Virus-Encoded Complement Regulators: Current Status
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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but are likewise nonpermissive for Ad4 and Ad7 vectors have been developed to address global needs for infections (unpublished data).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. -
Intracellular Trafficking of HBV Particles
cells Review Intracellular Trafficking of HBV Particles Bingfu Jiang 1 and Eberhard Hildt 1,2,* 1 Department of Virology, Paul-Ehrlich-Institut, D-63225 Langen, Germany; [email protected] 2 German Center for Infection Research (DZIF), TTU Hepatitis, Marburg-Gießen-Langen, D63225 Langen, Germany * Correspondence: [email protected]; Tel.: +49-61-0377-2140 Received: 12 August 2020; Accepted: 2 September 2020; Published: 2 September 2020 Abstract: The human hepatitis B virus (HBV), that is causative for more than 240 million cases of chronic liver inflammation (hepatitis), is an enveloped virus with a partially double-stranded DNA genome. After virion uptake by receptor-mediated endocytosis, the viral nucleocapsid is transported towards the nuclear pore complex. In the nuclear basket, the nucleocapsid disassembles. The viral genome that is covalently linked to the viral polymerase, which harbors a bipartite NLS, is imported into the nucleus. Here, the partially double-stranded DNA genome is converted in a minichromosome-like structure, the covalently closed circular DNA (cccDNA). The DNA virus HBV replicates via a pregenomic RNA (pgRNA)-intermediate that is reverse transcribed into DNA. HBV-infected cells release apart from the infectious viral parrticle two forms of non-infectious subviral particles (spheres and filaments), which are assembled by the surface proteins but lack any capsid and nucleic acid. In addition, naked capsids are released by HBV replicating cells. Infectious viral particles and filaments are released via multivesicular bodies; spheres are secreted by the classic constitutive secretory pathway. The release of naked capsids is still not fully understood, autophagosomal processes are discussed. This review describes intracellular trafficking pathways involved in virus entry, morphogenesis and release of (sub)viral particles. -
Tools for Cell Therapy and Immunoregulation
RnDSy-lu-2945 Tools for Cell Therapy and Immunoregulation Target Cell TIM-4 SLAM/CD150 BTNL8 PD-L2/B7-DC B7-H1/PD-L1 (Human) Unknown PD-1 B7-1/CD80 TIM-1 SLAM/CD150 Receptor TIM Family SLAM Family Butyrophilins B7/CD28 Families T Cell Multiple Co-Signaling Molecules Co-stimulatory Co-inhibitory Ig Superfamily Regulate T Cell Activation Target Cell T Cell Target Cell T Cell B7-1/CD80 B7-H1/PD-L1 T cell activation requires two signals: 1) recognition of the antigenic peptide/ B7-1/CD80 B7-2/CD86 CTLA-4 major histocompatibility complex (MHC) by the T cell receptor (TCR) and 2) CD28 antigen-independent co-stimulation induced by interactions between B7-2/CD86 B7-H1/PD-L1 B7-1/CD80 co-signaling molecules expressed on target cells, such as antigen-presenting PD-L2/B7-DC PD-1 ICOS cells (APCs), and their T cell-expressed receptors. Engagement of the TCR in B7-H2/ICOS L 2Ig B7-H3 (Mouse) the absence of this second co-stimulatory signal typically results in T cell B7-H1/PD-L1 B7/CD28 Families 4Ig B7-H3 (Human) anergy or apoptosis. In addition, T cell activation can be negatively regulated Unknown Receptors by co-inhibitory molecules present on APCs. Therefore, integration of the 2Ig B7-H3 Unknown B7-H4 (Mouse) Receptors signals transduced by co-stimulatory and co-inhibitory molecules following TCR B7-H5 4Ig B7-H3 engagement directs the outcome and magnitude of a T cell response Unknown Ligand (Human) B7-H5 including the enhancement or suppression of T cell proliferation, B7-H7 Unknown Receptor differentiation, and/or cytokine secretion. -
The Munich Outbreak of Cutaneous Cowpox Infection: Transmission by Infected Pet Rats
