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The subsequent course of chronic hepatitis B is quite variable. Most persons remain HBsAg-positive for years if not for life and have some degree of chronic liver injury chronic hepatitis that can lead to significant fibrosis and cirrhosis.

The diagnosis of acute hepatitis B is reliably made by the finding of IgM anti-HBc in serum, particularly in a patient with HBsAg and signs, symptoms, or laboratory features of acute hepatitis. Nevertheless, in some instances, HBsAg is cleared rapidly from the serum, and IgM anti-HBc is the only marker detectable when the patient presents with hepatitis. About two-thirds of patients with acute HBV infection have a mild, asymptomatic and subclinical illness that usually goes undetected.

The clinical incubation period of acute hepatitis B averages 2—3 months and can range from 1—6 months after exposure, the length of the incubation period correlating, to some extent, with the level of virus exposure. The preicteric phase lasts a few days to as long as a week and is followed by onset of jaundice or dark urine. The icteric phase of hepatitis B lasts for a variable period averaging 1—2 weeks, during which viral levels decrease.

In convalescence, jaundice resolves but constitutional symptoms may last for weeks or even months. Patients with acute liver failure due to hepatitis B require careful management and monitoring and should be referred rapidly to a tertiary medical center with the availability of liver transplantation. Chronic hepatitis B has a variable and dynamic course. The course and natural history of hepatitis B are discussed in detail elsewhere in these proceedings.

The overall prognosis of patients with chronic hepatitis is directly related to the severity of disease. Patients with more severe disease or cirrhosis may have significant constitutional symptoms, jaundice, and peripheral stigmata of end-stage liver disease including spider angiomata, palmar erythema, splenomegaly, gynecomastia, and fetor hepaticus.

Ascites, peripheral edema, encephalopathy, and gastrointestinal bleeding are seen in patients with more advanced cirrhosis. Bilirubin, prothrombin time, and albumin often become abnormal with progressive disease.

Decreasing platelet count is often a poor prognostic sign. Patients with chronic hepatitis may develop acute exacerbations with markedly elevated serum ALT. This scenario is more frequently described in those with HBeAg-negative chronic hepatitis B. However anti-HBc of the IgM class can be detected occasionally in patients with chronic hepatitis B with exacerbation. An estimated one-third of persons with chronic HBV infection will ultimately develop a long-term consequence of the disease, such as cirrhosis, end-stage liver disease, or HCC.

The serum-sickness—like syndrome occurs in the setting of acute hepatitis B, often preceding the onset of jaundice. The symptoms often subside shortly after the onset of jaundice, but can persist throughout the duration of acute hepatitis B. The course of this syndrome often parallels the duration and level of HBV viremia: rapid clearance of the virus leads to rapid resolution of the illness. This disorder resembles experimental serum sickness, in which immune complexes activate the complement pathways leading to complement-mediated injury.

Patients with this syndrome have low complement levels and high-level circulating immune complexes containing HBV antigens and complement components. Immune-mediated vascular injury can involve large, medium, and small vessels. Early clinical features are marked constitutional symptoms, high fever, anemia, and leukocytosis. Multisystem involvement is common, including arthritis, renal disease proteinuria and hematuria , heart disease pericarditis and congestive heart failure , hypertension, gastrointestinal disease acute abdominal pain and bleeding , skin involvement vasculitic lesions , and neurological disorders mononeuritis multiplex and central nervous system abnormalities.

HBV-associated nephropathy has been described in adults but is more common in children. Liver disease may be mild or absent in many of these patients. This disorder is frequently observed in countries with high prevalence of HBV infection. Papular acrodermatitis Gianotti-Crosti syndrome is a distinct skin manifestation of acute HBV infection in childhood. The syndrome lasts about 15—20 days and can either precede or follow the onset of jaundice in acute hepatitis B.

Generalized lymphadenopathy and hepatomegaly have been described. Other immune-mediated hematological disorders, such as essential mixed cryoglobulinemia and aplastic anemia have been described as part of the extrahepatic manifestations of HBV infection, but their association is not as well-defined; therefore, they probably should not be considered etiologically linked to HBV.

Some of these patients have underlying liver disease, suggestive of ongoing hepatocellular injury from persistent HBV infection. Existing evidence supports the notion that it indeed indicates low-level viral replication, capable of transmission. Patients with serologic evidence of recovery probably have low-level viral replication that is effectively controlled by an active immune response.

The possibility that these occult infections are caused by HBV mutants has been proposed. Although mutations have been reported in various regions of the viral genome, 60 — 63 definitive evidence in support of a pathogenic role of these mutants is lacking.

Furthermore, whether liver disease can indeed result from these occult HBV infections is controversial. At present, there are no convincing studies in support of a causal relationship. Therefore, these occult HBV infections, other than the special situations described above, may not be clinically important. How does HBV establish productive infection in vivo and what is the host response early during the infection? Despite well-described information on the clinical manifestations and natural history of acute HBV infection, detailed knowledge of the virus-host interaction during this stage remains poorly defined.

Advances in this area would offer a better understanding of the pathogenesis of HBV infection and its associated disease. What is the immunologic basis of chronic infection and hepatocellular injury? There have been great strides in understanding the virology and immune response of HBV infection, but the molecular mechanisms whereby the host fails to clear the virus and develops chronic infection remain largely unknown.

In addition, the adaptive evolution of virus under host immune pressure remains to be elucidated. Finally, the pathogenesis of various extra-hepatic manifestations associated with HBV infection is poorly understood. Further research in these areas is crucial not only in better understanding the natural history and disease progression but also in improving treatment for chronic hepatitis B. What is the genetic basis of the diverse clinical manifestations and disease outcomes of HBV infection?

