Zuckerman / Howard / Tinsley Hepatitis Viruses of Man

1. Auflage 2014
ISBN: 978-1-4832-2078-9
Verlag: Elsevier Science & Techn.
Format: EPUB
Kopierschutz: 6 - ePub Watermark

E-Book, Englisch, 278 Seiten

Hepatitis Viruses of Man covers the advances and developments in the study of viral hepatitis. The book discusses the history, epidemiology, and clinical features of viral hepatitis; the nomenclature and morphology of hepatitis viruses and their antigens; and the pathology of the liver in acute viral hepatitis. The text also describes the biochemical and biophysical properties of hepatitis B surface antigen; the nature and immunopathogenesis of hepatitis B; and the laboratory tests for hepatitis B surface antigen and antibody and hepatitis B core antigen and antibody. The carrier state; maternal transmission of hepatitis B and neonatal infection; and Hepatitis B virus and primary liver cancer are also considered. The book further tackles the laboratory tests for hepatitis A and the nature of the virus; immunization against hepatitis; and interferon and antiviral therapy in chronic hepatitis B infection. Microbiologists, pathologists, and medical doctors will find the book useful.

APPOINTMENTS 1989-1999 AND CURRENT APPOINTMENTS Principal and Dean of the Royal Free and University College Medical School of University College London 1998-October 1999 (and of the Royal Free Hospital School of Medicine since 1989) Professor of Medical Microbiology in the University of London 1975-1999. Professor Emeritus since October 1999 Honorary Consultant Medical Microbiologist, Royal Free Hampstead NHS Trust since 1990 Non-Executive Director of the Royal Free Hampstead NHS Trust 1990-October 1999 Director, World Health Organisation Collaborating Centre for Reference and Research on Viral Hepatitis, London (1974-1989) and on Viral Diseases since 1990 Member of the WHO Expert Advisory Panel on Virus Diseases since 1974 Founder and Editor-in-Chief of the Journal of Medical Virology (Wiley-Liss, New York) since 1976, and of the Journal of Virological Methods (Elsevier, Amsterdam) since 1979 Member of the Council of University College London since 1995 PREVIOUS APPOINTMENTS London School of Hygiene and Tropical Medicine (Senior Lecturer 1965-1968; Reader in Virology 1968-1972; Professor of Virology 1972-1975; Professor of Medical Microbiology 1975-1989). Member of several Expert and Advisory Groups to the Department of Health 1970-2000. Member of the Council of the Royal College of Pathologists (1983-1986), Public Health Laboratory Service Board (1983-1989), Council of the Zoological Society of London (1989-1992),Court and Council of the University of London (1992-1998). MILITARY SERVICE Royal Air Force Medical Branch (1959-1962). AUTHOR AND EDITOR of 16 textbooks and numerous publications in learned journals.

Autoren/Hrsg.

Zuckerman, Arie J.

Howard, Colin R.

Tinsley, T. W.

Brown, F.

