Prevention & Control of Viral Hepatitis Infection
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Immunogenicity and Efficacy Testing in Chimpanzees of an Oral Hepatitis B Vaccine Based on Live Recombinant Adenovirus
Proc. Natl. Acad. Sci. USA Vol. 86, pp. 6763-6767, September 1989 Medical Sciences Immunogenicity and efficacy testing in chimpanzees of an oral hepatitis B vaccine based on live recombinant adenovirus (adenovirus animal model/adenovirus-vectored vacdnes) MICHAEL D. LUBECK*, ALAN R. DAVIS*, MURTY CHENGALVALA*, ROBERT J. NATUK*, JOHN E. MORIN*, KATHERINE MOLNAR-KIMBER*, BRUCE B. MASON*, BHEEM M. BHAT*, SATOSHI MIZUTANI*, PAUL P. HUNG*, AND ROBERT H. PURCELLO *Wyeth-Ayerst Research, Biotechnology and Microbiology Division, P.O. Pox 8299, Philadelphia, PA 19101; and tLaboratory of Infectious Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892 Contributed by Robert H. Purcell, May 30, 1989 ABSTRACT As a major cause of acute and chronic liver which, because oftheir wide prior usage, are good candidates disease as well as hepatocellular carcinoma, hepatitis B virus as vectors. Other less well-characterized small animal models (HBV) continues to pose significant health problems world- for human adenoviruses have been occasionally reported wide. Recombinant hepatitis B vaccines based on adenovirus (11-13) but are likewise nonpermissive for Ad4 and Ad7 vectors have been developed to address global needs for infections (unpublished data). An early study of animal effective control of hepatitits B infection. Although consider- species including nonhuman primates indicated that human able progress has been made in the construction ofrecombinant adenoviruses do not induce acute respiratory disease in adenoviruses that express large amounts of HBV gene prod- monkeys or chimpanzees following intranasal inoculations ucts, preclinical immunogenicity and efficacy testing of candi- (14). Serological data, however, indicated that such experi- date vaccines has remained difficult due to the lack ofa suitable mental infections occasionally induced anti-adenovirus anti- animal model. -
Viral Hepatitis Testing Effective Date: January 1, 2012
Viral Hepatitis Testing Effective Date: January 1, 2012 Scope This guideline provides guidance for the use of laboratory tests to diagnose acute and chronic viral hepatitis in adults (> 19 years) in the primary care setting. General Considerations for Ordering Laboratory Tests Prior to ordering tests for hepatitis, consider the patient’s history, age, risk factors (see below), hepatitis vaccination status, and any available previous hepatitis test results. Risk Factors for Viral Hepatitis include: • Substance use (includes sharing drug snorting, smoking or injection equipment) • High-risk sexual activity or sexual partner with viral hepatitis • Travel to or from high-risk hepatitis endemic areas or exposure during a local outbreak • Immigration from hepatitis B and/or C endemic countries • Household contact with an infected person especially if personal items (e.g., razors, toothbrushes, nail clippers) are shared • Recipient of unscreened blood products* • Needle-stick injury or other occupational exposure (e.g., healthcare workers) • Children born to mothers with chronic hepatitis B or C infection • Attendance at daycare • Contaminated food or water (hepatitis A only) • Tattoos and body piercing • History of incarceration • HIV or other sexually transmitted infection • Hemodialysis *screening of donated blood products for hepatitis C (anti-HCV) began in 1990 in Canada.1 Types of Viral Hepatitis Hepatitis A: causes acute but not chronic hepatitis Hepatitis B: causes acute and chronic hepatitis Hepatitis C: causes chronic hepatitis but rarely manifests as acute hepatitis Hepatitis D: rare and only occurs in patients infected with hepatitis B Hepatitis E: clinically similar to hepatitis A, mostly restricted to endemic areas and occasionally causes chronic infection in immunosuppressed people Others: e.g. -
Hepatitis B Fast Facts Everything You Need to Know in 2 Minutes Or Less!
