Biological Sciences
Hepatitis Viruses
Hepatitis viruses are a group of viruses that cause inflammation of the liver, known as hepatitis. There are several types of hepatitis viruses, including hepatitis A, B, C, D, and E. Each type is transmitted differently and can lead to acute or chronic liver disease, with symptoms ranging from mild illness to severe liver damage.
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12 Key excerpts on "Hepatitis Viruses"
eBook - ePubStudies on Hepatitis Viruses
Life Cycle, Structure, Functions, and Inhibition
- Satya Prakash Gupta(Author)
- 2018(Publication Date)
- Academic Press(Publisher)
Chapter 1Viral Hepatitis
Historical Perspective, Etiology, Epidemiology, and Pathophysiology
Abstract
The chapter discusses the types of Hepatitis Viruses that are mainly hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV) and presents their etiology, epidemiology, and pathophysiology, which refer to manner of causation of a disease or condition, study of cause of a disease, and physiology of abnormal states, respectively.Keywords
Epidemiology; Etiology; Hepatitis Viruses; Pathophysiology1. Introduction
Hepatitis refers to inflammation of the liver, which is primarily caused by viruses called Hepatitis Viruses. So far, there are five known Hepatitis Viruses, called hepatitis A virus (HAV), hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and hepatitis E virus (HEV). In United States, the first three viruses, i.e., HAV, HBV, and HCV, are more prevalent. The symptoms of their infection are usually nausea, abdominal pain, fatigue, malaise, and jaundice (Wasley et al., 2008 ). Hepatitis may be temporary (acute) or long term (chronic), depending on whether it lasts for less or more than 6 months. Acute hepatitis can sometimes resolve on its own or progress to chronic hepatitis, which over time may progress to liver failure or liver cancer. HBV and HCV may lead to chronic infection, causing cirrhosis and hepatocellular carcinoma (HCC) (Wasley et al., 2008 ). The most common effect of HAV and HEV is the sudden onset of fever and systemic symptoms, followed a few days later by jaundice. HDV may also cause chronic infection, but it affects only in presence of HBV infection; hence an individual protected against HBV is hardly affected by HDV. Three viruses—HBV, HCV, and HDV—are transmitted in the body parenterally, while the remaining two—HAV and HEV—can be transmitted enterally.Compared to human immunodeficiency virus (HIV), Hepatitis Viruses are less publicized. They are recognized as silent killers. According to World Health Organization (WHO), about 400 million people worldwide are suffering with chronic hepatitis viral infection. More than 1 million people die of liver cirrhosis caused by Hepatitis Viruses, and HCC is the third leading cause of cancer deaths, claiming more than 500,000 lives each year. In spite of the prevalence of hepatitis, no symptoms of chronic viral hepatitis are recognized until patients develop complications of cirrhosis or liver cancer, and once symptoms occur, currently available remedies are often ineffective and/or expensive. Given the large burden of viral hepatitis, governments around the world have made various efforts to mitigate its impact. WHO has set a goal to eliminate viral hepatitis as a major public health threat by 2030.
