La hepatitis B puede transmitirse cuando alguien:. En , , muertes en todo el mundo se debieron al VHB, principalmente como resultado de complicaciones como estas. Actualmente no hay cura para el VHB.
Sin embargo, los CDC estiman que 33, infecciones ocurrieron en , que incluye las que no se reportaron. Estructura y simetria del capsomero. Propiedades fisicas del virion. Masa molecular. Densidad de flotacion. Coeficiente de ssedimentacion.
Estabilidad ante cambios del pH. Termo estabilidad. Estabilidad a solventes. Estabilidad a detergentes. Estabilidad a la radiacion. Propiedades del genoma. Tipo de hebra — simple o doble. Lineal o circular. Numero de segmentos. Presencia o ausencia y tipo de capsula terminal. Presencia o ausencia de uniones covalentes polipeptidicas. Secuencia de nucleotidos. Propiedades de proteinas. Numero de proteinas. Secuencia de aminoacidos. Presencia o ausencia de carbohidratos. Naturaleza de carbohidratos.
Estrategia de replicacion del acido nucleico. Caracteristicas de transcripcion. Successful cloning of portions of the viral genome permitted the development of new diagnostic tests for infection by the virus. Since the original antigen was detected by antibodies in the serum of an infected patient it was an obvious candidate for the basis of an ELISA to detect anti-HCV antibodies. A larger clone, C, was assembled from a number of overlapping clones and expressed in yeast as a fusion protein using human superoxide dismutase sequences to facilitate expression, and this fusion protein formed the basis of first generation tests for HCV infection.
The antigen comprises amino acid sequences from the non-structural, NS4, region of the genome and C contains both NS3 and NS4 sequences. It is now known that antibodies to C are detected relatively late following an acute infection. Furthermore, the first generation ELISAs were associated with a high rate of false positive reactions when applied to low incidence populations, and there were further problems with some retrospective studies on stored sera.
Data based on this test alone should, therefore, be interpreted with caution. Second generation tests include antigens from the nucleocapsid and further non-structural regions of the genome.
The former C22 is particularly useful and antibodies to the HCV core protein seem to appear relatively early in infection. These second generation tests confirm that HCV is the major cause of parenterally transmitted non-A, non-B hepatitis. Routine testing of blood donations is now in place in many countries and prevalence rates vary from 0.
Most of those with antibody have a history of parenteral risk such as a history of transfusion or administration of blood products or of intravenous drug abuse. There is little evidence for sexual or perinatal transmission of HCV and it is not clear what are the natural routes of transmission.
The availability of the nucleotide sequence of HCV made possible the use of the polymerase chain reaction PCR as a direct test for the genome of the virus. Whether the virus is cytopathic or whether there is an immunopathological element remains unclear. HCV infection is also associated with progression to primary liver cancer.
For example, in Japan, where the incidence of hepatocellular carcinoma has been increasing despite a decrease in the prevalence of HBsAg, HCV is now considered the major risk factor. There is no DNA intermediate in the replication of the HCV genome or integration of viral nucleic acid and viral pathology may contribute to oncogenesis through cirrhosis and regeneration of liver cells.
HCV rarely seems to cause fulminant hepatitis. It has been proposed that HCV should be the prototype of a third genus in the family Flaviviridae. All of these genomes contain a single large open reading frame which is translated to yield a polyprotein of around amino acids in the case of HCV from which the viral proteins are derived by post-translational cleavage and other modifications. The amino acid sequence of the nucleocapsid protein seems to be highly conserved among different isolates of HCV.
The next domain in the polyprotein also has a signal sequence at its carboxyl-terminus and may be processed in a similar fashion.
These glycoproteins have not been visualized in vivo and the molecular sizes are estimated from sequence data and expression studies in vitro. Other post-translational modifications, including further proteolytic cleavages, are possible. These proteins are the focus of considerable interest because of their potential use in tests for the direct detection of viral proteins and for HCV vaccines. Nucleotide sequencing studies reveal that both domains contain hypervariable regions.
