List of Viral Targets
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Saint Louis Encephalitis Virus and Other Arboviruses in the Differential Diagnosis for Dengue
Revista da Sociedade Brasileira de Medicina Tropical 47(5):541-542, Sep-Oct, 2014 http://dx.doi.org/10.1590/0037-8682-0197-2014 Editorial Saint Louis encephalitis virus and other arboviruses in the differential diagnosis for dengue Luiz Tadeu Moraes Figueiredo[1] [1]. Centro de Pesquisa em Virologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP. Brazil is a tropical country with a wide variety of flora and SLEV-seropositive by an immunoglobulin G-enzyme-linked fauna that includes many arthropods, especially mosquitoes and immunosorbent assay (IgG-ELISA), and these findings were midges. This ecological diversity facilitates the maintenance confirmed by a highly specific neutralization test. In the following of arboviral cycles and the emergence of novel arboviral year, during a widespread dengue type 3 epidemic, six patients pathogens. Indeed, many outbreaks attributable to zoonotic tested positive for SLEV in the City of São José do Rio Preto3,4. arboviruses such as Oropouche, Mayaro, Rocio virus (ROCV), Recently, a patient from Ribeirão Preto who presented with acute Saint Louis encephalitis virus (SLEV) and yellow fever virus febrile illness was also found to be SLEV-positive5. have been seen in the recent past. Furthermore, due to the In contrast to SLEV, ROCV has only been isolated in the increase in international travel, arboviruses present in other southeastern region of Brazil in the 1970s during a large-scale American countries, such as the emergent viruses West Nile outbreak of encephalitis that resulted in many fatalities. During and Chikungunya, have already been introduced, or could this outbreak, ROCV was isolated from 3 sources, a patient, be introduced to this region in the future. -
(SLE) Frequently Asked Questions What Is Saint Louis Encephalitis?
Saint Louis Encephalitis (SLE) Frequently Asked Questions What is Saint Louis encephalitis? Saint Louis encephalitis (SLE) is a type of viral encephalitis (inflammation or swelling of the brain) caused by the Saint Louis encephalitis virus. The SLE virus is transmitted to humans by mosquitoes. This virus normally only circulates between birds and mosquitoes. Human‐biting mosquitoes can become infected, however, and can transmit this disease to people. These mosquitoes tend to live and breed in urban and suburban areas; most human cases are also found in these areas. Because of the life cycle of the mosquitoes that transmit SLE virus, most SLE infections occur in the late summer and in the fall. Saint Louis encephalitis is found throughout the United States, including Georgia. What are the symptoms of SLE? Most people do not become ill when a mosquito infected with the SLE virus bites them. People who do experience symptoms will start to feel ill approximately 5‐15 days after the mosquito bite. Most people who experience symptoms will only suffer from headaches or a mild flu‐like illness with muscle aches, weakness, or vomiting. A small number of persons may develop encephalitis or aseptic meningitis (inflammation/swelling of the protective covering of the brain and spinal cord), and may experience symptoms such as confusion, coma, and possibly death. How likely am I to have serious illness resulting from SLE infection? Less than 1% of persons infected with Saint Louis encephalitis virus will show symptoms. In children less than 10 years old, only 1 child out of 800 will experience symptoms. -
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. -
Saint Louis Encephalitis (SLE)
Encephalitis, SLE Annual Report 2018 Saint Louis Encephalitis (SLE) Saint Louis Encephalitis is a Class B Disease and must be reported to the state within one business day. St. Louis Encephalitis (SLE), a flavivirus, was first recognized in 1933 in St. Louis, Missouri during an outbreak of over 1,000 cases. Less than 1% of infections manifest as clinically apparent disease cases. From 2007 to 2016, an average of seven disease cases were reported annually in the United States. SLE cases occur in unpredictable, intermittent outbreaks or sporadic cases during the late summer and fall. The incubation period for SLE is five to 15 days. The illness is usually benign, consisting of fever and headache; most ill persons recover completely. Severe disease is occasionally seen in young children but is more common in adults older than 40 years of age, with almost 90% of elderly persons with SLE disease developing encephalitis. Five to 15% of cases die from complications of this disease; the risk of fatality increases with age in older adults. Arboviral encephalitis can be prevented by taking personal protection measures such as: a) Applying mosquito repellent to exposed skin b) Wearing protective clothing such as light colored, loose fitting, long sleeved shirts and pants c) Eliminating mosquito breeding sites near residences by emptying containers which hold stagnant water d) Using fine mesh screens on doors and windows. In the 1960s, there were 27 sporadic cases; in the 1970s, there were 20. In 1980, there was an outbreak of 12 cases in New Orleans. In the 1990s, there were seven sporadic cases and two outbreaks; one outbreak in 1994 in New Orleans (16 cases), and the other in 1998 in Jefferson Parish (14 cases). -
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. -
Prevention & Control of Viral Hepatitis Infection
Prevention & Control of Viral Hepatitis Infection: A Strategy for Global Action © World Health Organization 2011. All rights reserved. The designations employed and the presentation of the material in this publication do not imply the expression of any opinion whatsoever on the part of the World Health Organization concerning the legal status of any country, territory, city or area or of its authorities, or concerning the delimitation of its frontiers or boundaries. Dotted lines on maps represent approximate border lines for which there may not yet be full agreement. The mention of specific companies or of certain manufacturers’ products does not imply that they are endorsed or recommended by the World Health Organization in preference to others of a similar nature that are not mentioned. Errors and omissions excepted, the names of proprietary products are distinguished by initial capital letters. All reasonable precautions have been taken by WHO to verify the information contained in this publication. However, the published material is being distributed without warranty of any kind, either express or implied. The responsibility for the interpretation and use of the material lies with the reader. In no event shall the World Health Organization be liable for damages arising from its use. Table of contents Disease burden 02 What is viral hepatitis? 05 Prevention & control: a tailored approach 06 Global Achievements 08 Remaining challenges 10 World Health Assembly: a mandate for comprehensive prevention & control 13 WHO goals and strategy -
