg transcript using Lipofectamine 2000 transfection reagent (Invitrogen, USA) . The culture supernatant was collected after 24, 48 and 72 hr after incubation in fresh media and viral RNAs were isolated from it using Trizol LS reagent (Ambion, USA) and quantified by real-time quantitative RT-PCR. Total RNA was extracted from cells using Trizol reagent (Ambion, USA) and then RNA was subjected to cDNA synthesis using RevertAid reverse transcription (Thermo Fisher Scientific, USA). The PCR products were resolved by electrophoresis in 1.5% (w/v) agarose gels and images were captured by a Chemidoc XRS system (Bio-Rad, USA). Results: We observed Huh7.5 cells were cultured in DMEM. Plasmid FL-J6/JFH1 was linearized with the restriction enzyme XbaI and HCV RNA was obtained by In-vitro transcription and was transfected to grown Huh 7.5 cells shown by band on agarose gel and total RNA isolated after 24 hours of post infection followed by RT-PCR gave distinct band on gel whereas 48 and 72 hr did not. Infection of Huh 7.5 cells with cell culture supernatant from cells transfected with HCV in vitro transcript gave a distinct band. This will help in understanding entire viral life cycle and its non-structural gene products like NS4B and NS5A that enhance the replicative capacity of replicons in Huh 7.5 cell lines for development of drug and vaccines.
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Hepatitis c. diagnosis and treatment.assld guidelines.2016 .2017
A 45-year-old woman presented with fatigue, weakness, loss of appetite, and anemia. Liver function tests showed elevated AST, ALT, and bilirubin levels indicating liver inflammation and damage. A liver biopsy revealed necroinflammation and fibrosis. This suggests a diagnosis of chronic hepatitis C, which would be confirmed by a positive HCV RNA test. The best course of action would be to treat the patient with direct-acting antiviral therapy to cure the hepatitis C infection, advise lifestyle changes to protect the liver, and monitor for complications like cirrhosis or liver cancer.
Hepatitis C - Etiology Pathogenesis Clinical Features Diagnosis Management
Hepatitis C is a viral infection that affects an estimated 2-3% of the world's population. It is transmitted parenterally or through exposure to infected blood or bodily fluids. Approximately 70-130 million individuals are chronically infected. While some acute cases resolve, others progress to chronic infection which can lead to cirrhosis or liver cancer over time. Diagnosis involves testing for HCV antibodies and RNA. Genotypes 1-6 exist globally. Management involves antiviral therapy with pegylated interferon and ribavirin or newer direct acting antiviral agents targeting viral proteins. Treatment aims to achieve a sustained virologic response and prevent progression of liver disease.
Viral hepatitis
This document provides information on the clinical presentation and progression of viral hepatitis. It describes the prodromal symptoms including fatigue, nausea and low grade fever. Onset of jaundice is marked by diminishing constitutional symptoms and development of liver tenderness and pain. Various clinical syndromes can develop after viral exposure including acute, fulminant or chronic hepatitis. The morphologic lesions are similar between virus types and include lobular inflammation and necrosis. Serologic testing can identify exposure to hepatitis A, B, C and E viruses.
Viral hepatitis
This document provides information on the clinical presentation and progression of viral hepatitis. It describes the prodromal symptoms including fatigue, nausea and low grade fever. Onset of jaundice is characterized by diminishing constitutional symptoms and liver tenderness. Various clinical syndromes can develop after viral exposure including acute, fulminant or chronic hepatitis. The morphologic lesions are similar between virus types and include lobular inflammation and necrosis. Serologic testing can identify exposure to hepatitis A, B, C and E viruses.
Hepatitis ppt final
Hepatitis viruses include Hepatitis A, B, C, D, E, and G. Hepatitis A virus is transmitted through the fecal-oral route and causes an acute infection. Hepatitis B virus is transmitted through blood or bodily fluids and can cause either an acute or chronic infection. Hepatitis C virus is transmitted through blood exposure and commonly causes a chronic infection. Prevention strategies include vaccination, immunoglobulin treatment, and screening of blood donors.