eBook - ePub- (Author)
- 2012(Publication Date)
- Academic Press(Publisher)
Chapter 99 Viral Hepatitis Nicholas A. Shackel, Keyur Patel and John McHutchison Introduction Viral hepatitis is a significant global health problem. Hepatitis B virus (HBV) and hepatitis C virus (HCV) infect more than 300 million people. HBV and HCV are complicated by chronic, persistent infection, characterized in a proportion of patients by progressive hepatic injury leading to complications of end-stage liver disease, including hepatocellular carcinoma (HCC). HCC is the fifth most prevalent human malignancy, and the majority of cases can be directly attributed to liver injury secondary to chronic HBV and/or HCV infection. Although both hepatitis A and E are significant health problems, they are typically characterized by a self-limiting course and are not complicated by significant clinical sequelae in the majority of cases. Therefore, research into infectious hepatitis has focused mainly on HBV and HCV pathogenesis, including the development of liver fibrosis, the immune response in acute infection, mechanisms of viral persistence, and the development of HCC. The use of functional genomics approaches has significantly advanced our understanding of viral hepatitis pathogenesis, as well as our understanding of therapeutic strategies. Virology of Hepatitis Viruses The Hepatitis Viruses are characterized by specificity for the liver and in particular the hepatocyte (Figure 99.1). The mechanism by which these viruses are specific for the liver is largely unknown, but it is thought to involve hepatocyte receptor and co-receptor interactions and possible involvement of liver-specific pathways such as lipoprotein trafficking and synthesis. Figure 99.1 Hepatitis virus virology. (A) Summary of the virology of viral hepatitis (HAV to HEV). (B) The HBV circular DNA and the multiple overlapping reading frames. (C) In contrast to hepatitis B, the hepatitis C virus has a linear RNA genome encoding viral proteins
eBook - ePub- Alex P. Mowat(Author)
- 2013(Publication Date)
- Butterworth-Heinemann(Publisher)
Chapter 6Viral infections of the liver
Publisher Summary
This chapter discusses the clinical features, prevention, and treatment of various viral infections of the liver, such as acute viral hepatitis type A, viral hepatitis type B, viral hepatitis type C, delta hepatitis, herpes simplex hepatitis, and mosquito borne viral hepatitis. It also explains the viruses that have a high degree of hepatic trophism. Acute viral hepatitis type A is an acute inflammation of the liver with varying degrees of hepatocellular necrosis caused by the enterically transmitted hepatitis A virus (HAV), a member of the picornavirus family. The hepatitis is usually benign but severity may increase with age. There are no long-term sequelae but the disease may be relapsing. Viral hepatitis type B is caused by the hepatitis B virus (HBV), a double-stranded DNA virus of the hepadnavirus family which has unique biological properties. Unlike hepatitis A virus the host immunological response may be ineffective leading to chronic infection. Transmission of HBV occurs by the parenteral route; however, as minute quantities of blood are infective it may be blood-borne via unapparent fomites. In saliva and semen viral concentrations are 100–1000 times less than in blood but both have been shown to be infective in experimental studies. Hepatitis C virus (HCV) has been shown to cause the majority of cases of post-transfusion non-A non-B hepatitis and much sporadic, community acquired non-A non-B hepatitis in many parts of the world.Hepatitis
The term hepatitis indicates an inflammation of the liver, usually associated with hepatocyte degeneration or necrosis. The cause may be infective, toxic, genetically determined, physical, ischaemic or cryptogenic. The course may be acute or chronic. Although it is usual to characterize the hepatitis by the aetiological factor, the wide range of clinical manifestations seen in any of the above types is determined by the severity of the alterations in hepatocyte function. At one end of the scale is an asymptomatic hepatitis in which hepatocellular necrosis is minimal and revealed only by elevation of serum enzymes such as aspartate aminotransferase, at the other end is fulminant hepatitis associated with massive hepatocellular necrosis, hepatic encephalopathy and spontaneous haemorrhage. Hepatitis in infancy is considered in Chapter 4
eBook - PDF- E.A. Fagan, T.J. Harrison(Authors)
- 2003(Publication Date)
- Garland Science(Publisher)
Chapter 1 General Introduction 1.0 Issues Viral hepatitis in humans is caused by at least five viruses (Table 1.1) for which the liver is the major site of replication. A variety of other viruses (Table 1.2) occasionally show marked hepatotropism. The symptoms of acute and persistent virus replication in the liver are remarkably consistent despite the diversity of viruses involved. Hepatitis A virus (HAV) and hepatitis E virus (HEV) are considered together in Chapter 2. Both are small, non-enveloped viruses with positive-sense RNA genomes of around 7.5 kb. These viruses are spread by the fecal-oral route and probably replicate in the intestinal tract prior to infecting the liver. The usual outcome is an acute hepatitis that resolves without evidence of chronic liver disease. Occasionally, viral replication may be protracted. Rarely, the acute hepatitis may pursue a fulminant course (acute liver failure, Chapter 5). Hepatitis B virus (HBV) is considered in Chapter 3 with hepatitis D virus (HDV), the delta agent, which relies on HBV for transmission. HBV is a small (3.2 kb DNA genome), enveloped virus with a replication strategy similar to that of the retroviruses. HBV is spread predominantly by blood (parenteral) and sexual contact. HBV appears to replicate almost exclusively in the liver, although viral nucleic acids and antigens may be detected in peripheral white blood cells. HBV may cause persistent infections, especially following infection of babies and young children, and virus replication may persist for life. HBV infections persist in only around 1–5% of healthy adults. Liver damage relates mostly to immune-mediated mechanisms of the host, through lysis of infected hepatocytes by cytotoxic T lymphocytes. Chronic hepatitis may ensue, leading to cirrhosis and hepatocellular carcinoma. HDV is an unusual agent, with similarities to plant viroids, and the smallest virus (1.7 kb circular RNA genome) known to infect man.
