Why does hepatitis B virus only invade the liver?
Hepatitis B virus has hepatotropic properties. Previously, it was only known that hepatitis B virus could mainly cause liver lesions and lead to liver necrosis. Later, evidence of virus replication and reproduction in liver cells was found. In recent years, it has been recognized that there are corresponding chimeric sites or receptors between hepatitis B virus and liver cells. This site is located on the surface antigen of hepatitis B virus, and its material basis is polymerized human serum albumin receptor, which consists of 55 amino acid residues encoded by the pre-S2 region in the structure of viral deoxyribonucleic acid. There are receptors on the membrane of human hepatocytes, which can bind to polymerized human serum albumin.
Experts speculate that when hepatitis B virus enters the blood of infected people, it first forms a complex of hepatitis B virus and polymerized human serum albumin. When the receptor bound on the liver cell membrane was found on the polymerized human serum albumin in the complex, hepatitis B virus escaped into liver cells through the bridge of binding sites.
It was found that the binding site of polymerized human serum albumin was specific. Only aggregated human serum albumin of hepatitis B virus susceptible people and chimpanzees can bind to hepatitis B surface antigen. Some animals that are not easily infected, such as pigs, sheep, horses, cats and mice. Although there are polymerized human serum albumin components in blood and liver, they cannot bind to hepatitis B surface antigen.
In addition, it was also found that the amount of polymerized human serum albumin receptor in the serum of patients with positive E antigen was particularly high, while the amount of polymerized human serum albumin receptor in the serum of patients with positive hepatitis B E antibody was lacking. Polymerized human serum albumin receptor is related to the infectivity of hepatitis B virus. Measuring the number of polymerized human serum albumin receptors in blood has been used as a sign of whether hepatitis B virus is actively replicating in patients. The determination of polymerized human serum albumin receptor in the blood of patients with chronic hepatitis can judge whether the chronic liver is active or not and whether there is circumstantial evidence of acute attack.
What are hepatitis B virus DNA and DNA polymerase, and what does positive mean?
The genome of the core region of hepatitis B virus consists of hepatitis B virus deoxyribonucleic acid molecule (HBV-DNA) and deoxyribonucleic acid polymerase (DNA polymerase for short, or DNA-P). Hepatitis B virus DNA and DNA polymerase dominate hepatitis B virus replication, that is, asexual reproduction. So they are all positive, indicating that there are hepatitis B virus particles, which are active in replication and highly contagious.
The DNA of hepatitis B virus consists of two DNA chains, one is long and the other is short, and the directions are opposite. The two chains are strictly matched into a ring, and the short chain has a gap, so there is only one chain here. Modern molecular biology research has proved that HBV-DNA has 3200 pairs of nucleotides, and the combination of nucleotide pairs has strict regularity in the process of forming nucleic acid chains. When the virus begins to replicate, DNA polymerase first makes up for the missing part of the short chain, just like the long chain, and then the two chains separate to form a single chain. This single-stranded DNA can be used as a template, and each nucleotide of it is paired with a new nucleotide according to the pairing rule, thus forming a new strand, and then copying a new strand. At present, polymerase chain reaction (PCR) can be used to detect HBV-DNA, which has been widely used in clinic with strong specificity and high sensitivity, but the detection method of DNA polymerase is still not ideal.
What kind of virus is the pathogen of hepatitis B?
The pathogen of hepatitis B is deoxyribonucleic acid virus. It belongs to hepatotropic DNA virus family with woodchuck hepatitis virus, ground squirrel hepatitis virus and duck hepatitis virus. These viruses are race-specific and do not cross-infect each other. For example, hepatitis B virus is only susceptible to humans, orangutans and rhesus monkeys, and can be inherited in orangutans, but various tissue cultures have not been successful. Duck hepatitis virus can only infect ducks and is not contagious to humans and other animals.
Under the observation of electron microscope, the virus has three different forms.
① Small spherical particles: 22 nm in diameter.
② Tubular particles: the diameter is the same as that of spherical particles, and the length is 200 ~ 700 nm.