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The document provides an overview of hepatitis, focusing on hepatitis viruses A through E. It details the transmission, symptoms, testing, and treatment for acute and chronic cases of hepatitis B and C. Hepatitis A virus is transmitted through contaminated food or water, while hepatitis B and C viruses are transmitted through bodily fluids. Acute cases may show flu-like symptoms and jaundice, while chronic cases can lead to liver damage, cirrhosis, and liver cancer over many years if left untreated. Laboratory tests can identify viral antigens and antibodies to determine infection status and viral load. Treatment options aim to suppress viral replication through antiviral medications.
hep c.pptx diagnosis and management of hep c
The document discusses hepatitis C virus (HCV), including its structure, genome, genotypes, epidemiology, pathogenesis, diagnosis, and management. Some key points:
- HCV is a single-stranded RNA virus of the Flaviviridae family with a genome encoding both structural and nonstructural proteins.
- It exists as different genotypes globally, with genotypes 1, 2, 3 being most common. Genotype helps determine treatment duration and response.
- HCV is a major cause of liver disease worldwide and is transmitted through blood exposure. Diagnosis involves HCV antibody and RNA testing.
- Treatment aims to eradicate the virus and involves use of pegylated interferon and ribavirin
Presentation
The document discusses hepatitis C virus (HCV) infection in patients with kidney disease. It covers several topics:
1) HCV is highly prevalent among patients undergoing dialysis, with rates ranging from 1.4-28.3% in developed countries and 4.7-41.9% in developing countries.
2) HCV can accelerate progression of chronic kidney disease and increase risk of end-stage renal disease. Successful treatment of HCV with antiviral therapy can improve kidney function and reduce dialysis risk.
3) Several direct-acting antiviral regimens, including paritaprevir/ritonavir/ombitasvir/dasabuvir, paritaprevir/
Management of Hepatitis C with Natural and Synthetic Medicine
This document summarizes a study comparing the management of Hepatitis C with natural and synthetic medicines. The study compared two Unani (Eastern medicine) formulations, Hepotin tablets and Vironil syrup, to the conventional allopathic drugs interferon alfa-2b and ribavirin. Sixty patients with Hepatitis C were randomly assigned to receive either the Unani medicines or allopathic drugs for six months. Clinical signs and symptoms, biochemical markers, and viral load were measured and statistically compared between the two groups. The results showed the Unani medicines were as effective as the allopathic drugs in improving clinical symptoms, liver enzymes, and reducing viral load, with fewer side effects. The study provides evidence that Unani
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Viral hepatitis is an infection that causes liver inflammation and damage. Several different viruses cause hepatitis, including hepatitis A, B, C, D, and E. The hepatitis A and E viruses typically cause acute infections. The hepatitis B, C, and D viruses can cause acute and chronic infections. Hepatitis A causes only acute infection and typically gets better without treatment after a few weeks. The hepatitis A virus spreads through contact with an infected person’s stool. Protection by getting the hepatitis A vaccine. Hepatitis E is typically an acute infection that gets better without treatment after several weeks. Some types of hepatitis E virus are spread by drinking water contaminated by an infected person’s stool. Other types are spread by eating undercooked pork or wild game. Hepatitis B can cause acute or chronic infection. Recommendation for screening for hepatitis B in pregnant women or in those with a high chance of being infected. Protection from hepatitis B by getting the hepatitis B vaccine. Hepatitis C can cause acute or chronic infection. Doctors usually recommend one-time screening of all adults ages 18 to 79 for hepatitis C. Early diagnosis and treatment can prevent liver damage. The hepatitis D virus is unusual because it can only infect those who have a hepatitis B virus infection. A coinfection occurs when both hepatitis D and hepatitis B infections at the same time. A superinfection occurs already have chronic hepatitis B and then become infected with hepatitis D. The aim of this study is to find the effect of each type of viral hepatitis on the bilirubin (TB , DSB) , and liver enzymes; AST, ALT, ALP,GGT among viral hepatitis patients. 200 patients were selected from the viral hepatitis units in the central public health laboratory in Baghdad city, all the chosen cases were confirmed as a positive samples , they are classified into four equal group each with fifty individual and with a single serological viral hepatitis type either; anti-HAV( IgM ) , HBs Ag , anti-HCV ,or anti-HEV(IgM ). All patients were tested for; serum bilirubin ( TB ,D.SB ) , AST , ALT , ALP , GGT. Another fifty quite healthy and normal person was selected as a control group for comparison. . Liver enzymes and bilirubin changes are more pronounced in HAV, HEV than HCV and HBVAST and ALT lack some sensitivity in detecting HCV ,HBV and mild elevations of ALT or AST in asymptomatic patients can be evaluated efficiently by considering ,hepatitis B, hepatitis C. ALT is generally a more sensitive indicator of acute liver cell damage than AST, It is relatively specific for hepatocyte necrosis with a marked elevations in viral hepatitis. Liver enzymes and bilirubin changes are more pronounced in HAV, HEV than HCV and HBV.AST and ALT lack some sensitivity in detecting HCV ,HBV and mild elevations of ALT or AST in asymptomatic patients can be evaluated efficiently by considering ,hepatitis B, hepatitis C. ALT is generally a more sensitive indicator of acute liver
Hepatitis c infection, causes, treatment, and prevention
1) Hepatitis C virus (HCV) was identified in 1989 and is a leading cause of liver disease. Egypt has the largest HCV epidemic in the world with a prevalence of 14.7% based on antibody testing.