eBook - PDF- R Holland Cheng, Tatsuo Miyamura(Authors)
- 2008(Publication Date)
- World Scientific(Publisher)
91 Chapter 5 Hepatitis Viruses, Signaling Events and Modulation of the Innate Host Response Syed Mohammad Moin, Anindita Kar-Roy and Shahid Jameel* Viruses and their vertebrate hosts have co-evolved for millions of years. While the host has developed an immune system to deal with invading pathogens, including viruses, the latter have developed counter strategies. The host response comprises an early nonspecific innate system and an antigen-specific adaptive immune system. Accordingly, viruses have also evolved strategies to overcome these, based largely on modulation of host signaling pathways. Here we outline components of the innate host response and cell death and survival strategies, and summarize work on how Hepatitis Viruses modulate these responses. At least five separate viral agents are known to cause hepatitis, lead-ing to significant human morbidity and mortality. Their spectrum ranges from acute and self-limited infections to those that become chronic and stay with the host for its entire lifespan. This varied presentation of viral hepatitis is rational-ized here in terms of the virus’ ability to deal with the innate host response. Viral hepatitis is an ancient disease that had been recorded in early Babylonian, Greek and Chinese scriptures. 1 “Hepatitis,” which means inflammation of the liver, is not a single disease, but is caused by a spectrum of agents, viral or otherwise. It was not until 1969 that the first human hepatitis virus — the hepatitis B virus (HBV) — was * Virology Group, International Centre for Genetic Engineering and Biotechnology, Aruna Asaf Ali Marg, New Delhi 110067, India. 92 Structure-based Study of Viral Replication isolated, followed by the hepatitis A virus (HAV) in 1973. In the following years viral agents causing disease similar to HAV and HBV, but negative for tests specific for these viruses, were reported and named as non-A, non-B (NANB) Hepatitis Viruses, with distinct post-transfusion or enteric epidemiology.
eBook - PDF- Arnold Reif(Author)
- 2012(Publication Date)
- Academic Press(Publisher)
THE BIOLOGY OF HEPATITIS Β VIRUS AND HEPATOCELLULAR CARCINOMA* Arie J. Zuckerman Department of Medical Microbiology and WHO Collaborating Centre for Reference and Research on Viral Hepatitis London School of Hygiene and Tropical Medicine University of London London WC1E 7HT I. INTRODUCTION Viral hepatitis is a major public health problem in all parts of the world. The term human viral hepatitis refers to infections caused by four or more different viruses or groups of viruses, hepatitis A, hepatitis B, the more recently identified forms of hepatitis, non-Α, non-B hepatitis which are caused by more than two viruses and probably by several different viruses, epidemic non-Α hepatitis (previously referred to as epidemic non-Α, non-B hepatitis) and the delta virus. Hepatitis A and hepatitis Β can be differentiated by sensitive laboratory tests for specific antigens and antibodies and the viruses have been characterised. Specific laboratory tests are available for the delta agent, a defective virus which replicates in individuals ^The hepatitis research programme at the London School of Hygiene and Tropical Medicine is supported by generous grants from the Medical Research Council, the Department of Health and Social Security, the Wellcome Trust, the World Health Organiza-tion and Organon B.V. The hepatitis Β vaccine development at the London School of Hygiene and Tropical Medicine is generously supported by the British Technology Group (formerly the National Research Develop-ment Corporation), the Department of Health and Social Security, and the Wellcome Trust and the Commission of the European Economic Community. Copyright © 1985 by Academic Press, Inc. IMMUNITY TO CANCER 619 All rights of reproduction in any form reserved. ISBN 0-12-586270-9 620 Arie J. Zuckerman infected with hepatitis Β virus. Laboratory tests are under development for epidemic non-Α hepatitis, which is not caused by the recognised serotype of hepatitis A.