③ Spherical large particles: Dane particles or complete hepatitis B virus, with a diameter of 42nm.
Hepatitis B virus has a double-layer structure, consisting of a 7-nanometer outer membrane and a 27-nanometer inner core. The outer membrane of spherical, tubular and salvia miltiorrhiza granules consists of surface antigens and contains no nucleic acid. The outer layer of Dan's granule is a surface antigen coating film, and the content is a uniform icosahedron with a diameter of 27nm, which is called hepatitis B core antigen (HBcAg). Nucleic acid can be isolated from it, that is, the genetic composition of the virus.
Because of the particularity of hepatitis B virus morphology, its outer membrane can also be combined with hepatitis D virus. In the process of infecting people, it can be an acute lesion or a chronic infection. Once the virus gene is integrated into human hepatocytes, it can become the cause of primary liver cancer.
With the development of science and technology and in-depth research, the structure and pathogenic principle of hepatitis B virus, as well as the unknown mysteries, are being revealed one after another. We will answer the unclear questions later.
hepatitis B virus
In 1963, Blumberq found an abnormal antibody in the sera of two patients who received blood transfusions many times, which could react with the sera of an Australian aborigine. It was not until 1967 that it was clear that this antigen was related to hepatitis B. In 1970, the morphology of HBV was observed under electron microscope, and it was classified as hepatotropic DNA virus in 1986.
I. Biological characteristics
(1) form and structure
1. Large spherical particle: Also known as Dane particle, it is a virus particle consisting of an envelope and a core-shell containing DNA molecules, with a diameter of about 42nm. Core-shell is icosahedral symmetric structure. The free nucleocapsid can only be observed in the nucleus of hepatocytes. The concentration of Dana granules in blood is the highest in the late incubation period of acute hepatitis, and it drops rapidly after the onset. Dane particles contain HBsAg on the surface, and the core contains double-stranded DNA chains and DNA-dependent DNA polymerase. At present, Dion granules are considered to be completely HBV.
The two strands of HBV DNA are different in length, and the long chain (L) is a complete negative chain with a constant length of about 3200 nucleotides. Short chain is a positive chain with variable length, which is about 50 ~ 100% of the length of long chain, and chain proliferation is carried out in the order of 5 ′-3 ′. In different molecules, the position of 3' end of short chain is variable, while the fixed point of 5' end of short chain and long chain is sticky end, and the circular structure of DNA molecule is maintained by 250-300 nucleotide base pairs. On both sides of the sticky end, the 5' ends of the two chains each have a direct repeat sequence (5'ttcacctTCC) consisting of 1 1 bp, which is called DR 1 at nucleotide 1824 and DR2 at nucleotide 1590.
2. Small spherical particles: Small spherical particles with a diameter of about 22 nanometers are the most common in blood after HBV infection. It consists of the envelope HBsAg of the virus. The chemical component is lipoprotein, which can be separated from normal serum protein according to its unique density. No DNA polymerase activity was detected in this particle. At present, it is considered that the small particles of HBV are not HBV, which may be due to the excessive synthesis of capsules when infected hepatocytes leave the blood circulation.
3. Tubular particles: the diameter is about 22nm, and the length can be between 100 ~ 700 nm. In fact, it is a string of polymerized small particles, but it also has the antigenicity of HBsAg.
(2) Gene structure
At present, circular double-stranded DNA can be separated from the serum of patients infected with HBV virus and the purified virus core infected with liver, so as to determine HBV DNA virus.
The DNA structure of Dane granules was studied, and it was found that the DNA molecule contained about 3200 nucleotides. It includes two chains; Negative chain with fixed length and positive chain with uncertain length. Because the biosynthesis of DNA is completed by the formation of phosphodiester bond between 3'-OH at the growth end of DNA primer and 5'- phosphate group of added deoxynucleotides under the action of polymerase, the chain proliferation is carried out in the order of 5'-3', and each deoxynucleotide added in the chain is carried out according to the complementary law of base pairing of template DNA, and the long chain is 1, 800 or/kloc. The 5' end of the short chain maintains the cyclic structure of the molecule through base pairing of 250-300 nucleotides. The 3' end of the short chain is continuously extended by DNA polymerase to repair the gap. This gap may be related to the integration of HBV DNA in infected cells.
