HEPATITIS B

Hepatitis B HB ) is an infectious disease caused by the hepatitis B virus (HBV) that affects the liver . It can cause both acute and chronic infections . Many people have no symptoms during the initial infection. Some people develop rapidly when they are sick with vomiting, yellow skin , fatigue , dark urine and abdominal pain. Usually these symptoms last a few weeks and rarely the initial infection leads to death. It may take 30 to 180 days for the symptoms to begin. In people infected around the time of birth 90% were hepatitis B chronic while less than 10% teaser ng people infected after five. Most people with chronic illness have no symptoms; However, cirrhosis and liver cancer, c –utans can grow together. Cirrhosis or liver cancer occurs in about 25% of people with chronic disease.         

Infection has been prevented by vaccination since 1982. Vaccination is recommended by the World Health Organization on the first day of life if possible. Two or three more doses are required then for full effect. And c-apply approximately 95% of this activity. About 180 countries have been vaccinated as part of the national program since 200 6. We also recommend that all blood be tested for hepatitis B before a blood transfusion and a condom is used to prevent infection. During an initial infection, care is based on the symptoms a person has. In people who develop chronic illness, antiviral drugs like tenofovir or interferon may be helpful; However, these drugs are expensive. Double liver transplantation is sometimes used for cirrhosis.                

About a third of the world’s population has been infected at one point in their lives, including 343 million people with chronic infections. An additional 129 million new infections occurred in 2013. More than 750,000 people die from hepatitis B each year. About 300,000 of these are due to cancer . The disease is currently only common in East Asia and sub-Saharan Africa where 5 to 10% of adults are chronically infected. Rates in Europe and North America are less than 1%. It was originally called “serum hepatitis”. Research is looking at ways to make foods containing HBV vaccines. The disease can also affect other great apes .         

Signs and symptoms

Acute infection with hepatitis B virus -related hepatitis micro acute , the disease starts with general health, loss of appetite, nausea, vomiting, body aches, mild fever and urine dark color, then progress to jaundice . It has been noted that itchy skin has been a sign as a possible symptom of all hepatitis viruses. The disease lasts for a few weeks and then gradually improves in most of the affected people. A small number of people may have a more serious form of liver disease called supreme liver failure and may result in death. The infection may be completely asymptomatic and may not be recognized.               

Chronic infection with the hepatitis B virus may be asymptomatic or may be related to chronic hepatitis (chronic hepatitis), leading to cirrhosis in a few years. This type of infection significantly increases the incidence of hepatocellular carcinoma (HCC; liver cancer). Across Europe, hepatitis B and C cause about 50% of HCC. People carriers of chronic disease are encouraged to avoid consuming alcohol as it increases the risk of cirrhosis and liver cancer. The hepatitis B virus is involved in the development of membranous glomerulonephritis (MGN).                 

Symptoms outside the liver in 1 10% of those infected with HBV and include the syndrome similar to serum sickness , syndrome, vasculitis necrotizing acute ( inflammation multi cornea ), membranous glomerulonephritis membrane and inflammatory membrane pecan in children ( syndrome folliculitis in children ). Like syndrome, serum sickness occurs in the context of hepatitis B acute , often discharge care before starting jaundice. Clinical features are fever, skin rash, and polygonal inflammation . Symptoms usually subside after the onset of jaundice but may persist during acute hepatitis B infection . About 30 people 50% 50% of people with acute necrotizing vasculitis ( polygonal inflammation ) are carriers of HBV. HBV-related kidney disease has been described in adults but is more common in children. Membranous glomerulonephritis is the most common form. Other immunologically mediated hematologic disorders , such as essential mixed blood pressure and aplastic anemia, have been described as part of the non-infectious manifestations of HBV infection, but the association their are not well defined; therefore, they probably should not be considered to be causally related to HBV.                                     

Reason

Transmission

The transmission of hepatitis B virus is the result of contact with infectious blood or body fluids containing blood. It is 50 to 100 times more infectious than the human immunodeficiency virus (HIV) . The modes of transmission may include sexual intercourse , blood transfusion and transfusion v ới blood products others, reused needles and syringes contaminated , and vertical transmission from mother to child (MTCT) during birth. Without intervention, mothers who are positive for HBsAg have a 20% risk of transmitting the disease to their babies at birth. This risk is as high as 90% if the mother is also positive for HBeAg. HBV can be transmitted between family members in households, possibly through contact with skin without membranes or mucous membranes with secretions or saliva containing HBV. However, at least 30% of hepatitis B reported in adults may be associated with an identifiable risk factor. Breastfeeding after treatment with appropriate immunotherapy does not seem to contribute to HBV- to-mother transmission (MTCT). The virus can be detected within 30 to 60 days after infection and can survive and develop into chronic hepatitis B. The incubation period for hepatitis B virus is 75 days on average but can be replaced. change from 30 to 180 days.                   