2) HCV is a small enveloped RNA virus that is classified into 6 major genotypes. Genotypes 1 and 4 typically require longer treatment than genotypes 2, 3, 5 and 6.
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A Review Paper of Hepatitis C virus (HCV) Include Risk Factors, Diagnostic Te...
A Review Paper of Hepatitis C virus (HCV) Include Risk Factors, Diagnostic Te...Associate Professor in VSB Coimbatore
Every year universal expiries after viral hepatitis are 1.4 million. The organization has known a method to treat 80% of HCV patients by 2030. In Pakistan, HCV occurrence is 1%. There is no correct indication about the real occurrence of HCV chronic infection, though current meta-analyses approximation that currently, about 130-150 million people live with chronic hepatitis C and that HCV reasons about 500,000 deaths each year The purpose of this review article to describes the introduction of HCV, risk factors of HCV, Early treatment option sand result of sofosbuvir plus Ribavirin on the treatment of HCV.Hcv
Hepatitis C is a global problem caused by the hepatitis C virus (HCV). HCV is a blood-borne virus that infects approximately 200 million people worldwide. Laboratory testing plays an important role in diagnosing HCV, evaluating patients for treatment, monitoring patients during treatment, and following up after treatment. There are 6 major genotypes of HCV with genotypes 1 and 4 being more difficult to treat and less responsive to interferon-based therapy.
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In vitro transcription and transfection of HCV genomic replicon
Introduction: Hepatitis C virus (HCV) is a positive stranded RNA virus that causes acute and chronic hepatitis and hepatocellular carcinoma. Aims & Objectives: The study was conducted to establish the transfection of Huh 7.5 derived cell lines with In-vitro transcript of HCV pF6/JFH-1 for production of infectious virus particles in naïve Huh 7.5 cells, its detection by RT-PCR. Materials and Method: Huh 7.5 cells, a highly permissive cell lines for HCV replication, were grown in Dulbecco’s Modified Eagle’s Medium and pFL-J6/JFH plasmid was linearized with XbaI and subjected to in-vitro transcription using MEGAscript Kit (Ambion, USA) Huh-7.5 cells were transfected with 2.5 μg transcript using Lipofectamine 2000 transfection reagent (Invitrogen, USA) . The culture supernatant was collected after 24, 48 and 72 hr after incubation in fresh media and viral RNAs were isolated from it using Trizol LS reagent (Ambion, USA) and quantified by real-time quantitative RT-PCR. Total RNA was extracted from cells using Trizol reagent (Ambion, USA) and then RNA was subjected to cDNA synthesis using RevertAid reverse transcription (Thermo Fisher Scientific, USA). The PCR products were resolved by electrophoresis in 1.5% (w/v) agarose gels and images were captured by a Chemidoc XRS system (Bio-Rad, USA). Results: We observed Huh7.5 cells were cultured in DMEM. Plasmid FL-J6/JFH1 was linearized with the restriction enzyme XbaI and HCV RNA was obtained by In-vitro transcription and was transfected to grown Huh 7.5 cells shown by band on agarose gel and total RNA isolated after 24 hours of post infection followed by RT-PCR gave distinct band on gel whereas 48 and 72 hr did not. Infection of Huh 7.5 cells with cell culture supernatant from cells transfected with HCV in vitro transcript gave a distinct band. This will help in understanding entire viral life cycle and its non-structural gene products like NS4B and NS5A that enhance the replicative capacity of replicons in Huh 7.5 cell lines for development of drug and vaccines.