Inhaltsverzeichnis

1;Front Cover;1
2;Hepatitis Viruses of Man;4
3;Copyright Page;5
4;Table of Contents;8
5;PREFACE;6
6;Chapter 1. The history of viral hepatitis;10
6.1;THE ORIGIN OF THE TERM JAUNDICE;10
6.2;EPIDEMIC JAUNDICE UNTIL THE NINETEENTH CENTURY;11
6.3;CATARRHAL JAUNDICE;12
6.4;CAMPAIGN JAUNDICE;13
6.5;THE VIRAL AETIOLOGY OF HEPATITIS;15
6.6;THE EMERGENCE OF A SECOND TYPE OF HEPATITIS;16
6.7;A CHURCHILLIAN STORY;20
6.8;HUMAN EXPERIMENTATION;21
6.9;HEPATITIS A AND B;22
6.10;SPECIFIC SEROLOGICAL TESTS FOR VIRAL HEPATITIS;24
6.11;DISCOVERY OF AUSTRALIA ANTIGEN;25
7;Chapter 2. Nomenclature of hepatitis viruses and their antigens;28
7.1;SUBDETERMINANTS OF HEPATITIS B SURFACE ANTIGEN;29
7.2;SUBDETERMINANTS OF HEPATITIS B e ANTIGEN;30
8;Chapter 3. The epidemiology of viral hepatitis;31
8.1;HEPATITIS A;31
8.2;HEPATITIS B;33
9;Chapter 4. Pathology of the liver in acute viral hepatitis;43
9.1;ULTRASTRUCTURAL CHANGES IN THE LIVER IN VIRAL HEPATITIS;45
9.2;INTRACELLULAR VIRUS PARTICLES IN HEPATITIS A;47
9.3;INTRACELLULAR VIRUS PARTICLES IN HEPATITIS B;47
10;Chapter 5. The clinical features of viral hepatitis;49
10.1;ACUTE ANICTERIC HEPATITIS;50
10.2;ACUTE ICTERIC HEPATITIS;50
10.3;OTHER FORMS OF VIRAL HEPATITIS AND SEQUELAE;51
11;Chapter 6. The morphology of the hepatitis viruses;54
11.1;HEPATITIS B VIRUS;55
11.2;HEPATITIS A VIRUS;63
11.3;THE GB HEPATITIS AGENT;65
12;Chapter 7. Biochemical and biophysical properties of hepatitis B surface antigen;68
12.1;PROPERTIES OF THE SURFACE ANTIGEN;68
12.2;IMMUNOCHEMISTRY OF HEPATITIS B SURFACE ANTIGEN;75
13;Chapter 8. Laboratory tests for hepatitis B surface antigen and antibody;81
13.1;IMMUNODIFFUSION;81
13.2;COUNTER-IMMUNOELECTROPHORESIS;82
13.3;COMPLEMENT-FIXATION;83
13.4;INERT PARTICLE AGGLUTINATION;84
13.5;PASSIVE HAEMAGGLUTINATION AND HAEMAGGLUTINATION INHIBITION;84
13.6;REVERSE PASSIVE HAEMAGGLUTINATION;85
13.7;RADIOIMMUNOASSAY;86
13.8;ENZYME-LINKED IMMUNOSORBENT ASSAY (ELISA OR EIA);88
13.9;IMMUNE ADHERENCE HAEMAGGLUTINATION;89
13.10;ELECTRON MICROSCOPY;89
14;Chapter 9. Laboratory tests for hepatitis B core antigen and antibody;91
14.1;IMMUNOFLUORESCENCE;91
14.2;COMPLEMENT-FIXATION;91
14.3;IMMUNE ADHERENCE HAEMAGGLUTINATION;92
14.4;RADIOIMMUNOASSAY;92
15;Chapter 10. The hepatitis B e antigen-antibody system;94
15.1;SEROLOGICAL DETECTION;94
15.2;THE NATURE OF e ANTIGEN;98
15.3;POSSIBLE ASSOCIATION OF e ANTIGEN WITH HEPATITIS B VIRUS AND THE SURFACE ANTIGEN;103
15.4;CLINICAL SIGNIFICANCE;106
16;Chapter 11. The nature of hepatitis B virus;111
16.1;HEPATITIS B VIRUS-ASSOCIATED DNA POLYMERASE;112