BK Virus: Current Understanding of Pathogenicity and Clinical Disease in Transplantation
This is a repository copy of BK virus: Current understanding of pathogenicity and clinical disease in transplantation. White Rose Research Online URL for this paper: http://eprints.whiterose.ac.uk/146942/ Version: Accepted Version Article: Chong, S, Antoni, M orcid.org/0000-0002-3641-7559, Macdonald, A orcid.org/0000-0002-5978-4693 et al. (3 more authors) (2019) BK virus: Current understanding of pathogenicity and clinical disease in transplantation. Reviews in Medical Virology, 29 (4). ARTN: e2044. ISSN 1052-9276 https://doi.org/10.1002/rmv.2044 © 2019 John Wiley & Sons, Ltd. This is an author produced version of a paper published in Reviews in Medical Virology. Uploaded in accordance with the publisher's self-archiving policy. Reuse Items deposited in White Rose Research Online are protected by copyright, with all rights reserved unless indicated otherwise. They may be downloaded and/or printed for private study, or other acts as permitted by national copyright laws. The publisher or other rights holders may allow further reproduction and re-use of the full text version. This is indicated by the licence information on the White Rose Research Online record for the item. Takedown If you consider content in White Rose Research Online to be in breach of UK law, please notify us by emailing [email protected] including the URL of the record and the reason for the withdrawal request. [email protected] https://eprints.whiterose.ac.uk/ BK virus: Current understanding of pathogenicity and clinical disease in transplantation Running head: BK Virus: current understanding in Transplantation Stephanie Chong1, Michelle Antoni2, Andrew Macdonald2, Matthew Reeves3, Mark Harber1 and Ciara N. -
Merkel Cell Polyomavirus DNA in Immunocompetent and Immunocompromised Patients with Respiratory Disease
Journal of Medical Virology 83:2220–2224 (2011) Merkel Cell Polyomavirus DNA in Immunocompetent and Immunocompromised Patients With Respiratory Disease Bahman Abedi Kiasari,1,3* Pamela J. Vallely,1 and Paul E. Klapper1,2 1Department of Virology, Genomic Epidemiology Research Group, School of Translational Medicine, University of Manchester, Manchester, United Kingdom 2Clinical Virology, Manchester Medical Microbiology Partnership, Manchester Royal Infirmary, Oxford Road, Manchester, United Kingdom 3Human Viral Vaccine Department, Razi Vaccine & Serum Research Institute, Hesarak, Karaj, Iran Merkel cell polyomavirus (MCPyV) was identi- INTRODUCTION fied originally in association with a rare but aggressive skin cancer, Merkel cell carcinoma. In the past few years, a number of new human poly- The virus has since been found in the respirato- omaviruses, KI, WU, human polyomavirus 6 (HPyV6), ry tract of some patients with respiratory human polyomavirus 7 (HPyV7), trichodysplasia spi- disease. However, the role of MCPyV in the nulosa virus (TSV), human polyomavirus 9 (HPyV9), causation of respiratory disease has not been and Merkel cell polyomavirus (MCPyV) have been established. To determine the prevalence of discovered [Allander et al., 2007; Gaynor et al., 2007; MCPyV in 305 respiratory samples from Feng et al., 2008; Schowalter et al., 2010; van der immunocompetent and immunocompromised Meijden et al., 2010; Scuda et al., 2011]. MCPyV was patients and evaluate their contribution to re- discovered by digital transcriptome subtraction from a spiratory diseases, specimens were screened human skin cancer, Merkel cell carcinoma [Feng for MCPyV using single, multiplex, or real-time et al., 2008]. The finding of MCPyV in human Merkel PCR; co-infection with other viruses was exam- cell carcinoma suggests a role for this virus in the ined. -
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. -
An Overview on Human Polyomaviruses Developing Cancer
The Journal of Medical Research 2020; 6(4): 125-127 Review Article An overview on human polyomaviruses developing cancer in JMR 2020; 6(4): 125-127 humans July- August ISSN: 2395-7565 Mohammad Salim1, Mohammad Shahid Masroor2, Shagufta parween3, I.P. Prajapati1 © 2020, All rights reserved 1 Sanjay Gandhi Smriti Govt. Autonomous P.G. College, Sidhi, (affiliated to APS University, Rewa), Madhya Pradesh- www.medicinearticle.com 486661, India Received: 22-06-2020 2 People’s College of Dental Sciences & Research Center, People's University, Bhopal, Madhya Pradesh- 462037, Accepted: 14-07-2020 India 3 All India Institute of Medical sciences (AIIMS), Bhopal, Madhya Pradesh-462020, India Abstract The family Polyomaviridae included about a dozen of human polyomaviruses (HPyVs), of which MCPyV, SV-40, JCV and BKV viruses have been reported to cause cancer in human. Merkel cell carcinoma is a very aggressive type of skin cancer caused by the MCPyV5. Similarly, while SV-40 and JCV viruses developed brain tumor cancer, the BK virus has been linked to renal transplantations and nephropathy producing urinary bladder tumor and prostate cancer in human. In this paper we have tried to summarize the recent information gained in the field of human polyomaviruses causing cancer in human. Keywords: Human polyomaviruses, Cancer, Virus. INTRODUCTION Viruses are among the few causes of cancer contributing to a variety of malignancies. In 1966, when Peyton Rous was awarded a Nobel prize in physiology and medicine for his discovery of Rous chicken sarcoma virus as a cause of cancer, a renewed interest came in the field of microbial origin of cancer. -
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.