It is possible that this divergence has been driven by antibody pressure and that these regions specify important immunogenic epitopes. In the flaviviruses, NS3 has two functional domains, a protease which is involved in cleavage of the non-structural region of the polyprotein and a helicase which is presumably involved in RNA replication.
Motifs within this region of the HCV genome have homology to the appropriate consensus sequences, suggesting similar functions. Hepatitis C virus consists of a family of highly related but nevertheless distinct genotypes, numbering at present 6 genotypes and various subtypes with differing geographical distribution, and with a complex nomenclature. The C, NS3 and NS4 domains are the most highly conserved regions of the genome, and therefore these proteins are the most suitable for use as capture antigens for broadly reactive tests for antibodies to HCV.
The sequence differences observed between HCV groups suggest that virus-host interactions may be different, which could result in differences in pathogenicity and in response to antiviral therapy.
It is important, therefore, to develop group- and virus-specific tests. The degree of divergence apparent within the viral envelope proteins implies the absence of a broad cross-neutralizing antibody response to infection by viruses of different groups. Indeed, sequence changes within this region may occur during the evolution of disease in individual patients and may play an important role in progression to chronicity. Neutralizing antibodies have not been identified so far.
The virus has not been cultivated in vitro cf. Yellow fever flavivirus, which has been cultured and from which vaccines have been prepared. Nevertheless, approaches to vaccine development could be based on techniques used for the development of vaccines against the Flaviviruses and Pestiviruses.
About 30 years ago, a series of transmission studies of human viral hepatitis were initiated in small South American tamarins or marmosets, which were chosen because of their very limited contact with man, implying that they were unlikely to have been infected with human viruses. A serum which was obtained on the third day of jaundice from a young surgeon GB with jaundice-induced hepatitis in each of four inoculated marmosets and was passaged serially in these animals.
These important observations remained controversial until the application recently of modern molecular virological techniques. Cross-challenge experiments showed that infection with the original infectious tamarin inoculum conferred protection from reinfection with GBV-B but not GBV-A.
The organization of the genes of the GBV-A, B, and C genomes shows that they are related to other positive-strand RNA viruses with local regions of sequence identity with various flaviviruses. Diagnostic reagents were prepared with recombinant antigens, and limited testing was carried out in groups of patients, blood donors and other selected individuals: patients with non-A, B, C, D, E hepatitis, multitransfused patients, intravenous drug addicts and other populations with a high incidence of viral hepatitis.
The development and availability of specific diagnostic reagents will establish the epidemiology of these newly identified viruses, their pathogenic significance in man and their clinical and public health importance. Turn recording back on. National Center for Biotechnology Information , U. Show details Baron S, editor. Search term. Chapter 70 Hepatitis Viruses Arie J. General Concepts Viral hepatitis has emerged as a major public health problem throughout the world affecting several hundreds of millions of people.
The hepatitis viruses include a range of unrelated and often highly unusual human pathogens. Hepatitis A virus Hepatitis A virus HAV , classified as hepatovirus, is a small, unenveloped symmetrical RNA virus which shares many of the characteristics of the picornavirus family, and is the cause of infectious or epidemic hepatitis transmitted by the fecal-oral route. Hepatitis C virus Hepatitis C virus HCV , is an enveloped single-stranded RNA virus which appears to be distantly related possibly in its evolution to flaviviruses, although hepatitis C is not transmitted by arthropod vectors.
Hepatitis E virus Hepatitis E virus HEV , the cause of enterically-transmitted non-A, non-B hepatitis, is another non-enveloped, single-stranded RNA virus, which shares many biophysical and biochemical features with caliciviruses. Hepatitis A Outbreaks of jaundice have been frequently described for many centuries and the term infectious hepatitis was coined in to describe the epidemic form of the disease.
Distinctive properties Electron microscopic examination of concentrates of filtered fecal extracts from patients during the early stages of infection reveals 27 nm icosahedral particles typical of the Picornaviridae Fig.
Figure Hepatitis A virus particles found in fecal extracts by immunoelectron microscopy. Pathogenesis The clinical expression of infection with hepatitis A virus varies considerably, ranging from subclinical, anicteric, and mild illnesses in children to the full range of symptoms with jaundice in adults.