16.2;BIOPHYSICAL PROPERTIES OF HEPATITIS B CORE ANTIGEN;113
16.3;CORE ANTIGEN POLYPEPTIDES;115
16.4;IMMUNOCHEMISTRY OF HEPATITIS B CORE ANTIGEN;117
16.5;THE NUCLEIC ACID OF HEPATITIS B VIRUS;118
17;Chapter 12. Immunopathogenesis of hepatitis B;123
17.1;THE HUMORAL RESPONSE;123
17.2;CELLULAR IMMUNE RESPONSES;125
17.3;AUTOIMMUNE REACTIONS;127
17.4;THE ROLE OF CORE ANTIGEN IMMUNE COMPLEXES;129
17.5;EXTRAHEPATIC LESIONS IN HEPATITIS B;131
17.6;ARTHRITIS;131
17.7;POLYARTERITIS NODOSA;133
17.8;GLOMERULONEPHRITIS;134
17.9;POLYMYALGIA RHEUMATICA;135
17.10;ESSENTIAL MIXED CRYOGLOBULINAEMIA;136
17.11;INFANTILE PAPULAR ACRODERMATITIS;137
17.12;THE DELTA ANTIGEN–ANTIBODY SYSTEM;137
17.13;AN ANTIBODY REACTING WITH DANE PARTICLES;138
18;Chapter 13. The carrier state;139
18.1;HEPATITIS A;139
18.2;HEPATITIS B;140
18.3;LIVER DISEASE IN CARRIERS;142
18.4;SEX DIFFERENCES IN THE CARRIER STATE;143
18.5;GENETIC SUSCEPTIBILITY TO HEPATITIS B;146
18.6;THE HISTOCOMPATIBILITY LOCI (HLA);149
18.7;MANAGEMENT OF THE ASYMPTOMATIC CARRIER STATE OF HEPATITIS B;152
19;Chapter 14. Maternal transmission of hepatitis B and neonatal infection;155
19.1;CONTROL OF HEPATITIS B INFECTION IN THE NEWBORN;158
20;Chapter 15. Hepatitis B virus and primary liver cancer;161
21;Chapter 16. Laboratory tests for hepatitis A and the nature of the virus;166
21.1;IMMUNE ELECTRON MICROSCOPY;166
21.2;NON-HUMAN PRIMATES, HEPATITIS A AND THE DEVELOPMENT OF SEROLOGICAL TECHNIQUES;169
21.3;COMPLEMENT-FIXATION;170
21.4;IMMUNE ADHERENCE HAEMAGGLUTINATION;170
21.5;IMMUNOFLUORESCENCE;171
21.6;RADIOIMMUNOASSAY;171
21.7;ENZYME LINKED IMMUNOSORBENT ASSAY (ELISA OR EIA);172
21.8;DETECTION OF SPECIFIC HEPATITIS A IgM;173
21.9;THE NATURE OF HEPATITIS A VIRUS;174
22;Chapter 17. Viral hepatitis in non-human primates;176
22.1;HEPATITIS A;177
22.2;HEPATITIS B;179
22.3;THE PATHOLOGY OF HEPATITIS A AND B IN CHIMPANZEES;184
22.4;TRANSMISSION OF HEPATITIS B TO RHESUS MONKEYS;186
22.5;THE THIRD FORM OF HEPATITIS (NON-A: NON-B HEPATITIS) IN CHIMPANZEES;188
23;Chapter 18. Non-A: non-B hepatitis;194
23.1;NON-A: NON-B POST-TRANSFUSION HEPATITIS;194
23.2;SPORADIC FORM OF NON-A: NON-B HEPATITIS;197
23.3;BLOOD FRACTIONS AND NON-A: NON-B HEPATITIS;199
23.4;LABORATORY MARKERS FOR NON-A: NON-B HEPATITIS;202
24;Chapter 19. Hepatitis viruses: tissue and organ culture studies;204
25;Chapter 20. Immunization against hepatitis;209
25.1;HEPATITIS A;209
25.2;HEPATITIS B;210
26;Chapter 21. Interferon and antiviral therapy in chronic hepatitis B infection;229
26.1;INTERFERON;229
26.2;ANTIVIRAL DRUGS;232
27;References;236
28;Subject Index;270