Virology

Hepatitis B virus

CA The structure

The structure of the hepatitis B virus

The hepatitis B virus (HBV) is a member of the hepadnavirus family . The viral particles ( virions ) consist of an outer lipid envelope and a core icosahedral nucleocapsid consisting of protein . These virions have a diameter of 30 lines42. Nucleocapsid surrounds viral DNA and DNA polymerase has reverse transcription activity . The outer shell contains embedded proteins that are involved in viral binding and entering sensitive cells. This virus is one of the smallest enveloped animal viruses. The 42nm virions, capable of infecting liver cells called hepatocytes , are called ” Dane particles “. In addition to the Dane particles, fibrous and spherical-deficient bodies can be found in the sera of infected people. These particles are non-infectious and consist of lipids and proteins that form part of the surface of the virion, called surface antigen ( HBsAg ), and are over-produced during the virus’s life cycle.                       

Ministry gene

Genome organization of HBV. The genes overlap. 

The HBV genome is made up of circular DNA , but this is unusual because DNA is not completely double-stranded . One end of the full long chain is linked to the viral DNA polymerase . The genome has 30 nucleotides long 3020 (for full length chains) and 1700 nucle28ides long 1700 nucle otides (for short long chains). The negative (unencrypted) meaning is complementary to the viral mRNA . Viral DNA is found in the nucleus immediately after a cell infection . Partially double-stranded DNA is completed with a double chain upon completion of the sensory sequence (+) and removal of the molecular protein from the sensory chain (-) and a short RNA sequence from the sensory chain (+). Non-coding facilities are removed from the ends of the sensory sequence (-) and the ends are connected. There are four genes encoded by the genome, called C, X, P and S. The core protein is encoded by the C gene (HBcAg), and its starting codon is preceded by a starter codon in the frame. upstream from which pre-core proteins are produced. HBeAg is produced by processing proteolysis of proteins convenience. In some rare strains called the hepatitis B virus mutation , there is no HBeAg. DNA polymerase is encoded by gene P. Gene S is the gene encoding the antigen surface (HBsAg). The HBsAg gene is an extended reading frame but contains three “start” (ATG) codons in the gene division frame into three parts, pre-S1, pre-S2 and S. Because there are many starting codons, polypeptides of three sizes The difference is called big (order from surface to inside: before S1, before S2 and S) , between (before S2, S) and small (S) are created. The function of the protein encoded by the X gene is not fully understood but it is involved in the development of liver cancer. It stimulates genes that promote cell growth and inactivates molecules that regulate growth.                                                   

Pathophysiology

Replication of the hepatitis B virus

The life cycle of the hepatitis B virus is very complicated. Hepatitis B is one of the few types parar RNA known : not the kind of retrovirus still uses reverse transcriptase during their replication. The virus enters the cell by binding to the surface NTCP and is endotoxic . Because the virus replicates through RNA generated by a host enzyme, the viral genomic DNA must be transferred to the cell nucleus by host proteins called chaperones. Partially double-stranded viral DNA is then made up of double chains completely by a viral polymerase and transformed into chemotherapy circular DNA (cccDNA). This CccDNA serve as templates to copy four mRNAs of the virus by the host’s RNA polymerase. The largest MRNA, (longer than the viral genome), is used to make new copies of the genome and create viral capsid core proteins and DNA polymerases . These four copies of the virus undergo additional processing and continue to form prenatal virions released from the cell or returned to the nucleus and reprocessed to make more copies. The long mRNA is then transported back to the cytoplasm where the virion P protein (DNA polymerase) synthesizes DNA through its reverse transcription activity.                             

Serotype and genotype

This virus is divided into four categories of serum primary (adr, ADW, ayr, ayw) based on the epitopes antigen presented on its envelope proteins, and into eight major genotypes (A soup H). Genotypes have a distinct geographical distribution and are used to track the growth and transmission of viruses. Differences between genotypes affect the severity of the disease, the process and the likelihood of complications, and the response to treatment and possibly vaccinations. There are two other genotypes I and J but they were not popularly accepted in 2015.          

Genotypes differ at least 8% of their sequence and were first reported in 1988 when the six original descriptions (AFF). Two other types have been described (G and H). Most current genotypes are divided into genotypes with distinct attributes.

Mechanism

The hepatitis B virus primarily interferes with liver functions by copying within the liver cells . A functional receptor is NTCP . There is evidence that the receptor in the closely related virus Duck Hepatitis B is carboxypeptidase D . The virions bind to the host cell through the preS domain of the viral surface antigen and are later endogenized by endocytosis. HBV-preS specific receptors are expressed primarily on liver cells; however, viral DNA and proteins have also been detected in the extrasensory sites, suggesting that cell receptors for HBV can also exist on the telepathy cells.               