eBook - ePub- Douglas D. Richman, Richard J. Whitley, Frederick G. Hayden, Douglas D. Richman, Richard J. Whitley, Frederick G. Hayden(Authors)
- 2016(Publication Date)
- ASM Press(Publisher)
32 Hepatitis B Virus DARREN J. WONG, STEPHEN A. LOCARNINI, AND ALEXANDER J.V. THOMPSONIt has been over 40 years since the discovery of the hepatitis B virus (HBV), and yet the disease it causes remains a major public health challenge. Worldwide, over 240 million people have chronic hepatitis B (CHB), with the majority being in the Asia-Pacific region, and there are almost 800,000 deaths each year as a direct consequence of infection (2 ). HBV infection is the ninth leading cause of death worldwide. The main public health strategy to control hepatitis B infection for the last 30 years has been primary prevention through vaccination. According to WHO, as of 2013, more than 180 countries have now adopted a national policy of immunizing all infants with hepatitis B vaccine. However, a strategy of secondary prevention is clearly necessary to reduce the risk of long-term complications (cirrhosis, liver failure, and hepatocellular carcinoma) in those individuals who have CHB. The risk of these complications is strongly associated with persistent high-level HBV replication (3 –5 ). Antiviral agents active against HBV are available. The long-term suppression of HBV replication has been shown to prevent progression to cirrhosis and reduce the risk of hepatocellular carcinoma (HCC) and liver-related deaths. However, currently available treatments fail to eradicate the virus in most of those treated, necessitating potentially lifelong treatment. WHO has set targets for both morbidity and mortality. A cure for CHB remains elusive, and a significant research effort is now being directed toward this goal.VIROLOGY
Classification
The HBV is an enveloped 3.2-kb double-stranded DNA virus and prototypical member of the family Hepadnaviridae. HBV can be classified into ten major genotypes (A to J) based on nucleotide (nt) diversity of 8% or more over the entire genome (6 –10 ). These genotypes show distinct geographical distributions (Table 1 ). As genotype designation is now based on the entire genomic sequence, it is a more reliable classification than the earlier serological subtype nomenclature (adw , adr , ayw, and ayn ) used previously, which was based on the immunoreactivity of particular antibodies to a limited number of amino acids in the envelope protein. Particular HBV genotypes have unique insertions or deletions. For example, HBV genotype A varies from the other genotypes by an insertion of six nucleotides at the C-terminus of the core gene (11 ). HBV genotype D has a 33-nt deletion at the N-terminus of the Pre-S1 region (11 ). HBV genotypes E and G have a 3-nt deletion also in the N-terminus of the Pre-S1 region. HBV genotype G also has a 36-nt insertion in the N-terminus of the core gene (8 ), and the precore/core region has two translational stop codons at positions 2 and 28 and results in a HBeAg-negative phenotype. A very large number of subgenotypes (of <8% but greater than 4% nt diversity) have been described in a number of these genotypes (A, B, C, D, and F), and recombination between two HBV genotypes has also been reported for genotypes B and C (12 ) and genotypes A and D (13
eBook - PDFMolecular Genetic Medicine
Volume 2
- Theodore Friedmann(Author)
- 2013(Publication Date)
- Academic Press(Publisher)
3. Hepatitis B Virus Biology and Pathogenesis 91 viral vectors carrying HBV DNA sequences. Much has been learned using these systems with regard to the regulation of HBV gene expression (Spandau and Lee, 1988; Shaul et al, 1985; Tur-Kaspa et al, 1986; Treinin and Laub, 1987; H. K. Chang et al, 1987; Elfassi, 1987; Ganem and Varmus, 1987; Siddiqui et al, 1987; Tognoni et al, 1985) and particle structure, assembly, and transport (Ou et al, 1986; Roossinck et al, 1986; Uy et al, 1986; McLachlan et al, 1987; Schlicht et al, 1987; C. Chang et al, 1987a; Persing et al, 1986; Ou and Rutter, 1987; Molnar-Kimber et al, 1988; Cheng and Moss, 1987; Cheng et al, 1986; Marquardt et al, 1987; Moss et a/., 1984; Standring et a!., 1986; Yaginuma et ., 1987). Furthermore, among these systems are those that have opened the door for development of alternative vaccines (Heermann et al, 1984; Moss et al, 1984) and for production of immunological models to study the immu-nopathogenesis of HBV-induced liver cell injury in humans (McLachlan et al, 1987). Until recently, however, these in vitro systems did not support viral replication, thereby limiting their experimental value and restricting in vitro analysis of viral replication to the primary duck hepatocyte system described above (Tuttleman et al., 1986a,b). Because of the difficulties inherent in primary hepatocyte cell culture, it is not surprising that considerable effort was made to establish a system for viral replication in continuous cell lines. Indeed, several laboratories have demonstrated that cloned, tandemly repeated, multimers of hepadnavirus genomes transfected into human hepato-cellular carcinoma cell lines yield transformed cellular clones that support viral replication (Yaginuma et al, 1987; C. Chang et al, 1987b; Sells et al, 1987; Sureau et al, 1986; Tsurimoto et al, 1987) and produce complete HBV viral particles that are infectious in chimpanzees (Acs et al, 1987).