Leseproben

3 The epidemiology of viral hepatitis
Publisher Summary
Morbidity rates of hepatitis A are based on notification and statistical records; Sweden and Denmark have kept statistical records of hepatitis with jaundice since 1928. Viral hepatitis became notifiable in the United States of America in January 1952, and since 1966, hepatitis A and hepatitis B have been notifiable separately. Thus, statistical records of morbidity and mortality are available for a number of countries. Notifications tend to be extremely variable not only from city to city and from region to region but also with a number of poorly definable factors such as holiday seasons, physician awareness, and many more. Hepatitis B has been defined in the past on the basis of infection occurring in patients about 40–200 days after the injection of human blood or plasma fractions. However, the mode of spread of hepatitis B continues to present intriguing and unexpected findings. The huge reservoir of hepatitis B virus in the human population with a prevalence of hepatitis B surface antigen among apparently healthy adults varying from about 0.02–0.1% in parts of Europe, North America and Australia, over 5% in parts of eastern and southern Europe, the Middle and Far East, to as many as 20% in some tropical areas poses a major public health problem. Hepatitis A Incidence Age incidence Seasonal pattern Mode of spread Incubation period Hepatitis B Hepatitis B surface antigen in various body fluids other than blood Incubation period Incidence Age incidence Modes of transmission Clustering of hepatitis B in families HEPATITIS A
Incidence
Morbidity rates of hepatitis A are based on notification and statistical records; Sweden and Denmark have kept statistical records of hepatitis with jaundice since 1928, Viral hepatitis became notifiable in the United States of America in January 1952, and since 1966 hepatitis A and hepatitis B have been notifiable separately. Hepatitis has also been reported for a number of years in many European countries and in June 1968, the notification of infective jaundice became compulsory in England and Wales. Thus statistical records of morbidity and mortality are available for a number of countries. However, no account is taken of subclinical infections and anicteric cases, which occur with a generally accepted rate of some 10 cases or more for each patient with clinical jaundice. Notifications tend to be extremely variable, not only from city to city and from region to region but also with a number of poorly definable factors such as holiday seasons, physician awareness and so on. Furthermore, the degree of under-reporting is believed to be very high and it is doubtful whether more than perhaps 50% of cases of jaundice are actually notified. Age incidence
All age groups are susceptible to hepatitis. Until recent years the highest incidence in the civilian population was observed in children of school age but in a number of countries, including Sweden and the U.S.A., as many as 60–70% of the notified cases occur in adults. This shift in age incidence is reminiscent of the change of age incidence which occurred with poliomyelitis during and after the Second World War, reflecting improvement in socio-economic conditions. Seasonal pattern
In temperate zones the characteristic seasonal trend is for a marked rise in incidence in the autumn and early winter months with a rapid and progressive fall from January to a minimum during midsummer. Mosley (1972) noted, however, that since 1966 the seasonal peak has been lost in the U.S.A. Mode of spread
Hepatitis A is spread by the intestinal–oral route, most commonly by close contact, and infection occurs readily in conditions of poor sanitation and overcrowding. Food or waterborne transmission is not a major factor in the maintenance of this infection in the developed countries. Ingestion of shellfish cultivated in polluted water is associated with a high risk of acquiring hepatitis A. This infection is also not infrequently acquired by travellers to areas of high endemicity. Outbreaks of hepatitis A have also been described in handlers of newly captured non-human primates. Hepatitis A is not transmitted by blood and blood products and rarely if ever by the parenteral route (Szmuness et al., 1977; Papaevangelou et al., 1978), although this has been achieved experimentally in volunteers. Incubation period
The incubation period of hepatitis A is between 3 and 5 weeks and most commonly 4 weeks. This period of incubation has been confirmed by human volunteer experiments and by transmission to susceptible chimpanzees. The incubation period of the MS-1 strain of hepatitis A transmitted either by the oral route or parenterally to volunteers was between 35 and 50 days. HEPATITIS B
Hepatitis B has been defined in the past on the basis of infection occurring in patients about 40–200 days after the injection of human blood or plasma fractions. However, the mode of spread of hepatitis B continues to present intriguing and unexpected findings. The huge reservoir of hepatitis B virus in the human population with a prevalence of hepatitis B surface antigen among apparently healthy adults varying from about 0·02–0·1% in parts of Europe, North America and Australia, over 5% in parts of eastern and southern Europe, the Middle and Far East, to as many as 20% in some tropical areas, poses a major public health problem. As sensitive laboratory techniques for markers of hepatitis B infection were developed the epidemiological concepts of this infection have undergone significant changes, and it is now clear that the direct inoculation of blood and certain blood products cannot be the principal method of spread of the infection, nor account for the some 176 million carriers of hepatitis B. The question of whether an apparently healthy carrier can transmit frequently the infectious agent by means other than blood is thus of great importance and much has been written on the subject. Hepatitis B surface antigen, a marker of the virus, has been found repeatedly in blood and in a variety of body fluids including saliva, menstrual and vaginal discharges, seminal fluid, amniotic fluid, colostrum and breast milk. The presence of the antigen in urine, bile, faeces, sweat and even tears has also been reported but not always confirmed. It is therefore not surprising that contact-associated hepatitis B is apparently of major significance. Hepatitis B surface antigen in various body fluids other than blood
Hepatitis B surface antigen has been detected repeatedly in blood and certain plasma fractions, saliva, semen, breast milk, amniotic fluid and in certain exudates including pleural effusions and ascitic fluid. The antigen has also been reported in various tissue and body fluids contaminated with blood. Occasionally, the surface antigen was reported in bile and urine and a variety of other fluids including sweat and tears but confirmation of these is still awaited. Saliva Hepatitis B surface antigen has been detected in the saliva and mouth washings obtained from patients with acute hepatitis B, from persistent carriers and from patients with chronic liver disease and antigenaemia. Although occult blood was found in many samples of saliva, the presence of antigen in saliva was independent of the presence of blood. The titre of antigen in saliva is always low but tends to be higher in specimens containing occult blood. The antigen was never detected beyond 4 weeks after the onset of symptoms in acute hepatitis B and its finding in saliva was related to the titre of antigen in the blood (Lun Wong et al., 1976). In persistent carriers the antigen was found intermittently in repeated saliva specimens (Feinman et al., 1975). Bancroft et al. (1977) collected a pool of whole-mouth saliva from five carriers of hepatitis B surface antigen. Occult blood was present in the saliva and immune electron microscopy revealed all the morphological entities associated with hepatitis B including the complete virus. Two gibbons (Hylobates lar) were injected subcutaneously with a small quantity of the saliva pool every other day for 3 days. One gibbon developed antigenaemia for 2 weeks accompanied by elevated alanine aminotransferase 12 weeks after inoculation. Surface antibody was detected in all subsequent serum samples. The second gibbon had elevated alanine and aspartate aminotransferases, 10 weeks and 4 days after exposure, and surface antibody was detected at 22 weeks. Eight gibbons were exposed to the saliva pool by the oral and nasal routes and by spray and brushing of teeth or by ingestion of saliva injected into a banana, but none were successfully infected. Thus although saliva was demonstrated to be infective, this was not achieved by a natural mode of transmission. Alter et al....