At present, because the complete nucleotide of cloned DNA has been determined, it has been confirmed that HBsAg and HBcAg are both encoded by the DNA of Dane particles, and the two types of genes exist in the same DNA molecule. Some people compare the coding ability of virus genes with the number of viruses, and find that the negative strand of HBV DNA can encode all known HBV proteins, while the positive strand of HBV DNA cannot encode virus proteins because of its open reading region.
The negative strand of HBV DNA has four open regions, namely S, C, P and X, which can encode all known HBV proteins. S region can be divided into two parts, S gene and pre-S gene. S gene (nucleotide 155 ~ 833) can encode major surface proteins. S gene is preceded by pre-S gene, which can encode 163 amino acids (2,848-154), and encode pre-S 1 and pre-S2 protein. The genes in C region include pre-C gene and C gene, which encode HBeAg and HBcAg respectively. P region is the longest, accounting for more than 75% of the genome, and it encodes viral DNA polymerase. X region (nucleotide 1, 374 ~ 1, 835) may encode an alkaline polypeptide with 154 amino acids, and the long-chain gap is located in this region.
(III) Antigen composition of HBV
1.HBsAg: HBsAg is unique to the genome of HBV, and it is possessed by the above three forms of particles.
HBsAg antigen activity belongs to lipoprotein with high floating density. By CsCl density gradient centrifugation, the average density of surface antigens (small particles and tubular particles) is 1.20g/cm2. Dion particle density is slightly higher, which is 1.25g/cm2. The average sedimentation coefficient of purified 22-nanometer particles is 33-54S, and the molecular weight is about 24-2.5× 106.
The purified HBsAg contains lipids, carbohydrates, lipids, protein and glycoproteins. It consists of 8 kinds of polypeptides, named P 1 to P8. At least two or three peptides were positive in periodic acid Schiff test, suggesting the existence of carbohydrate structure. The extracted HBsAg was detected by ultraviolet spectrophotometer, showing a typical protein absorption spectrum. Protein accounts for more than 70 ~ 90% of the total, and HBsAg in a broad sense consists of three protein: (1) major surface protein (S protein, small molecule HBsAg), which consists of 226 amino acids encoded by S gene. (2) The middle molecular protein (middle molecular HBsAg) consists of pre-S2 and S genes, and a pre-S2 protein with 55 amino acids is added to the N-terminal of 226 amino acids of S protein, ***28 1 amino acid. (3) Macromolecular protein (macromolecular HBsAg) is composed of S, pre-S 1 and pre-S2 genes, and a11protein with 9 amino acids is added to the N-terminal of a molecular protein with * * 400 amino acids.
S protein, that is, HBsAg in a narrow sense, is the main component of the main surface antigen of HBV envelope, including glycosylated GP27 and non-glycosylated P24, which are connected by disulfide bonds to form dimers, representing the structural unit of HBsAg and having complete antigenicity. If the dimer dissociates, the antigenicity of HBsAg will decrease obviously.
HBsAg can stimulate the body to produce corresponding antibody-anti-HBS, which is a neutralizing antibody of HBV and has immune protection. The detection of HBsAg is one of the signs of HBV infection.
Pre-S protein 2 (pre-S2) is linked to HBsAg terminal at its C terminal. Pre-S2 is exposed to the outer layer of HBV envelope and has a receptor for polymerized human serum albumin (PHSA-R), which can bind to PH-SA. Because there is also PHSA-R on the surface of liver cells, HBV can be adsorbed to the surface of liver cells through the mediation of PHSA existing in blood circulation, and finally enter liver cells through pinocytosis. If pre-S2 virus is detected in the patient's serum, it means that HBV virus replicates in liver cells. S2 precursor has good immunogenicity and can stimulate the body to produce corresponding antibody-anti-S2 precursor. This antibody appeared in the early stage of recovery from acute infection, earlier than anti -HBs, and maintained for the same time as anti -HBs. Anti-pre-S2 has a neutralizing effect, which can be used as one of the indicators of physical rehabilitation.