With the recent advances in genetic and genomic medicine, there are increasing opportunities to elucidate the genetic basis for variations in expression and susceptibility to HBV-associated diseases. Genome-wide association studies and other genomic technological advances would provide crucial information to identify useful genetic markers for disease outcome, clinical manifestations, and treatment response of HBV-associated disease.

Potential conflict of interest: Nothing to report. National Center for Biotechnology Information , U. Author manuscript; available in PMC Jan Jake Liang. Author information Copyright and License information Disclaimer. Copyright notice. The publisher's final edited version of this article is available at Hepatology. See other articles in PMC that cite the published article. Abstract Hepatitis B virus HBV infects more than million people worldwide and is a common cause of liver disease and liver cancer.

Open in a separate window. Diagnosis and Serology HBV infection leads to a wide spectrum of liver disease ranging from acute hepatitis including fulminant hepatic failure to chronic hepatitis, cirrhosis, and hepatocellular carcinoma HCC. The clinical course and serologic profiles of A acute and B chronic hepatitis B. Acute Hepatitis B About two-thirds of patients with acute HBV infection have a mild, asymptomatic and subclinical illness that usually goes undetected.

Chronic Hepatitis B Chronic hepatitis B has a variable and dynamic course. Important Questions and Needs for Future Research How does HBV establish productive infection in vivo and what is the host response early during the infection?

Footnotes Potential conflict of interest: Nothing to report. References 1. Ganem D, Schneider RJ. Hepadnaviridae and their replication.

Fields Virology. Hepatitis B virus. Structure of hepatitis B surface antigen: characterization of the lipid components and their association with the viral proteins. J Biol Chem. Gerlich W, Robinson WS. J Virol. Milich D, Liang TJ. Exploring the biological basis of hepatitis B e antigen in hepatitis B virus infection.

X-deficient woodchuck hepatitis virus mutants behave like attenuated viruses and induce protective immunity in vivo. J Clin Invest. Altered proteolysis and global gene expression in hepatitis B virus X transgenic mouse liver. The enigmatic X gene of hepatitis B virus.

Genetic and biochemical evidence for the hepatitis B virus replication strategy. Yee J. A liver-specific enhancer in the core promoter region of human hepatitis B virus.

Hepatitis B virus DNA contains a glucocortcoid response element. Huang J, Liang TJ. Mol Cell Biol. Klingmuller U, Schaller H. Hepadnavirus infection requires interaction between the viral pre-S domain and a specific hepatocellular receptor. Carboxypeptidase D gp , a Golgi-resident protein, functions in the attachment and entry of avian hepatitis B viruses.

Phosphorylation of hepatitis B virus Cp at Ser87 facilitates core assembly. Biochem J. Kock J, Schilicht H-J. Analysis of the earliest steps of hepadnavirus replication genome repair after infectious entry into hepatocytes does not depend on viral polymerase activity. Internal entry of ribosomes and ribosomal scanning involved in hepatitis B virus P gene expression.

The preS1 protein of hepatitis B virus is acylated at its amino terminus with myristic acid. Pollack J, Ganem D. Replication strategy of human hepatitis B virus. Viral hepatitis, type B. Studies on natural history and prevention re-examined. Try the modernized ClinicalTrials. Learn more about the modernization effort. Hide glossary Glossary Study record managers: refer to the Data Element Definitions if submitting registration or results information.

Search for terms. Save this study. Warning You have reached the maximum number of saved studies Listing a study does not mean it has been evaluated by the U. Federal Government. Read our disclaimer for details. Last Update Posted : November 13, Study Description. Detailed Description:. Study design: prospective observational cohort study. The antibody levels will be measured prior to vaccination, and after 3,7 and 12 months.

The secondary outcome is safety of vaccination, measured as activity of the underlying autoimmune disease. In addition, frequency of common adverse effects, and immunological changes induced by HPV vaccination, such as number and function of cytotoxic T cells and Tregs will be described.

Nature and extent of the burden and risks associated with participation, benefit and group relatedness: Burden: included patients will be asked to visit the hospital 4 times in a period of 12 months. Resource links provided by the National Library of Medicine MedlinePlus Genetics related topics: Juvenile idiopathic arthritis Systemic lupus erythematosus. Drug Information available for: Human Papillomaviruses.

FDA Resources. Arms and Interventions. Outcome Measures. Primary Outcome Measures : the immunogenicity of HPV vaccination in patients with immune system disorders. Secondary Outcome Measures : difference in the activity of underlying disease before versus after vaccination. Eligibility Criteria. Information from the National Library of Medicine Choosing to participate in a study is an important personal decision. Inclusion Criteria: Females Clinical diagnosis of JIA, SLE or JDM And who are in the following age groups: 12 years these girls are vaccinated via the National Vaccination Program from September years these girls are vaccinated during a national vaccination campaign from March-May Current co-medication: all co-medication prescribed may be continued And in the control group: healthy girls aged years these girls are vaccinated during a national vaccination campaign from March-May Exclusion Criteria: No HPV vaccination Refusal to allow venous puncture Proven or suspected cervical carcinoma.

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Please refer to this study by its ClinicalTrials. More Information. Safety of measles, mumps and rubella vaccination in juvenile idiopathic arthritis. Ann Rheum Dis. Epub Feb 6. Safety and efficacy of meningococcal c vaccination in juvenile idiopathic arthritis.

Arthritis Rheum. Immunogenicity and safety of the bivalent HPV vaccine in female patients with juvenile idiopathic arthritis: a prospective controlled observational cohort study. Epub May National Library of Medicine U. National Institutes of Health U. Department of Health and Human Services.