- Nejat Düzgünes(Author)
- 2019(Publication Date)
- Quintessence Publishing Co, Inc(Publisher)
• HBsAg can be detected during acute or chronic HBV infection, and its presence indicates that a person can pass the virus to others. Donated blood is screened for HBsAg. The presence of the core antigen (HbcAg) is the best indicator for the presence of infectious virus.• Liver necrosis, inflammation, and fibrosis are observed in chronic hepatitis, leading to the development of cirrhosis. Liver damage results from immune system attack on hepatocytes expressing viral antigens.• HBV is transmitted through transfusion of blood and blood products, accidental injection of contaminated blood, exchange of fluids, and transplantation. • Chronic hepatitis B can be treated with pegylated interferon, 3TC, adefovir, entecavir, and tenofovir. • The HBV vaccine is based on recombinant HBsAg produced in yeast. • HCV is an enveloped, positive-strand RNA virus with an icosahedral capsid. • Acute HCV infection is usually asymptomatic. However, it can lead to rapid progression to cirrhosis in 15% of patients and chronic infection in 70% of patients. • Liver pathogenesis is most likely mediated by cytotoxic T cells attaching to hepatocytes that express viral antigens. • HCV is spread via blood, blood-derived products, sexual contact, and from mother to child.• Treatment of HCV infections involves the use of pegylated interferon-α with or without ribavirin. The protease inhibitors telaprevir and boceprevir can be added to this regimen. Newer drugs include sofosbuvir, simeprevir, and daclatasvir.• HDV is an RNA virus that requires the presence of HBV to replicate. The range of clinical presentation varies from mild disease to fulminant liver failure. • HEV resembles HAV. Most infections are subclinical, but when symptomatic, the virus causes fulminant hepatitis that may be fatal. • HGV is a flavivirus, similar to HCV. It replicates in lymphocytes and not hepatocytes and may inhibit HIV replication.
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The Herpesviridae family has three subfamilies: α- , β- , and γ- herpesvirinae (Table 33-1 ). The α-herpesvirinae include the genera Simplexvirus and Varicellovirus that grow rapidly in cultured cells and establish latent infection in sensory ganglia. The β-herpesvirinae comprise Cytomegalovirus and Roseolovirus
eBook - PDF- John I. Gallin, Anthony S. Fauci(Authors)
- 2000(Publication Date)
- Academic Press(Publisher)
8 I M M U NOPATHOGEN ESIS OF HEPATITIS C BARBARA REHERMANN Liver Diseases Section National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health Bethesda, Maryland INTRODUCTION More than 170 million people in the world are estimated to be infected with the hepatitis C virus (HCV) and the prevalence of HCV infection among healthy blood donors varies between 0.01 and 0.02% in northern Europe, (1,2) 6.5% in equatorial Africa, (3) and 20% in Egypt. (4,5) In the United States, infec- tion with HCV accounts for 16-21% of all cases of acute and 45 % of chronic viral hepatitis. In total, 4 million people, i.e., 1.8% of the U.S. population, are infected. (6) The immunological correlates of viral clearance are still unknown. This is mainly due to the fact that most de novo HCV infections are clinically inappar- ent and in 40% of cases neither the time nor the routes of infection are known. Accordingly, many patients are diagnosed with hepatitis C when they present with symptoms and signs of chronic rather than acute liver disease. (7-9) For similar reasons, most studies on the HCV-specific immune response have been performed in chronically rather than in acutely infected or recovered patients. Collectively, these data imply that the immune response can mediate chronic in- flammatory liver cell injury if it is not able to clear the virus early after infection. COMPONENTS AND KINETICS OF THE CELLULAR IMMUNE RESPONSE Induction of a Virus-Specific, Cellular Immune Response It is generally assumed that the outcome of an acute viral infection, i.e., viral clearance or persistence, is determined in its earliest phase. Several factors, such as size, route, and genetic composition of the infecting virus as well as its rate of replication, cell tropism, and level of antigen expression, determine the kinetics with which host cells become infected and an opposing cellular immune response is induced.