Pre S 1 has strong immunogenicity, which can enhance the immunogenicity of pre S2 and HBsAg. Pre S 1 stimulates the body to produce corresponding antibodies-pre s1. There are two kinds of antibodies, lgM and lgG, in which anti-Pre1is produced in the incubation period of HBV infection, that is, before anti-HBV~lgM appears, so it can be used as a specific indicator of early HBV infection. However, the anti-Pre S 1 lgG appeared a little later and stayed in the body for a long time, which had a neutralizing effect.
HBsAg is stable to some compounds that promote denaturation, such as ether, 1: 1 chloroform-urea, sodium dodecyl sulfate, Tween 30 and various proteolytic enzymes. After several hours incubation in acid, HBsAg is still stable. Under alkaline conditions, freezing and melting can not inactivate it. The lipid on the surface may protect some antigenic determinants mainly composed of protein.
HBsAg has several specific antigenic components, including antigenic determinant A with the same subtype, and two groups of mutually exclusive subtype determinants d/y and W/R. The main subtypes of HBsAg are adr, adw, ayr and ayw4. Adr in Europe and America is the main factor, while in China, the majority of Han people are adr in central China and ayw in minority areas (Tibet, Xinjiang, Inner Mongolia, etc.). ).
2.HBCAG: HBCAG exists in the core of Dane Granule and the hepatocyte nucleus of hepatitis B patients. HBcAg is generally extracted from the liver of autopsy with HBcAg positive or the liver of experimental infected chimpanzee. Anti-~HBc can often be detected in acute phase, recovery phase and HBcAg carriers of hepatitis B, and the antibody has no neutralizing effect on the virus. If ~HBcAg or anti -HBc is found in the body, it means that HBV continues to replicate in the liver.
3. The essence of HBeAg: E antigen is not very clear, but most people think it is the core part of Dane Granule. So far, it has not appeared in HbsAg negative serum. HBeAg is a soluble antigen. There are three subtypes of antigens: e 1, e2 and e3. Because the growth and decline of HBeAg and DNA polymerase in blood are consistent, the existence of HBcAg can be used as a sign of HBV replication and serum infectivity in vivo. The higher the HBsAg titer in blood, the higher the detection rate of HBeAg. Some patients may produce HBe antibody, which may also be a protective antibody.
(D) the cultivation of HBV
Tissue culture of HBV has been unsuccessful. In recent years, the methods of primary culture of purulent cells obtained from human embryonic liver, preparation of semi-continuous human hepatocyte lines and adult embryonic tissue of diagnostic liver stab culture have been developed, but it is still difficult to culture HBV in vitro using various liver tissues. Although some "hepatitis undetermined" viruses were obtained by boldly trying to isolate HBV from various cells and organs, it was difficult to make them pass through tissue culture continuously, so none of them were confirmed as HBV. Recently, it has not been realized that HBV can spread by extracting HBV DNA and saving the virus through cell fusion.
South African scholar (1976) reported that HBsAg replication was found in the cell line (PLC/PRF/5) established from HBsAg positive primary liver cancer tissue. The main feature of this cell line is that it can produce more and more HBsAg. 104/ day cells can produce 500ng HBsAg, mostly 22nm particles, which are round and slightly submicroscopic. Its antigenicity and immunity are the same as HBsAg in blood. Dane particles and tubes were not found. At present, this cell line has been used to study the useful model of viral genome expression in vitro.
Chimpanzees are susceptible animals to HBV, while marmosets can be infected, but they are not as sensitive as the former. In foreign countries, chimpanzees are used to study the pathogenesis of HBV, and the effects of active and passive immunization and the safety of HBV vaccine are tested. However, chimpanzees are short in source and difficult to be widely used.