During HBV infection, the host ‘s immune response causes both liver cell damage and virus clearance. Although the innate immune response does not play an important role in these processes, the adaptive immune response, especially virus-specific cytotoxic T lymphocytes (CTL), contributes to in most liver damage related to HBV infection. CTL eliminates HBV infection by destroying infected cells and producing antiviral cytokines , which are then used to clear HBV from viable liver cells. Although liver damage is initiated and mediated by CTL, the inflammatory cell antigens not specifically may worsen pathological immune CTL and sub caukich works at the site of infection may facilitate for CTL accumulation in the liver.                

Diagnose

Tests, called tests , to detect infection with the hepatitis B virus involve serological tests or blood tests for viral antigens (viral proteins) or antibodies produced by the host. Interpreting these tests is complicated.            

The hepatitis B surface antigen ( HBsAg ) is most frequently used to screen for the presence of this infection. This is the first virus antigen that can be detected during infection. However, in the early stages of infection, this antigen may not appear and it may not be detected later in the infection because it is being cleared by the host. Infectious virions contain an “core particle” inside the virus genome. The icosah core is made up of 180 or 240 copies of the core protein, also known as the hepatitis B core antigen , or HBcAg . In the ‘window’ of this, in which the host remains infected but is successfully removed the virus, antibodies to IgM specific for hepatitis Bkhang integer cores ( IgM anti-HBc ) may be evidence of serum only disease . Therefore, most hepatitis B diagnostic tables contain HBsAg and total anti-HBc (both IgM and IgG).                         

Immediately after the appearance of HBsAg, another antigen called the hepatitis B e antigen ( HBeAg ) will appear. Traditionally, the presence of HBeAg in the host serum has been associated with higher viral replication rates and increased infection; however, variants of the hepatitis B virus do not produce the ‘e’ antigen, so this rule is not always true. During a natural infection, HBeAg may be removed and antibodies to the ‘e’ antigen ( anti-HBe ) will arise soon after. This conversion is often associated with a significant decrease in virus replication.           

Ground glass liver cells as seen in a chronic hepatitis B biopsy liver .   

If the host is able to remove the infection, eventually HBsAg will not be detected and will be followed by resistance to IgG against surface antigen of hepatitis B and core antigen ( anti-HBs and anti-HBc IgG ). The time between eliminating HBsAg and the appearance of anti-HB drugs is called the window period . A person who is negative for HBsAg but positive for anti-HBs has either removed the infection or has been previously vaccinated.              

Those who remain HBsAg positive for at least six months are considered human carriers of hepatitis B. The virus can bring chronic hepatitis B infection, this will be reflected by levels of alanine aminotransferase (ALT) in serum rose high and hepatitis, if they are in phase immune clearance of chronic infection. Carriers of HBeAg-negative pathogens, especially those infected with adulthood, have very little viral replication and therefore may be less likely to have long-term complications or transmission. sick to others. However, individuals may enter an “immune escape” with HBeAg-negative hepatitis.        

Prevent

Hepatitis B vaccine

The hepatitis B vaccine has been regularly recommended for babies since 1991 in the United States. The first dose is usually recommended within one day of birth.

Most vaccines are given in three doses over a few months. The protective response to the vaccine is determined to be at least 10 mIU / ml antibody concentration in the recipient’s serum. The vaccine is more effective in children and 95 percent of people who get the vaccine have protective antibody levels. This decreases to about 90% in the 40s and about 75% in the people over 60. The protection provided by immunization is permanent even when the antibody concentration drops below 10 mIU / ml. For infants of mothers with HBsAg-positive: only vaccine for hepatitis B immune globulin hepatitis B or combination vaccine plus immunoglobulin hepatitis B, all of which prevent ng ừa the appearance of hepatitis B. Moreover, the combination of the vaccine plus the hepatitis B immunoglobulin is superior to the simple vaccine. This combination prevents HBV transmission during the birth period in 86% to 99% of cases.     

Tenofovir used in the second or third trimester may reduce the risk of mother-to-child transmission by 77% when combined with hepatitis B immunoglobulin and hepatitis B vaccine, especially for pregnant women. have high levels of hepatitis B virus DNA. However, there is no sufficient evidence to suggest that the use of hepatitis B immune globulin alone during pregnancy may reduce the rate of transmission to infants. No randomized controlled trials were conducted to evaluate the effects of hepatitis B vaccine during pregnancy to prevent infection in newborn infants. 

Everyone at risk of contact with body fluids like blood should be vaccinated, if not. Testing to verify effective immunization is recommended and additional doses of vaccine should be given to those who are not eligible for immunization.