In vitro transcription and transfection of HCV genomic replicon
ABSTRACT:
Introduction: Hepatitis C virus (HCV) is a positive stranded RNA virus that causes acute and chronic hepatitis and hepatocellular carcinoma. Aims & Objectives: The study was conducted to establish the transfection of Huh 7.5 derived cell lines with In-vitro transcript of HCV pF6/JFH-1 for production of infectious virus particles in naïve Huh 7.5 cells, its detection by RT-PCR. Materials and Method: Huh 7.5 cells, a highly permissive cell lines for HCV replication, were grown in Dulbecco’s Modified Eagle’s Medium and pFL-J6/JFH plasmid was linearized with XbaI and subjected to in-vitro transcription using MEGAscript Kit (Ambion, USA) Huh-7.5 cells were transfected with 2.5 μg transcript using Lipofectamine 2000 transfection reagent (Invitrogen, USA) . The culture supernatant was collected after 24, 48 and 72 hr after incubation in fresh media and viral RNAs were isolated from it using Trizol LS reagent (Ambion, USA) and quantified by real-time quantitative RT-PCR. Total RNA was extracted from cells using Trizol reagent (Ambion, USA) and then RNA was subjected to cDNA synthesis using RevertAid reverse transcription (Thermo Fisher Scientific, USA). The PCR products were resolved by electrophoresis in 1.5% (w/v) agarose gels and images were captured by a Chemidoc XRS system (Bio-Rad, USA). Results: We observed Huh7.5 cells were cultured in DMEM. Plasmid FL-J6/JFH1 was linearized with the restriction enzyme XbaI and HCV RNA was obtained by In-vitro transcription and was transfected to grown Huh 7.5 cells shown by band on agarose gel and total RNA isolated after 24 hours of post infection followed by RT-PCR gave distinct band on gel whereas 48 and 72 hr did not. Infection of Huh 7.5 cells with cell culture supernatant from cells transfected with HCV in vitro transcript gave a distinct band. This will help in understanding entire viral life cycle and its non-structural gene products like NS4B and NS5A that enhance the replicative capacity of replicons in Huh 7.5 cell lines for development of drug and vaccines.
Non Invasive Biomarkers in NASH (non-alcoholic steatohepatitis) Webinar Slides
This document discusses non-invasive biomarkers for non-alcoholic steatohepatitis (NASH). It provides an agenda for a meeting on this topic, including discussions of the need for non-invasive biomarkers in NASH, current and future methods for non-invasive diagnosis of NASH and liver fibrosis, leveraging genomics in biomarker development, and the strategic use of non-invasive testing in NASH drug development and clinical practice. Specific non-invasive tests are discussed, such as blood-based biomarkers, imaging techniques, and genomic and proteomic profiling methods for assessing liver fat, inflammation, fibrosis and other aspects of NASH.
Hepatitis c. diagnosis and treatment.assld guidelines.2016 .2017
A 45-year-old woman presented with fatigue, weakness, loss of appetite, and anemia. Liver function tests showed elevated AST, ALT, and bilirubin levels indicating liver inflammation and damage. A liver biopsy revealed necroinflammation and fibrosis. This suggests a diagnosis of chronic hepatitis C, which would be confirmed by a positive HCV RNA test. The best course of action would be to treat the patient with direct-acting antiviral therapy to cure the hepatitis C infection, advise lifestyle changes to protect the liver, and monitor for complications like cirrhosis or liver cancer.
Hepatitis C - Etiology Pathogenesis Clinical Features Diagnosis Management
Hepatitis C is a viral infection that affects an estimated 2-3% of the world's population. It is transmitted parenterally or through exposure to infected blood or bodily fluids. Approximately 70-130 million individuals are chronically infected. While some acute cases resolve, others progress to chronic infection which can lead to cirrhosis or liver cancer over time. Diagnosis involves testing for HCV antibodies and RNA. Genotypes 1-6 exist globally. Management involves antiviral therapy with pegylated interferon and ribavirin or newer direct acting antiviral agents targeting viral proteins. Treatment aims to achieve a sustained virologic response and prevent progression of liver disease.