(5) Resistance
HBV has a strong resistance to the outside world. Resistant to low temperature, dryness, ultraviolet rays and general chemical disinfectants. The infectivity of hepatitis B virus and antigenicity of hepatitis B surface antigen are completely consistent in external resistance. Their activity can be maintained at 37℃ for 7 days, at -20℃ for 20 years, and heating at 100℃ 10 min can make HBV lose infectivity, but still maintain its surface antigen activity. HBV is sensitive to 0.5% peracetic acid, 5% sodium chlorate and 3% bleaching powder and can be used for disinfection.
Second, the pathogenicity and immunity of HBV
(1) Source of infection and route of transmission
The main sources of infection of hepatitis B are patients and HBV antigen carriers. In the incubation period and acute period, the patient's serum is contagious. The spread of type B pneumonia is very extensive, and it is estimated that there are about 200 million HBsAg carriers in the world. Because they have no clinical symptoms, HBsAg carries for a long time (months to years), and it is more harmful to become a source of infection than patients.
HBV is highly contagious. It is reported that 0.00004 ml of blood containing virus is enough to infect people. Blood transfusion or injection is an important route of infection and delicious. Surgery and oral surgery, acupuncture, the use of public razors, toothbrushes and other items, as well as minor skin surgery that pollutes blood containing a small amount of virus can all become sources of infection. It is also reported that hepatitis B is spread by breathing blood and sucking insects. Recently, it was reported that HBsAg and Dane particles were detected in saliva samples of patients with acute hepatitis B and chronic HBsAg carriers. Therefore, the route of oral transmission of HBsAg with saliva should be paid attention to. Pregnant women suffer from acute hepatitis B in the third trimester of pregnancy, and their newborns are prone to the disease. Because hepatitis B is easily infected with this disease. Because hepatitis B surface antigen can be detected in semen and vaginal secretions of patients with hepatitis B and carriers of hepatitis B surface antigen, it is possible to spread hepatitis B through sexual contact.
(2) Pathogenic mechanism and immunity
The pathogenesis of HBV is not completely clear. In view of the diversity of clinical types of hepatitis B (such as acute hepatitis, chronic active hepatitis, chronic persistent hepatitis, severe hepatitis and asymptomatic carriers of HBsAg), it is generally believed that the pathogenic effect of HBV is different from that of virus. It is possible that the target cells are not directly destroyed by the virus proliferation in the captured cells, but may be caused by the immune response of the body to the virus.
1. Specific antibody: After hepatitis B virus infection, the body can produce three kinds of antibodies, anti-HBs, anti-HBc and anti-HBe. Anti -HBs usually appears 4 weeks after HBV infection, which has protective effect on hepatitis B. It is reported that less than 1% of 7 12 medical staff have hepatitis, while 1 1% who are not anti -HBS have hepatitis. However, anti -HBs can only act on extracellular HBV, which is more important in preventing infection, and the recovery of disease requires the synergistic effect of cellular immunity.
The appearance of anti-HBc reflects the recent infection and proliferation of HBV in the body, so it can be used as an indicator of HBV replication in the body. Anti -HBc usually appears 60 ~ 150 days after infection, often before or shortly after symptoms appear, 3 1 ~ 87 days earlier than anti -HBs, but it is not as persistent as anti -HBc. Anti -HBc is related to the amount of HBcAg in the liver. The anti -HBc titer of chronic HBsAg carriers is low, but it is higher in patients with chronic activity, liver cirrhosis and liver cancer. The fluctuation of titer is parallel to the condition. Because anti -HBc not only does not increase, but decreases in the process of disease recovery, it is considered that anti -HBc is different from anti -HBs and has nothing to do with protection, but with virus proliferation and liver cell damage.
Anti-Hbe can reduce virus activity, which may have protective effect, but the mechanism is different.
2. Damage of immune complex: HBsAg-anti-HBs immune complex can often be detected in the blood circulation of patients with hepatitis B, and immune complex can cause type III allergic reaction, among which arthritis and nephritis are the most common. Hepatitis B surface antigen-sometimes anti-hepatitis B surface antigen can be detected simultaneously in the blood of fulminant hepatitis. This patient has a poor prognosis and a high mortality rate. Therefore, it is considered that immune complex can cause a series of symptoms of patients outside the liver. If a large number of immune complexes are deposited in the liver, causing capillary embolism, it may cause acute liver necrosis and lead to death.