Hepatitis B Foundation Cause for a Cure www.hepb.org Hepatitis B Fast Facts Everything you need to know in 2 minutes or less! Hepatitis B is the most common serious liver infection in the world. It is caused by the hepatitis B virus (HBV) that attacks liver cells and can lead to liver failure, cirrhosis (scarring) or cancer of the liver. The virus is transmitted through contact with blood and bodily fluids that contain blood. Most people are able to fight off the hepatitis B infection and clear the virus from their blood. This may take up to six months. While the virus is present in their blood, infected people can pass the virus on to others. Approximately 5-10% of adults, 30-50% of children, and 90% of babies will not get rid of the virus and will develop chronic infection. Chronically infected people can pass the virus on to others and are at increased risk for liver problems later in life. The hepatitis B virus is 100 times more infectious than the AIDS virus. Yet, hepatitis B can be pre- vented with a safe and effective vaccine. For the 400 million people worldwide who are chronically infected with hepatitis B, the vaccine is of no use. However, there are promising new treatments for those who live with chronic hepatitis B. In the World: • This year alone, 10 to 30 million people will become infected with the hepatitis B virus (HBV). • The World Health Organization estimates that 400 million people worldwide are already chronically infected with hepatitis B. -
The Role of Hepatitis C Virus in Hepatocellular Carcinoma U
Viruses in cancer cell plasticity: the role of hepatitis C virus in hepatocellular carcinoma U. Hibner, D. Gregoire To cite this version: U. Hibner, D. Gregoire. Viruses in cancer cell plasticity: the role of hepatitis C virus in hepato- cellular carcinoma. Contemporary Oncology, Termedia Publishing House, 2015, 19 (1A), pp.A62–7. 10.5114/wo.2014.47132. hal-02187396 HAL Id: hal-02187396 https://hal.archives-ouvertes.fr/hal-02187396 Submitted on 2 Jun 2021 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Distributed under a Creative Commons Attribution - NonCommercial - ShareAlike| 4.0 International License Review Viruses are considered as causative agents of a significant proportion of human cancers. While the very Viruses in cancer cell plasticity: stringent criteria used for their clas- sification probably lead to an under- estimation, only six human viruses the role of hepatitis C virus are currently classified as oncogenic. In this review we give a brief histor- in hepatocellular carcinoma ical account of the discovery of on- cogenic viruses and then analyse the mechanisms underlying the infectious causes of cancer. We discuss viral strategies that evolved to ensure vi- Urszula Hibner1,2,3, Damien Grégoire1,2,3 rus propagation and spread can alter cellular homeostasis in a way that increases the probability of oncogen- 1Institut de Génétique Moléculaire de Montpellier, CNRS, UMR 5535, Montpellier, France ic transformation and acquisition of 2Université Montpellier 2, Montpellier, France stem cell phenotype. -
Rational Engineering of HCV Vaccines for Humoral Immunity
viruses Review To Include or Occlude: Rational Engineering of HCV Vaccines for Humoral Immunity Felicia Schlotthauer 1,2,†, Joey McGregor 1,2,† and Heidi E Drummer 1,2,3,* 1 Viral Entry and Vaccines Group, Burnet Institute, Melbourne, VIC 3004, Australia; [email protected] (F.S.); [email protected] (J.M.) 2 Department of Microbiology and Immunology, Peter Doherty Institute for Infection and Immunity, University of Melbourne, Melbourne, VIC 3000, Australia 3 Department of Microbiology, Monash University, Clayton, VIC 3800, Australia * Correspondence: [email protected]; Tel.: +61-392-822-179 † These authors contributed equally to this work. Abstract: Direct-acting antiviral agents have proven highly effective at treating existing hepatitis C infections but despite their availability most countries will not reach the World Health Organization targets for elimination of HCV by 2030. A prophylactic vaccine remains a high priority. Whilst early vaccines focused largely on generating T cell immunity, attention is now aimed at vaccines that gen- erate humoral immunity, either alone or in combination with T cell-based vaccines. High-resolution structures of hepatitis C viral glycoproteins and their interaction with monoclonal antibodies isolated from both cleared and chronically infected people, together with advances in vaccine technologies, provide new avenues for vaccine development. Keywords: glycoprotein E2; vaccine development; humoral immunity Citation: Schlotthauer, F.; McGregor, J.; Drummer, H.E To Include or 1. Introduction Occlude: Rational Engineering of HCV Vaccines for Humoral Immunity. The development of direct-acting antiviral agents (DAA) with their ability to cure Viruses 2021, 13, 805. https:// infection in >95% of those treated was heralded as the key to eliminating hepatitis C globally. -