Acta Derm Venereol 2012; 92: 126–131 INVESTIGATIVE REPORT The Munich Outbreak of Cutaneous Cowpox Infection: Transmission by Infected Pet Rats Sandra VOGEL1, Miklós SÁRDY1, Katharina GLOS2, Hans Christian KOrting1, Thomas RUZICKA1 and Andreas WOLLENBERG1 1Department of Dermatology and Allergology, Ludwig Maximilian University, Munich, and 2Department of Dermatology, Haas and Link Animal Clinic, Germering, Germany Cowpox virus infection of humans is an uncommon, another type of orthopoxvirus, from infected pet prairie potentially fatal, skin disease. It is largely confined to dogs have recently been described in the USA, making Europe, but is not found in Eire, or in the USA, Austral the medical community aware of the risk of transmission asia, or the Middle or Far East. Patients having contact of pox viruses from pets (3). with infected cows, cats, or small rodents sporadically Seven of 8 exposed patients living in the Munich contract the disease from these animals. We report here area contracted cowpox virus infection from an unusual clinical aspects of 8 patients from the Munich area who source: rats infected with cowpox virus bought from had purchased infected pet rats from a local supplier. Pet local pet shops and reputedly from the same supplier rats are a novel potential source of local outbreaks. The caused a clinically distinctive pattern of infection, which morphologically distinctive skin lesions are mostly res was mostly restricted to the patients’ neck and trunk. tricted to the patients’ necks, reflecting the infected ani We report here dermatologically relevant aspects of mals’ contact pattern. Individual lesions vaguely resem our patients in order to alert the medical community to ble orf or Milker’s nodule, but show marked surrounding the possible risk of a zoonotic orthopoxvirus outbreak erythema, firm induration and local adenopathy. -
Complement Recognition Pathways in Renal Transplantation
BRIEF REVIEW www.jasn.org Complement Recognition Pathways in Renal Transplantation Christopher L. Nauser, Conrad A. Farrar, and Steven H. Sacks Medical Research Council Centre for Transplantation, Division of Transplantation Immunology and Mucosal Biology, King’s College London, National Health Service Guy’s and St. Thomas’ Trust, London, United Kingdom ABSTRACT The complement system, consisting of soluble and cell membrane–bound compo- weigh its effect on organ injury and nents of the innate immune system, has defined roles in the pathophysiology of renal rejection with dampening the antimi- allograft rejection. Notably, the unavoidable ischemia-reperfusion injury inherent to crobial functions of the complement sys- transplantation is mediated through the terminal complement activation products tem, such as opsonisation, cell lysis, and C5a and C5b-9. Furthermore, biologically active fragments C3a and C5a, produced recruitment of neutrophils and other in- during complement activation, can modulate both antigen presentation and T cell flammatory cells.7 It is our belief that priming, ultimately leading to allograft rejection. Earlier work identified renal tubule therapeutic strategies can be designed cell synthesis of C3, rather than hepatic synthesis of C3, as the primary source of C3 to specificallytargetthekeyinitiators driving these effects. Recent efforts have focused on identifying the local triggers of of complement activation at the relevant complement activation. Collectin-11, a soluble C-type lectin expressed in renal tis- location, such as complement-binding sue, has been implicated as an important trigger of complement activation in renal anti-HLA antibodies in the vascular tissue. In particular, collectin-11 has been shown to engage L-fucose at sites of compartment or the initiator(s) of local ischemic stress, activating the lectin complement pathway and directing the innate complement activation in the extravas- immune response to the distressed renal tubule. -
How Macrophages Deal with Death
REVIEWS CELL DEATH AND IMMUNITY How macrophages deal with death Greg Lemke Abstract | Tissue macrophages rapidly recognize and engulf apoptotic cells. These events require the display of so- called eat-me signals on the apoptotic cell surface, the most fundamental of which is phosphatidylserine (PtdSer). Externalization of this phospholipid is catalysed by scramblase enzymes, several of which are activated by caspase cleavage. PtdSer is detected both by macrophage receptors that bind to this phospholipid directly and by receptors that bind to a soluble bridging protein that is independently bound to PtdSer. Prominent among the latter receptors are the MER and AXL receptor tyrosine kinases. Eat-me signals also trigger macrophages to engulf virus- infected or metabolically traumatized, but still living, cells, and this ‘murder by phagocytosis’ may be a common phenomenon. Finally , the localized presentation of PtdSer and other eat- me signals on delimited cell surface domains may enable the phagocytic pruning of these ‘locally dead’ domains by macrophages, most notably by microglia of the central nervous system. In long- lived organisms, abundant cell types are often process. Efferocytosis is a remarkably efficient business: short- lived. In the human body, for example, the macrophages can engulf apoptotic cells in less than lifespan of many white blood cells — including neutro- 10 minutes, and it is therefore difficult experimentally to phils, eosinophils and platelets — is less than 2 weeks. detect free apoptotic cells in vivo, even in tissues where For normal healthy humans, a direct consequence of large numbers are generated7. Many of the molecules this turnover is the routine generation of more than that macrophages and other phagocytes use to recognize 100 billion dead cells each and every day of life1,2. -
