Hepatitis b virus definition

Definition of hepatitis B. Examples of hepatitis B in a Sentence Recent Examples on the Web The pentavalent vaccine -- which protects against five diseases diphtheria, tetanus, pertussis, hepatitis B and Haemophilus influenzae type B -- is a great example. Thrasher, Scientific American , 10 May Vaccitech Chief Executive Bill Enright said Friday in an interview that the prospects for clinical-stage treatments for prostate cancer, hepatitis B and human papillomavirus were the biggest focus of investor interest.

First Known Use of hepatitis B , in the meaning defined above. Learn More About hepatitis B. Time Traveler for hepatitis B The first known use of hepatitis B was in See more words from the same year.

Style: MLA. Medical Definition of hepatitis B. Nevertheless, severe liver disease including cirrhosis may occur in a small proportion of patients during childhood [ 21 , 22 ]. Several studies have shown that seroconversion with marked reduction of HBV replication is associated with biochemical and histologic remission of inflammatory activity in the majority of patients [ 23 - 25 ]. Regression of fibrosis occurs gradually months to years after HBeAg seroconversion.

Older carriers and females are more likely to clear HBeAg [ 33 ]. These exacerbations usually last 2 to 4 months [ 34 ]. In some cases these spontaneous flares of hepatitis are not followed by subsequent HBeAg seroconversion and can be viewed as an abortive attempt at seroconversion. These flares of hepatitis are usually asymptomatic and frequently unrecognized, but some are accompanied by symptoms of acute hepatitis and rarely, primarily in patients with cirrhosis or advanced fibrosis, may lead to hepatic decompensation and even death due to massive necrosis [ 34 ].

Other causes of liver disease, such as superinfection with other hepatitis viruses, alcohol abuse, hepatotoxic drug use, and autoimmune or metabolic liver disease, should be excluded [ 3 , 4 ].

The most frequent variant has a G-to-A change at nucleotide GA , which creates a stop codon in the precore region of the HBV genome and completely abolishes the production of HBeAg [ 35 ]. Other variants include changes in the start codon of the precore region or a two-nucleotide substitution AT, GA in the core promoter region, which reduces precore messenger RNA synthesis and HBeAg production [ 36 ].

Patient with HBeAg negative are older than patients with HBeAg-positive chronic hepatitis median 40, range 36—45 years. The older age and the high rate of advanced liver damage at presentation suggest that HBeAg-negative chronic hepatitis represents a late phase in the natural history of chronic HBV infection rather than de novo infection with HBV variants that do not produce HBeAg.

Thus, the increasing prevalence of HBeAg-negative. Fluctuation in level of viremia and ALT are more common and sustained response is rare. Delayed spontaneous HBsAg clearance has been estimated to occur at a low rate of 0. Long-term follow- up up to 18 years of these carriers has indicated that the vast majority show sustained biochemical remission and very low risk of cirrhosis or hepatocellular carcinoma HCC [ 40 - 42 ].

Rarely, patients, even noncirrhotics, may develop liver cancer during the inactive HBsAg carrier state [ 40 - 43 ].

HBV reactivation is usually asymptomatic but on occasion can mimic acute viral hepatitis [ 44 ]. Acute flares of hepatitis should be differentiated from superinfection with other hepatotropic viruses. Clearance of HBsAg has been reported to be higher in women than in men and in older than younger carriers. Prognosis is improved by loss of HBsAg as liver disease is usually inactive and nonprogressive, but HBsAg clearance does not completely prevent occurrence of decompensation or HCC in patients who have already developed cirrhosis [ 45 , 46 ].

Chronic HBV infection is a dynamic process with a wide spectrum of spectrum of affliction. On one hand patients are asymptomatic with no clinical evidence of liver diseases, while on other being end-stage cirrhosis and hepatocellular carcinoma. For many decades the patients were considered to have a benign, non progression infection and were designated as hepatitis B "carriers". Probably the word 'carrier' was mistakenly chosen for hepatitis B as in true sense, a carrier is an individual who i harbors a specific infectious agent ii has no discernible clinical disease and iii serves as a potential source of infection.

For this infection the second and third points should be looked at carefully. One the basis of Asian collaborative survey the term 'carrier' was replaced by the term 'chronic hepatitis B virus infection' [ 47 , 48 ].

Later on for this infection the term 'Inactive HBsAg carrier' was adopted [ 49 ]. Treatment is not recommended as there is no evidence that available therapy affects HBsAg status. Family screening with HBsAg and anti-HBs, if negative vaccinate them and success of vaccination should be confirmed with anti-HBs testing. Protected sexual intercourse until partner has developed protective antibodies. The offspring need active and passive vaccination [ 4 , 47 ].

Use of alcohol should be avoided, possibility of reactivation or super infection by other viruses and advised if there is jaundice, malaise or increased fatigue. Regular follow-up at every 6—12 months intervals with ALT [ 4 ].