Host Defenses Antibody to hepatitis A virus develops late in the incubation period. Epidemiology Viral hepatitis type A previously named infectious or epidemic hepatitis occurs endemically in all parts of the world, with frequent reports of minor and major outbreaks. Figure Immune aggregate of hepatitis A virus following the addition of convalescent serum to a fecal extract during the acute phase of the illness X , from a series by Anthea Thornton and A J Zuckerman.
Diagnosis Various serologic tests are available for hepatitis A, including immune electron microscopy, complement-fixation, immune adherence hemagglutination, radioimmunoassay, and enzyme immunoassay. Control and Prevention of Hepatitis A In areas of high prevalence, most children are infected early in life and such infections are generally asymptomatic. Hepatitis E Retrospective testing of serum samples from patients involved in various epidemics of hepatitis associated with contamination of water supplies with human feces indicated that an agent other than HAV or hepatitis B was involved.
Structure of the Virus The hepatitis B virion is a nm particle comprising an electron-dense core nucleocapsid 27 nm in diameter surrounded by an outer envelope of the surface protein HBsAg embedded in membranous lipid derived from the host cell Fig. Figure Electron micrograph of serum containing hepatitis B virus after negative staining. Organization of the HBV Genome The genomes of more than a dozen isolates of hepatitis B virus have been cloned and the complete nucleotide sequences determined.
Figure Structure and genomic organization of hepatitis B virus. Host Defenses Antibody and cell-mediated immune responses to various types of antigens are induced during the infection. Epidemiology Although various body fluids blood, saliva, menstrual and vaginal discharges, serous exudates, seminal fluid, and breast milk have been implicated in the spread of infection, infectivity appears to be especially related to blood.
Diagnosis Direct demonstration of virus in serum samples is feasible by visualizing the virus particles by electron microscopy, by detecting virus-associated DNA polymerase, and by assay of viral DNA. Protection of hepatitis B The discovery of variation in the epitopes presented on the surface of the virions and subviral particles identified several subtypes of HBV which differ in their geographical distribution.
Hepatitis B Antibody Escape Mutants Production of antibodies to the group antigenic determinant a mediates cross-protection against all sub-types, as has been demonstrated by challenge with a second subtype of the virus following recovery from an initial experimental infection. HBV Precore mutants The nucleotide sequence of the genome of a strain of HBV cloned from the serum of a naturally infected chimpanzee has been reported.
HBV and Hepatocellular Carcinoma When tests for HBsAg became widely available, regions of the world where the chronic carrier state is common were found to be coincident with those where there is a high prevalence of primary liver cancer. Hepatitis D Delta hepatitis was first recognized following detection of a novel protein, delta antigen HDAg , by immunofluorescent staining in the nuclei of hepatocytes from patients with chronic active hepatitis B.
Hepatitis C Transmission studies in chimpanzees established that the main agent of parenterally acquired non-A, non-B hepatitis was likely to be an enveloped virus some 30 to 60 nm in diameter. Diagnosis of HCV Infection Successful cloning of portions of the viral genome permitted the development of new diagnostic tests for infection by the virus.
Figure Hepatitis C Viral Genome. The GB Hepatitis Viruses About 30 years ago, a series of transmission studies of human viral hepatitis were initiated in small South American tamarins or marmosets, which were chosen because of their very limited contact with man, implying that they were unlikely to have been infected with human viruses. Williams and Wilkins, Baltimore, Lancet II: , Lancet , Studies on the transmission of human viral hepatitis to marmoset monkeys.
Transmission of disease, serial passages, and description of liver lesions. Journal of Experimental Medicine. Krawczynski K. Hepatitis E. Lemon SM. Type A viral hepatitis. New developments in an old disease.
New Eng J Med. Preliminary evidence that a trpE- HEV fusion protein protects cynomolgus macaques against challenge with wild-type hepatitis E virus. J Med Viro. Con perro. Personal sanitario manipula unas muestras de sangre en el laboratorio.
EFE-Christian Brun. Cuarto propio.
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