Hepatitis B? HEPATITIS B Hepatitis B Is a Contagious Liver Disease That Results from Infection with the Hepatitis B Virus
What is Hepatitis B? HEPATITIS B Hepatitis B is a contagious liver disease that results from infection with the Hepatitis B virus. When first infected, a person can develop Are you at risk? an “acute” infection, which can range in severity from a very mild illness with few or no symptoms to a serious condition requiring hospitalization. Acute Hepatitis B refers to the first 6 months after someone is exposed to the Hepatitis B virus. Some people are able to fight the infection and clear the virus. For others, the infection remains and leads to a “chronic,” or lifelong, illness. Chronic Hepatitis B refers to the illness that occurs when the Hepatitis B virus remains in a person’s body. Over time, the infection can cause serious health problems. How is Hepatitis B spread? Hepatitis B is usually spread when blood, semen, or other body fluids from a person infected with the Hepatitis B virus enter the body of someone who is not infected. This can happen through having sex with an infected partner; sharing needles, syringes, or other injection drug equipment; or from direct contact with the blood or open sores of an infected person. Hepatitis B can also be passed from an infected mother to her baby at birth. Who should be tested for Hepatitis B? Approximately 1.2 million people in the United States and 350 million people worldwide have Hepatitis B. Testing for Hepatitis B is recommended for certain groups of people, including: Most are unaware of their infection. ■ People born in Asia, Africa, and other regions with moderate or high rates Is Hepatitis B common? of Hepatitis B (see map) Yes. -
Hepatitis A, B, and C: Learn the Differences
Hepatitis A, B, and C: Learn the Differences Hepatitis A Hepatitis B Hepatitis C caused by the hepatitis A virus (HAV) caused by the hepatitis B virus (HBV) caused by the hepatitis C virus (HCV) HAV is found in the feces (poop) of people with hepa- HBV is found in blood and certain body fluids. The virus is spread HCV is found in blood and certain body fluids. The titis A and is usually spread by close personal contact when blood or body fluid from an infected person enters the body virus is spread when blood or body fluid from an HCV- (including sex or living in the same household). It of a person who is not immune. HBV is spread through having infected person enters another person’s body. HCV can also be spread by eating food or drinking water unprotected sex with an infected person, sharing needles or is spread through sharing needles or “works” when contaminated with HAV. “works” when shooting drugs, exposure to needlesticks or sharps shooting drugs, through exposure to needlesticks on the job, or from an infected mother to her baby during birth. or sharps on the job, or sometimes from an infected How is it spread? Exposure to infected blood in ANY situation can be a risk for mother to her baby during birth. It is possible to trans- transmission. mit HCV during sex, but it is not common. • People who wish to be protected from HAV infection • All infants, children, and teens ages 0 through 18 years There is no vaccine to prevent HCV. -
Understanding Human Astrovirus from Pathogenesis to Treatment