If the age of the patient is more than 50 yrs family history of HCC-AFP and ultrasonography every 6—12 monthly should be done. Universal precaution should be taken while treating these patients in the hospital.

Treatment is directed at this latter group. Adapted from the European Association for the Study of the Liver guidelines. It should be noted that older patients may have cirrhosis with normal ALT levels. If ALT level increases, closer monitoring should be resumed and the potential need for therapy discussed. Asian men aged 40 years or older, Asian women aged 50 years or older, sub-Saharan African people older than 20 years, and those with family history of HCC should be monitored for HCC.

It should be noted that an elevated ALT level can be found in patients with HBV infection due to metabolic syndrome and non-alcoholic fatty liver disease. Patients with HBV infection plus obesity or metabolic syndrome have a higher risk of cirrhosis than those with HBV infection alone. Weight gain or central adiposity rather than body mass index, since this may be normal in some patients— eg, patients of Asian decent may increase suspicion that ALT level is increasing in this context; however, liver biopsy may be needed to determine whether the ALT level increase is associated with HBV-related damage or steatosis.

There are no contraindications for use of statins in individuals with HBV infection or for other drugs used in treatment of metabolic syndrome eg, antihypertensive agents or antidiabetic agents, including metformin. Currently approved treatments for HBV infection consist of interferon alfa-2b, lamivudine, adefovir, entecavir, peginterferon alfa-2a, telbivudine, tenofovir disoproxil TDF , and tenofovir alaf-enamide TAF.

Figure 1A provides data for the efficacy of the first-line treatments by showing histology and fibrosis improvements with entecavir therapy. Figure 1B shows data from different studies on the efficacy of entecavir and tenofovir compared with peginterferon in reducing HBV DNA to undetectable levels over the course of 3 years of treatment. A: Histologic and fibrosis improvement with long-term entecavir treatment. Adapted from Chang et al. Trials are not head-to-head comparisons and were conducted in different patient populations using different trial designs.

NA indicates not applicable. Functional cure consists of clinical resolution of infection that is sustained off drug treatment, with no inflammation present, as indicated by normal ALT level and negative liver biopsy, loss of HBsAg, and potential gain of anti-HBs. Complete cure is virologic cure, consisting of all the elements of functional cure plus loss of covalently closed circular ccc HBV DNA in the liver. This state is what is now our best treatment success—a patient still has HBV infection, but infection is inactive.

Rituximab and stem cell transplantation are the most potent reactivators of HBV. For those who are anti-HBs-seropositive, antiviral therapy should be started before immunosuppressive treatment. For other organ transplant, consultation with hepatology is recommended for management and follow-up.

Screening for HCC involves ultrasound performed and alpha fetoprotein level determined every 6 months, with use of computed tomography or magnetic resonance imaging to identify HCC if a lesion is detected during screening. Coinfection with HIV has been found to increase risk of HBV chronicity ie, reduce likelihood of HBsAg clearance in unvaccinated patients , increase antiretroviral-related hepatotoxicity, and increase risk of end-stage liver disease.

Flares may also be associated with use of antiretroviral therapy without anti-HBV therapy and with stopping of antiretroviral therapy. Atypical serologic findings occur in patients with HIV coinfection during antiretroviral therapy.

For example, reverse seroconversion may occur, in which patients who were anti-HBc-seropositive only become HBs-seropositive. All pregnant women should be tested for HBsAg. Infants born to mothers who are HBsAg-seropositive should receive both hepatitis B immune globulin HB1G and hepatitis B vaccine within 12 hours of birth, with subsequent vaccination at 1 then 3 or 6 months.

Current recommendations are to assess HBV DNA level in all pregnant women at 26 to 28 weeks of pregnancy to determine need for treatment in the mother.

Many people with hepatitis do not have symptoms and do not know they are infected. If symptoms occur with an acute infection, they can appear anytime from 2 weeks to 6 months after exposure. Symptoms of chronic viral hepatitis can take decades to develop.

Symptoms of hepatitis can include: fever, fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, light-colored stools, joint pain, and jaundice. Skip directly to site content Skip directly to page options Skip directly to A-Z link.

Viral Hepatitis. Section Navigation. Facebook Twitter LinkedIn Syndicate. What is Viral Hepatitis? Minus Related Pages. What causes it? Number of U. About 22, new infections in Estimated , people living with hepatitis B.

About 50, new infections in Estimated 2. Key facts Hepatitis A Hepatitis B Hepatitis C Effective vaccine available Outbreaks still occur in the United States; currently there are widespread person-to-person outbreaks Recent foodborne outbreaks in US traced to imported food Common in many countries, especially those without modern sanitation.

S are Asian Hepatitis B is a leading cause of liver cancer. How long does it last?