Viral hepatitis
This document provides information on the clinical presentation and progression of viral hepatitis. It describes the prodromal symptoms including fatigue, nausea and low grade fever. Onset of jaundice is marked by diminishing constitutional symptoms and development of liver tenderness and pain. Various clinical syndromes can develop after viral exposure including acute, fulminant or chronic hepatitis. The morphologic lesions are similar between virus types and include lobular inflammation and necrosis. Serologic testing can identify exposure to hepatitis A, B, C and E viruses.
Viral hepatitis
This document provides information on the clinical presentation and progression of viral hepatitis. It describes the prodromal symptoms including fatigue, nausea and low grade fever. Onset of jaundice is characterized by diminishing constitutional symptoms and liver tenderness. Various clinical syndromes can develop after viral exposure including acute, fulminant or chronic hepatitis. The morphologic lesions are similar between virus types and include lobular inflammation and necrosis. Serologic testing can identify exposure to hepatitis A, B, C and E viruses.
Hepatitis ppt final
Hepatitis viruses include Hepatitis A, B, C, D, E, and G. Hepatitis A virus is transmitted through the fecal-oral route and causes an acute infection. Hepatitis B virus is transmitted through blood or bodily fluids and can cause either an acute or chronic infection. Hepatitis C virus is transmitted through blood exposure and commonly causes a chronic infection. Prevention strategies include vaccination, immunoglobulin treatment, and screening of blood donors.
BCC4: Pierre Janin on 4 Newer Agents for Hepatitis C
Janin speaks on the dawn of a revolution for treating Hepatitis C. This was recorded at Bedside Critical Care Conference 4. Full postings can be found at www.intensivecarenetwork.com
Hepatitis simple review by kufamedst
The document provides an overview of hepatitis, focusing on hepatitis viruses A through E. It details the transmission, symptoms, testing, and treatment for acute and chronic cases of hepatitis B and C. Hepatitis A virus is transmitted through contaminated food or water, while hepatitis B and C viruses are transmitted through bodily fluids. Acute cases may show flu-like symptoms and jaundice, while chronic cases can lead to liver damage, cirrhosis, and liver cancer over many years if left untreated. Laboratory tests can identify viral antigens and antibodies to determine infection status and viral load. Treatment options aim to suppress viral replication through antiviral medications.
hep c.pptx diagnosis and management of hep c
The document discusses hepatitis C virus (HCV), including its structure, genome, genotypes, epidemiology, pathogenesis, diagnosis, and management. Some key points:
- HCV is a single-stranded RNA virus of the Flaviviridae family with a genome encoding both structural and nonstructural proteins.
- It exists as different genotypes globally, with genotypes 1, 2, 3 being most common. Genotype helps determine treatment duration and response.
- HCV is a major cause of liver disease worldwide and is transmitted through blood exposure. Diagnosis involves HCV antibody and RNA testing.
- Treatment aims to eradicate the virus and involves use of pegylated interferon and ribavirin
Presentation
The document discusses hepatitis C virus (HCV) infection in patients with kidney disease. It covers several topics:
1) HCV is highly prevalent among patients undergoing dialysis, with rates ranging from 1.4-28.3% in developed countries and 4.7-41.9% in developing countries.
2) HCV can accelerate progression of chronic kidney disease and increase risk of end-stage renal disease. Successful treatment of HCV with antiviral therapy can improve kidney function and reduce dialysis risk.
3) Several direct-acting antiviral regimens, including paritaprevir/ritonavir/ombitasvir/dasabuvir, paritaprevir/
Management of Hepatitis C with Natural and Synthetic Medicine
This document summarizes a study comparing the management of Hepatitis C with natural and synthetic medicines. The study compared two Unani (Eastern medicine) formulations, Hepotin tablets and Vironil syrup, to the conventional allopathic drugs interferon alfa-2b and ribavirin. Sixty patients with Hepatitis C were randomly assigned to receive either the Unani medicines or allopathic drugs for six months. Clinical signs and symptoms, biochemical markers, and viral load were measured and statistically compared between the two groups. The results showed the Unani medicines were as effective as the allopathic drugs in improving clinical symptoms, liver enzymes, and reducing viral load, with fewer side effects. The study provides evidence that Unani
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Hepatitis C E learning summary - Clinical features and treatment
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hepatitis c.pptx
- 1. HEPATITIS C Dr.HARDIK (R1 GENERAL MEDICINE DEPARTMENT ) PDU MEDICAL COLLEGE RAJKOT
- 2. DEFINITION Hepatitis c is contagious liver disease caused by hepatitis c virus. It accounts for 3% global population involved It can range in severity from mild illness lasting for few weeks to serve life threatening illness
- 3. INTRODUCTION Labelled as a "non-A, non-B hepatitis,“ Member of hepacivirus c. It is a linear, single-stranded enveloped RNA virus belonging to the flavivirus family.