3. Cell-mediated immune response: At present, it is considered that HBV is insoluble, that is, it will not proliferate and divide infected cells. Therefore, the elimination of hepatitis B virus mainly depends on T cells (Tc, T killer cells) or antibody-mediated K cells to kill the target cells, and release the virus into body fluids, and then through the action of antibodies. Experimental studies have found that the number and function of T cells in people transformed into chronic hepatitis are generally low. Therefore, it is speculated that the strength of T cell function in patients with hepatitis B may be related to the severity of clinical process and prognosis. Dudleuy believes that when T cell immune function is normal and not too many liver cells are infected by virus, hepatitis B virus will be quickly eliminated by cellular immunity combined with humoral immunity. At this time, the acute hepatocyte injury caused by cellular immunity can be completely recovered. For example, the immune function of T cells is low, the immune response is not enough to completely destroy the liver cells infected by the virus, or it can't produce effective anti -HBs, or even the virus that can't act on the cells. The virus that persists in the liver cells can cause immunopathological reactions and lead to chronic persistent hepatitis. If the body completely lacks cellular immune response to the virus, it can neither effectively clear the virus nor cause immunopathological reaction, resulting in asymptomatic HBsAg carrying symptoms. If the immune function of T cells is too strong and there are too many cells infected by the virus, the cellular immune response can quickly cause a large number of hepatocyte necrosis, and the clinical manifestation is fulminant hepatitis. However, the above theory has not been completely confirmed. Through further research, most people think that cellular immunity and humoral immunity cooperate with each other to play an immune role together. Therefore, more and more attention has been paid to antibody-mediated K cell function, which is considered as an important immune mechanism to kill target cells. In addition to the above-mentioned low function of T cells, some people think that the occurrence of chronic active hepatitis is related to the low inhibitory function of T cells and the excessive killing function of Tc cells or K cells, thus causing continuous damage to liver cells.
4. Autoimmune reaction: After HBV infects hepatocytes, on the one hand, it can change the surface antigen of hepatocytes and expose the liver-specific protein antigen (liver-specific protein:; LSP), on the other hand, HBsAg may contain the same antigen as the host hepatocyte protein, thus inducing the body to produce an autoimmune response to the antigenic components of the hepatocyte membrane. It is found that some patients with hepatitis B do have specific antibodies or cellular immune responses to LSP. It is generally believed that if patients have autoimmune reaction in the course of the disease, they can strengthen the damage to liver cells and develop into chronic active hepatitis.
5. Hepatitis B and primary liver cancer: In recent years, more and more attention has been paid to the relationship between HBV infection and primary liver cancer. Domestic and foreign data show that the incidence of liver cancer in patients with hepatitis is higher than that in natural population. The HBV infection index of patients with liver cancer is also higher than that of natural population. Maupas and others demonstrated the close relationship between HBV and primary liver cancer: ① there is a geographical correlation between the high prevalence area of hepatitis B infection and the high prevalence area of primary liver cancer; ② In epidemic and non-epidemic areas, the risk of primary liver cancer among male HBsAg chronic carriers is relatively constant. In this population, the annual mortality rate of primary liver cancer is 250-500/65438+ 10,000. It is roughly estimated that there are about 654.38+75 million chronic carriers of HBsAg in the world, and the annual incidence of primary liver cancer is 350,000 cases. This indicates that HBV-related primary liver cancer is one of the most popular cancers in the world. ③HBV infection can precede and often accompany the occurrence of primary liver cancer; ④ Primary liver cancer often occurs in the liver of chronic hepatitis B virus or cirrhosis; ⑤ HBV-specific DNA and antigen exist in the tissues of patients with primary liver cancer; ⑥ Some primary liver cancer cell lines have been able to produce HBsAg in culture, and it has been proved that HBV DNA can be integrated into the genomes of these cells. In addition, it contains biochemical and biophysical characteristics similar to HBV, and can induce cirrhosis and primary liver cancer in its host. A similar virus has been isolated from domestic chickens in China and the United States. However, there are still different opinions on the interpretation of the above data: ①HBV can cause cancer or promote cancer, and it must be combined with other factors such as heredity, endocrine, immunity and environment to cause liver cancer; ② Liver cancer is caused by factors unrelated to HBV, but these cancer cells may be so sensitive to HBV that they continue to carry the virus.