In follow-up studies of 10 to 22 years, no hepatitis B infection among people with normal immune systems was vaccinated. Only rare chronic infections have been noted. Special vaccinations are recommended for high-risk groups including health care workers, people with chronic kidney failure and men who have sex with men.    

Both hepatitis B vaccines, plasma-derived vaccines (PDV) and recombinant vaccines (RV) are equally effective at preventing infection in both health care workers. and chronic renal failure. With a noticeable difference between the medical staff group, that the RV intramuscular route was significantly more effective than the intravenous RV injection.

Other

In assisted reproductive technology , sperm washing is not necessary for men with hepatitis B to prevent transmission, unless the female partner has not been effectively vaccinated. In women with hepatitis B, the risk of mother-to-child transmission of IVF is no different from the risk of spontaneous conception.    

People at high risk of infection should be checked for effective treatment for those who are ill. The recommended screening groups include those who have not been vaccinated and one of the following: people from regions of the world where hepatitis B occurs in more than 2%, people with HIV, and users Intravenous drug, men who have sex with men, and those who live with a person with hepatitis B. Pregnancy screening is recommended in the United States.  

Treatment

Infection with hepatitis B Acute usually do not need treatment and most adults remove the infection naturally. Treatment with early antiviral drugs may be required in less than 1% of people who have a very active infection (fulminant hepatitis) or who are immunocompromised . On the other hand, treatment of chronic infection may be needed to reduce the risk of cirrhosis and liver cancer. People who are chronically infected with elevated serum alanine aminotransferase , a marker of liver damage and HBV DNA levels, are candidates for therapy. Treatment lasts from six months to a year, depending on the drug and genotype. The duration of treatment with oral medications, however, varies widely and is usually longer than a year.            

Although there are no drugs that can eliminate the infection, they can prevent the virus from multiplying, thereby minimizing liver damage. As of 2018, there are eight drugs licensed for the treatment of infection with hepatitis B in the United States. These include viral drug lamivudine , adefovir , tenofovir disoproxil , tenofovir alafenamide , telbivudine , and entecavir , and the two immune system modulators interferon alpha-2a and interferon alpha-2a . In 2015, the World Health Organization recommended tenofovir or entecavir as a first-class agent. People with cirrhosis currently need the most treatment.                         

The use of interferon, requiring daily injections or three times per week, has been replaced by the long-acting PEGylated interferon , given only once weekly. However, some individuals are much more responsive than others and this may be due to the genotype of the virus being infectious or hereditary. The treatment reduces the viral replication in the liver, thereby reducing the viral load ( viral particles measured in the blood). Response to treatment varies between genotypes. Interference treatment can produce serum conversion rate was 37% e antigen in genotype A but only 6% seroconversion in type D. Genotype B seroconversion rate similar kind A while type C seroconverted only in 15% of cases. Loss of antigen e maintained after treatment is ~ 45% in types A and B as indicated by 25 253030 in types C and D.          

Prognosis

Infectious virus hepatitis B can be acute (self-limiting) or chronic (long-term). People with self-limited infections naturally get rid of the infection within weeks to months.    

Children are less likely than adults to clear the infection. More than 95% of those infected as adults or children will fully recover and develop immunity to protect against the virus. However, this is reduced to 30% for babies and only 5% of babies who have an infection from the mother at birth will eliminate the infection. This population has a 40% risk of dying from cirrhosis or hepatocellular carcinoma . Of those infected one to six years of age, 70% will eliminate the infection.      

Hepatitis D (HDV) can only occur when infected with hepatitis B at the same time , because HDV uses HBV surface antigen to form capsid . Co-infection with hepatitis D increases the risk of cirrhosis and liver cancer. Polyarteritis nodosa is more common in people with hepatitis B infection.          

Cirrhosis

A number of different tests are available to determine the current level of cirrhosis. Transient elasticity (FibroScan) is the test of choice, but it is expensive. Aspartate aminotransferase to platelet ratio index can be used when cost is an issue.   

Strange activation

The hepatitis B virus DNA persists in the body after infection and in some patients relapses. Although rare, reactivation is most often seen after alcohol or drug use, or in immunocompromised individuals. HBV goes through replication and non-replication cycles. Approximately 50% of over-carriers experience acute reactivation. Men with a baseline ALT of 200 UL / L were three times more likely to reactivate than those with lower levels. Although reactivation can occur spontaneously, people undergoing chemotherapy are at higher risk. Immunosuppressants support an increase in HBV replication while inhibiting T-cell function that is cytotoxic in the liver. The risk of reactivation varies according to serological profile; People with HBsAg can detect in blood at highest risk, but those who only have antibodies to the core antigen are also at risk. The presence of antibodies to surface antigens, which is considered a sign of immunity, does not exclude reactivation. Prophylactic antiviral treatment can prevent serious illnesses related to reactivation of HBV disease.              

 

 

 

 

 

 

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