eBook - PDF- Joao Monjardino(Author)
- 1998(Publication Date)
- ICP(Publisher)
During this period both the liver enzymes and bile pigments are raised in serum. However in some cases, common amongst children but rare in adults, the disease is asymptomatic. 14 Molecular Biology of Human Hepatitis Viruses The patient is infectious between two and five weeks after exposure while the virus, which is secreted in the bile, is present in the stools. The infection is self-limiting with ultimate clearance of the virus. This occurs before the jaundice disappears and is associated with a strong neutralizing antibody response which confers life-long protection. The antibody response includes IgM, IgA and IgG. IgM can be detected days before the onset of symptoms and disappears by three months whereas IgG, being the primary defense against re-infection, becomes detectable within three months and persists throughout life. The strictly hepatotropic virus is not directly cytopathic and liver damage appears to occur as the result of the cellular immune response directed at the infected liver cells. Although the histological changes observed in the infected liver are common to other forms of viral hepatitis some features are suggestive of HAV infection. These include the periportal distribution of the inflammatory changes with bile stasis (cholestasis) and prominent hepatocyte damage with multivesicular bodies in the cells showing cytopathic changes. The virus gets across the intestinal wall and reaches the liver by a mechanism which has not been fully elucidated. Replication in the liver is accompanied by virus release into the blood stream and excretion into the bile and faeces. Epidemiology The ocurrence of hepatitis A is closely related to socio-economic development with high incidence, endemic areas corresponding to the poorest regions of the world.
eBook - PDF- Edward K. Wagner, Martinez J. Hewlett, David C. Bloom, David Camerini(Authors)
- 2009(Publication Date)
- Wiley-Blackwell(Publisher)
This is not a latent infection because the harboring cells can express viral antigens, which lead to lifelong immunity, but infectious virus can never be recovered. Other lasting types of virus-induced damage can be much more difficult to establish without extensive epidemiological records. Chronic liver damage due to hepatitis B virus infection is a major factor in hepatic carcinoma. Persistent virus infections can lead to immune dysfunction. Virus infections may also result in the appearance of a disease or syndrome (a set of diagnostic symptoms displayed by an affected individual) years later that has no obvious relation to the initial infection. It has been suggested that diseases such as diabetes mellitus, multiple sclerosis, and rheumatoid arthritis have viral etiologies (ultimate causative factors). Virus factors have also been implicated in instances of other diseases such as cancer and schizophrenia. QUESTIONS FOR CHAPTER 2 1 A good general rule concerning the replication of RNA viruses is that they require what kind of molecular process? 2 What is the role of a vector in the transmission of a viral infection? 3 It is said that viruses appear to “violate the cell theory” (“cells only arise from preexisting cells”). To which phase of a virus life cycle (growth curve) does this refer? What is the explanation for this phase of the growth curve? 4 Viruses are called “obligate intracellular parasites.” For which step of gene expression do all viruses completely depend on their host cell? 5 Viruses are said to “violate the cell theory,” indicating that there are differences between viruses and cells. In the following table are listed several features of either viruses or cells or both. Indicate which of these features is true for viruses and which for cells. Write a “Yes” if the feature is true or a “No” if the feature is not true in each case.
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