University of Tennessee Health Science Center UTHSC Digital Commons Theses and Dissertations (ETD) College of Graduate Health Sciences 6-2020 Understanding Human Astrovirus from Pathogenesis to Treatment Virginia Hargest University of Tennessee Health Science Center Follow this and additional works at: https://dc.uthsc.edu/dissertations Part of the Diseases Commons, Medical Sciences Commons, and the Viruses Commons Recommended Citation Hargest, Virginia (0000-0003-3883-1232), "Understanding Human Astrovirus from Pathogenesis to Treatment" (2020). Theses and Dissertations (ETD). Paper 523. http://dx.doi.org/10.21007/ etd.cghs.2020.0507. This Dissertation is brought to you for free and open access by the College of Graduate Health Sciences at UTHSC Digital Commons. It has been accepted for inclusion in Theses and Dissertations (ETD) by an authorized administrator of UTHSC Digital Commons. For more information, please contact [email protected]. Understanding Human Astrovirus from Pathogenesis to Treatment Abstract While human astroviruses (HAstV) were discovered nearly 45 years ago, these small positive-sense RNA viruses remain critically understudied. These studies provide fundamental new research on astrovirus pathogenesis and disruption of the gut epithelium by induction of epithelial-mesenchymal transition (EMT) following astrovirus infection. Here we characterize HAstV-induced EMT as an upregulation of SNAI1 and VIM with a down regulation of CDH1 and OCLN, loss of cell-cell junctions most notably at 18 hours post-infection (hpi), and loss of cellular polarity by 24 hpi. While active transforming growth factor- (TGF-) increases during HAstV infection, inhibition of TGF- signaling does not hinder EMT induction. However, HAstV-induced EMT does require active viral replication. -
Host Cell Functions in Vesicular Stomatitis Virus Replication Phat X
University of Nebraska - Lincoln DigitalCommons@University of Nebraska - Lincoln Papers in Veterinary and Biomedical Science Veterinary and Biomedical Sciences, Department of 2016 Host Cell Functions In Vesicular Stomatitis Virus Replication Phat X. Dinh University of Nebraska - Lincoln Anshuman Das University of Nebraska-Lincoln Asit K. Pattnaik University of Nebraska - Lincoln, [email protected] Follow this and additional works at: https://digitalcommons.unl.edu/vetscipapers Part of the Biochemistry, Biophysics, and Structural Biology Commons, Cell and Developmental Biology Commons, Immunology and Infectious Disease Commons, Medical Sciences Commons, Veterinary Microbiology and Immunobiology Commons, and the Veterinary Pathology and Pathobiology Commons Dinh, Phat X.; Das, Anshuman; and Pattnaik, Asit K., "Host Cell Functions In Vesicular Stomatitis Virus Replication" (2016). Papers in Veterinary and Biomedical Science. 237. https://digitalcommons.unl.edu/vetscipapers/237 This Article is brought to you for free and open access by the Veterinary and Biomedical Sciences, Department of at DigitalCommons@University of Nebraska - Lincoln. It has been accepted for inclusion in Papers in Veterinary and Biomedical Science by an authorized administrator of DigitalCommons@University of Nebraska - Lincoln. Published in Biology and Pathogenesis of Rhabdo and Filoviruses Copyright © 2016 World Scientific Publishing Co Pte Ltd digitalcommons.unl.edu HOST CELL FUNCTIONS IN VESICULAR STOMATITIS VIRUS REPLICATION Phat X. Dinh, Anshuman Das, and Asit K. Pattnaik School of Veterinary Medicine and Biomedical Sciences and the Nebraska Center for Virology, University of Nebraska-Lincoln, 109 Morrison Life Science Research Center, 4240 Fair Street, Lincoln, * Nebraska 68583, USA E-mail: [email protected] Summary Vesicular stomatitis virus (VSV), the prototypic rhabdovirus, has been used as an excellent paradigm for understanding the mechanisms of virus replication, pathogenesis, host response to virus infection and also for myriads of studies on cellular and molecular biology. -
Hepatitis a Transmitted by Food
INVITED ARTICLE FOOD SAFETY David Acheson, Section Editor Hepatitis A Transmitted by Food Anthony E. Fiore Division of Viral Hepatitis, Centers for Disease Control and Prevention, Atlanta Hepatitis A is caused by hepatitis A virus (HAV). Transmission occurs by the fecal-oral route, either by direct contact with an HAV-infected person or by ingestion of HAV-contaminated food or water. Foodborne or waterborne hepatitis A outbreaks are relatively uncommon in the United States. However, food handlers with hepatitis A are frequently identified, and evaluation of the need for immunoprophylaxis and implementation of control measures are a considerable burden on public health resources. In addition, HAV-contaminated food may be the source of hepatitis A for an unknown proportion of persons whose source of infection is not identified. FEATURES OF HEPATITIS A and 40%–70% are jaundiced [6]. Children and occasionally young adults can also have inapparent infection, in which Hepatitis A virus (HAV) is classified