Third, microbial diagnosis.
(A) detection methods of hepatitis B antigen and antibody
At present, the detection methods of HBsAg, HBcAg, HBeAg and their antibody systems have been established. Radioimmunoassay, enzyme-linked immunosorbent assay and enzyme-linked immunosorbent assay are the most sensitive, followed by reverse passive hemagglutination and immunoadhesion hemagglutination. Although immunodiffusion and convection electrophoresis are not very sensitive, they are still widely used in China. Among these three antigen systems, HBsAg is the most commonly used.
(B) the practical significance of detection of hepatitis B antigen antibody
1.HBsAg: HBsAg was detected in serum, indicating that the body was infected with HBV virus, so it is a specific marker. HBsAg positive can be found in: ① acute hepatitis B in the latent period or acute period (mostly short-term positive); ② Chronic liver disease, persistent and chronic active hepatitis, posthepatitic cirrhosis or primary liver cancer caused by ②HBV. ③ asymptomatic carriers.
2. Anti -HBs: It means that you have been infected with HBV. No matter what the clinical symptoms of hepatitis are, you have recovered and have certain immunity to HBV.
3.HBcAg and anti-HBc: HBCAG mainly exists in the nucleus of hepatocytes and only exists in Dane granules. Therefore, HBcAg can not be detected in patients' serum, but anti-HBc can be detected. Serum anti -HBc positive reaction: ① recent infection with HBc② HBV proliferation in vivo; ③ It is helpful to diagnose acute and chronic hepatitis B, especially a few cases are in the early stage of acute recovery, and HBsAg has disappeared from the blood. At this time, only anti-HBc exists in the blood. Therefore, it is possible to engage in the career of rehabilitating patients.
4.HBCAG and anti-HBE: The existence of HBCAG often indicates that the patient's blood is infectious. The positive HBcAg suggests that the patient's liver may have chronic damage, which is helpful to predict the prognosis. Anti-HBe positive may have some protective effects on patients.
(b) Practical application of detecting hepatitis B antigen and antibody.
1. Screening blood donors: Screening HBsAg-positive blood donors can greatly reduce the incidence of hepatitis B after blood transfusion.
2. It can be used as a specific diagnosis for hepatitis B patients or carriers.
3. To provide reference for the prognosis and prognosis of patients with hepatitis B.. It is generally believed that about 2/3 patients with acute hepatitis B, such as those with HBsAg lasting for more than 2 months, can turn into chronic hepatitis. HBeAg positive people are more likely to develop chronic hepatitis and cirrhosis after illness.
4. Study the epidemiology of hepatitis B, and understand the infection of hepatitis B among people in different places.
5. To judge the immune level of people to hepatitis B, and understand the seroconversion and titer increase of antibodies after vaccination.
Fourth, the prevention and control principles
Interferon-α is the definitive drug for treating hepatitis B at present, and it has been reported at home and abroad that HBsAg turns negative after continuous high-dose injection of interferon-α for half a year. But recently, it was found that some patients who turned negative turned negative after stopping interferon. Others, such as thymosin and transfer factor, have also been reported to treat chronic hepatitis, but the effect is not good.
In recent years, the research and application of hepatitis B vaccine is very active. Hepatitis B genetic engineering (yeast recombinant HBsAg) vaccine has been put into large-scale application and achieved gratifying results. The development of polypeptide vaccine, fusion protein vaccine and gene vaccine is in the ascendant, and it is believed that the desire to control hepatitis B will be realized through various efforts.
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