- 5. VIRAL PROTEINS STRUCTURAL: 1) C: core protein nucleocapsid 2) E1, E2:envelope Glycoprotein 3) P7:ion channel for viral release NON STRUCTURAL:1) NS3:serine proteas 2) NS5A:RNA binding site within replication complex 3) NS5B:RNA dependent RNA polymerase DIRECTLY ACTING ANTIVIRAL ACT ON:NS5A,NS5B NS5A(-) :declatasavir Velpatasavir NS5B: Sofosbuvir
- 6. TRANSMISSION
- 7. INCUBATION PERIOD 15days to 160 days
- 8. VIRAL CYCLE
- 9. PATHOGENESIS
- 11. SYMPTOMS-ACUTE
- 12. CHRONIC
- 14. WHOM TO TEST 1. People who inject drugs ( PWID) 2. Men who have sex with men 3. Female sex workers 4. People who received blood transfusion before routine testing for hepatitis C 5. People who need frequent blood transfusion, such as, thalessemic and dialysis patients 6. People living with HIV 7. Inmates of prisons and other closed settings
- 15. LAB DIAGNOSIS >As illustrated in figure,following an initial eclipse phase of 1–2 weeks when no virological or serological markers of infection may be detected, the natural course of HCV infection is characterized by the appearance of HCV RNA, then HCV core p22 Ag in the absence of an antibody response for a further 6–10 weeks. >after that ANTI-HCVantibody appears in blood
- 16. DIAGNOSIS IN CHILDREN anti-HCV antibodies from an infected mother may persist in children <18 months of age, HCV RNA detection is also used to diagnose HCV infection in this age group (after 2 months of age)
- 17. LAB INVESTIGATION Complete blood cell (CBC) count with differential International normalized ratio (INR) Liver function tests, including levels of ALT and AST, alkaline phosphatase, albumin, and total and direct bilirubin Calculated glomerular filtration rate (eGFR Screening tests for coinfection with human immunodeficiency virus (HIV) or hepatitis B virus (HBV)
- 18. Serum pregnancy testing in women of childbearing age before initiating a treatment regimen that includes ribavirin or that includes direct-acting antiviral agents (DAAs) without ribavirin The World Health Organization (WHO) recommends nucleic acid testing for qualitative or quantitative HCV RNA detection as well as for test of cure at 12 or 24 weeks following antiviral treatment completion.[50]In areas with limited resources, the WHO suggests using the aminotransferase/platelet ratio index (APRI) or the fibrosis-4 (FIB-4) score for evaluating hepatic fibrosis rather than other noninvasive tests that require more resources (eg, elastography, FibroTest), as follows[50]:
- 19. >APRI = [(AST (IU/L)/AST_ULN (IU/L))×100]/platelet count (109 /L) >FIB-4= age (years) × AST (IU/L)/platelet count (109)/L × [ALT (IU/L)1/2 APRI>0.2 FIB-4>3.2 are suggestive of hepatic fibrosis
- 21. TREATMENT Whom To Treat Any individual diagnosed to have infection with hepatitis C virus (viremia +) needs treatment. The duration of treatment will depend on the several situations such as, cirrhosis versus non-cirrhosis, presence of decompensation (ascites, variceal bleeding, hepatic encephalopathy, or infection(s), treatment naïve versus treatment experienced (to peg IFN, DAAs, etc).
- 22. WHAT REGIME TO USE
- 25. DOSE ADJUSTMENT FOR RIBAVIRIN ANEMIA: IF 1) HB<10: 600mg 2) HB<8.5: discontinue RENAL FAILURE: patients with an eGFR <50 mL/ min/1.73 m2 should not be treated with ribavirin and those on haemodialysis must have the dose lowered to 200 mg per day or take it three times per week.
- 26. Management of treatment experienced