Discovery of a Highly Divergent Hepadnavirus in Shrews from China
Virology 531 (2019) 162–170 Contents lists available at ScienceDirect Virology journal homepage: www.elsevier.com/locate/virology Discovery of a highly divergent hepadnavirus in shrews from China T Fang-Yuan Niea,b,1, Jun-Hua Tianc,1, Xian-Dan Lind,1, Bin Yuc, Jian-Guang Xinge, Jian-Hai Caof, ⁎ ⁎⁎ Edward C. Holmesg,h, Runlin Z. Maa, , Yong-Zhen Zhangb,h, a State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China b State Key Laboratory for Infectious Disease Prevention and Control; Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases; Department of Zoonoses, National Institute for Communicable Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Changping, Beijing, China c Wuhan Center for Disease Control and Prevention, Wuhan, China d Wenzhou Center for Disease Control and Prevention, Wenzhou, Zhejiang Province, China e Wencheng Center for Disease Control and Prevention, Wencheng, Zhejiang Province, China f Longwan Center for Disease Control and Prevention, Longwan District, Wenzhou, Zhejiang Province, China g Marie Bashir Institute for Infectious Diseases and Biosecurity, Charles Perkins Centre, School of Life and Environmental Sciences and Sydney Medical School, The University of Sydney, Sydney, NSW 2006, Australia h Shanghai Public Health Clinical Center & Institute of Biomedical Sciences, Fudan University, Shanghai, China ARTICLE INFO ABSTRACT Keywords: Limited sampling means that relatively little is known about the diversity and evolutionary history of mam- Hepadnaviruses malian members of the Hepadnaviridae (genus Orthohepadnavirus). An important case in point are shrews, the Shrews fourth largest group of mammals, but for which there is limited knowledge on the role they play in viral evo- Phylogeny lution and emergence. -
Human Astrovirus 1–8 Seroprevalence Evaluation in a United States Adult Population
UC Santa Cruz UC Santa Cruz Previously Published Works Title Human Astrovirus 1-8 Seroprevalence Evaluation in a United States Adult Population. Permalink https://escholarship.org/uc/item/9nz336gs Journal Viruses, 13(6) ISSN 1999-4915 Authors Meyer, Lena Delgado-Cunningham, Kevin Lorig-Roach, Nicholas et al. Publication Date 2021-05-25 DOI 10.3390/v13060979 Peer reviewed eScholarship.org Powered by the California Digital Library University of California viruses Article Human Astrovirus 1–8 Seroprevalence Evaluation in a United States Adult Population Lena Meyer , Kevin Delgado-Cunningham, Nicholas Lorig-Roach, Jordan Ford and Rebecca M. DuBois * Department of Biomolecular Engineering, University of California Santa Cruz, Santa Cruz, CA 95064, USA; [email protected] (L.M.); [email protected] (K.D.-C.); [email protected] (N.L.-R.); [email protected] (J.F.) * Correspondence: [email protected] Abstract: Human astroviruses are an important cause of viral gastroenteritis globally, yet few studies have investigated the serostatus of adults to establish rates of previous infection. Here, we applied biolayer interferometry immunosorbent assay (BLI-ISA), a recently developed serosurveillance technique, to measure the presence of blood plasma IgG antibodies directed towards the human astrovirus capsid spikes from serotypes 1–8 in a cross-sectional sample of a United States adult population. The seroprevalence rates of IgG antibodies were 73% for human astrovirus serotype 1, 62% for serotype 3, 52% for serotype 4, 29% for serotype 5, 27% for serotype 8, 22% for serotype 2, 8% for serotype 6, and 8% for serotype 7. Notably, seroprevalence rates for capsid spike antigens correlate with neutralizing antibody rates determined previously. -
CD2 Molecules Redistribute to the Uropod During T Cell Scanning: Implications for Cellular Activation and Immune Surveillance