as a picornavirus. Primates symptoms and elevation of ALT levels are absent but serocon are the only natural host [1]. There is only 1 HAV serotype, version occurs [7]. and immunity after infection is lifelong [2]. After ingestion, Hepatitis A begins with symptoms such as fever, anorexia, uptake in the gastrointestinal tract, and subsequent replication nausea, vomiting, diarrhea, myalgia, and malaise. Jaundice, in the liver, HAV is excreted in bile, and high concentrations dark-colored urine, or light-colored stools might be present at are found in stool specimens. Transmission occurs by the fecal- onset or might follow constitutional symptoms within a few oral route, either by direct contact with an HAV-infected person days. -
HEPATITIS D the Most Virulent Hepatitis Virus of All
HEPATITIS D The Most Virulent Hepatitis Virus Of All The hepatitis D virus is perhaps the most unique of all hepatitis viruses, and also the most virulent. As a virus, it is flawed. The hepatitis D virus (HDV) cannot replicate and infect someone unless the person is already infected with the hepatitis B virus (HBV). The hepatitis D virus requires the outer coating of the hepatitis B virus—called the surface antigen—in order to reproduce itself in a human host. The virus currently infects 15 million worldwide, nearly all adults, and it is most common among injecting drug user populations and in countries bordering the Mediterranean Sea. Most children with HDV infection live in Italy and Greece, with a few in northern Africa. There are no reports or estimates of There are two types of HDV infection, the number of children infected with coinfection and super-infection: HDV worldwide. • Coinfection occurs when a patient is Despite widespread hepatitis B in simultaneously infected with HDV and Asian populations, HDV infection is HBV. The majority of these patients virtually unknown there and appears completely recover but there is a higher rate of fulminant hepatic failure and primarily in injecting drug user death than with HBV infection alone. populations. • Super-infection occurs when someone HDV is transmitted through blood and with an existing chronic HBV infection body fluids, similar to the hepatitis B becomes infected with HDV. These patients usually experience a sudden virus. Hepatitis D symptoms are worsening of liver disease. Patients with similar to other viral hepatitis diseases hepatitis B who become chronically and include jaundice, fever, malaise, infected with HDV experience a very dark urine and nausea. -
The Role of Hepatitis C Virus in Hepatocellular Carcinoma A63
Review Viruses are considered as causative agents of a significant proportion of human cancers. While the very Viruses in cancer cell plasticity: stringent criteria used for their clas- sification probably lead to an under- estimation, only six human viruses the role of hepatitis C virus are currently classified as oncogenic. In this review we give a brief histor- in hepatocellular carcinoma ical account of the discovery of on- cogenic viruses and then analyse the mechanisms underlying the infectious causes of cancer. We discuss viral strategies that evolved to ensure vi- Urszula Hibner1,2,3, Damien Grégoire1,2,3 rus propagation and spread can alter cellular homeostasis in a way that increases the probability of oncogen- 1Institut de Génétique Moléculaire de Montpellier, CNRS, UMR 5535, Montpellier, France ic transformation and acquisition of 2Université Montpellier 2, Montpellier, France stem cell phenotype. We argue that 3Université Montpellier 1, Montpellier, France a useful way of analysing the conver- gent characteristics of viral infection and cancer is to examine how viruses affect the so-called cancer hallmarks. Introduction This view of infectious origin of cancer It is estimated that close to 20% of human cancers are due to infections is illustrated by examples from hep- atitis C infection, which is associated with known pathogens, mainly with viruses [1]. Given the difficulties in un- with a high proportion of hepatocellu- ambiguously assigning their causative role [2] and the fast rate of discovery lar carcinoma. of new viruses [3], it is likely a conservative estimate. Different pathogens are associated with increased cancer risk. One of the Key words: viruses, cancer cell plas- first identified cancer-causing infectious disease was schistosomiasis, ini- ticity, HCV, hepatocellular carcinoma.