CD2 molecules redistribute to the uropod during T cell scanning: Implications for cellular activation and immune surveillance Elena V. Tibaldi*†, Ravi Salgia†‡, and Ellis L. Reinherz*†§ *Laboratory of Immunobiology and ‡Division of Adult Oncology, Lowe Center for Thoracic Oncology, Dana-Farber Cancer Institute, and †Department of Medicine, Harvard Medical School, Boston, MA 02115 Communicated by Stuart F. Schlossman, Dana-Farber Cancer Institute, Boston, MA, April 9, 2002 (received for review February 14, 2002) Dynamic binding between CD2 and CD58 counter-receptors on op- cells, whereas its counter-receptor CD58 is expressed on a posing cells optimizes immune recognition through stabilization of diverse array of nucleated and non-nucleated cells including cell–cell contact and juxtaposition of surface membranes at a distance APCs and stromal cells (reviewed in refs. 11 and 12). CD2 suitable for T cell receptor–ligand interaction. Digitized time-lapse functions in both T cell adhesion and activation processes (13). Ϸ differential interference contrast and immunofluorescence micros- Of note, the weak affinity of the CD2-CD58 interaction (Kd copy on living cells now show that this binding also induces T cell 1 M) is associated with remarkably fast on and off rates that polarization. Moreover, CD2 can facilitate motility of T cells along foster rapid and extensive exchange between CD2 and CD58 antigen-presenting cells via a movement referred to as scanning. Both partners on opposing cell surfaces (14–16). These biophysical activated CD4 and CD8 T cells are able to scan antigen-presenting cells characteristics are reminiscent of the selectin–ligand interactions surfaces in the absence of cognate antigen. -
Genetic Susceptibility to Chronic Wasting Disease in Free-Ranging White-Tailed Deer: Complement Component C1q and Prnp Polymorphisms Julie A
Natural Resource Ecology and Management Natural Resource Ecology and Management Publications 12-2009 Genetic susceptibility to chronic wasting disease in free-ranging white-tailed deer: Complement component C1q and Prnp polymorphisms Julie A. Blanchong Iowa State University, [email protected] Dennis M. Heisey United States Geological Survey Kim T. Scribner Michigan State University Scot V. Libants Michigan State University Chad Johnson UFonilvloerwsit ythi of sW aiscondn asiddn - itMionadisoaln works at: http://lib.dr.iastate.edu/nrem_pubs Part of the Animal Diseases Commons, Genetics Commons, Natural Resources Management See next page for additional authors and Policy Commons, Veterinary Infectious Diseases Commons, and the Zoology Commons The ompc lete bibliographic information for this item can be found at http://lib.dr.iastate.edu/ nrem_pubs/84. For information on how to cite this item, please visit http://lib.dr.iastate.edu/ howtocite.html. This Article is brought to you for free and open access by the Natural Resource Ecology and Management at Iowa State University Digital Repository. It has been accepted for inclusion in Natural Resource Ecology and Management Publications by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. Genetic susceptibility to chronic wasting disease in free-ranging white- tailed deer: Complement component C1q and Prnp polymorphisms Abstract The eg netic basis of susceptibility to chronic wasting disease (CWD) in free-ranging cervids is of great interest. Association studies of disease susceptibility in free-ranging populations, however, face considerable challenges including: the need for large sample sizes when disease is rare, animals of unknown pedigree create a risk of spurious results due to population admixture, and the inability to control disease exposure or dose. -
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. -
Activation Regulates Alternative Pathway Complement Necrotic
Properdin Binds to Late Apoptotic and Necrotic Cells Independently of C3b and Regulates Alternative Pathway Complement Activation This information is current as of September 27, 2021. Wei Xu, Stefan P. Berger, Leendert A. Trouw, Hetty C. de Boer, Nicole Schlagwein, Chantal Mutsaers, Mohamed R. Daha and Cees van Kooten J Immunol 2008; 180:7613-7621; ; doi: 10.4049/jimmunol.180.11.7613 Downloaded from http://www.jimmunol.org/content/180/11/7613 References This article cites 56 articles, 27 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/180/11/7613.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 27, 2021 • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Properdin Binds to Late Apoptotic and Necrotic Cells Independently of C3b and Regulates Alternative Pathway Complement Activation1,2 Wei Xu,* Stefan P. Berger,* Leendert A.