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Hepatitis D. Causes, symptoms and treatment of hepatitis D

Viral hepatitis is a large heterogeneous in etiology, but similar in clinical manifestations, a group of severe consequences of diseases that are widespread in the world. Many viruses can cause liver damage among other effects (eg some serotypes of ECHO viruses), but there is a large group of viruses with a predominantly hepatotropic effect. According to ecological and epidemiological features, they can be divided into two groups - with a predominantly fecal-oral transmission mechanism (hepatitis viruses A and E) and with parenteral (blood contact) transmission (B, C, G, D). The hepatitis D virus (delta) is a defective virus - a satellite of the hepatitis B virus, transmitted parenterally and vertically (from mother to fetus). Hepatitis A virus - enterovirus 72, B - hepadnovirus, C and G - flaviviruses, D - unclassified virus, E - calicivirus.

Hepatitis b virus.

The hepatitis B virus (HBV) causes serum hepatitis, belongs to the family hepadnoviruses- shell DNA - viruses that cause hepatitis in various animal species (marmots, ducks, etc.).

Hepatitis B is a serious public health problem worldwide. This is facilitated by an increase in the incidence, the frequent formation of adverse outcomes (chronic hepatitis, cirrhosis of the liver, hepatocarcinoma, rather high mortality).

Hepadnoviruses primarily infect liver cells. The HBV genome is represented by a double-stranded circular DNA molecule, the outer chain is longer than the inner one.

reproduction cycleHBV is very complex and passes through an intermediate link - RNA (DNA RNA DNA), i.e. with a reverse transcription mechanism. During transcription of the viral genome in the nucleus of the hepatocyte, cellular DNA - dependent RNA - polymerase synthesizes two types of mRNA - larger (pregenome) and smaller (for the synthesis of viral proteins). The pregenome and viral DNA polymerase are packaged into a capsid and transported into the cytoplasm. Under the action of a virus-induced reverse transcriptase, a new minus-strand of DNA is synthesized on the pregenome template (RNA). Virion DNA polymerase on the minus chain synthesizes the plus chain. If the viral double-stranded DNA does not enter into further replication, the formed nucleocapsid, passing through the cell membrane, is covered by the supercapsid and buds from the cell.

Structure and antigenic structure.

Virus particles 42 - 45 nm in size ( Dane particles) have a rather complex structure and include DNA, its associated DNA polymerase and four antigens - surface (HBs Ag - “Australian”), core or cow (HBc Ag or cor Ag), infectivity antigen (HBe Ag, detected in the blood at active replication of HBV) and the least studied HBx Ag.

Circulating strains of HBV differ in the antigenic structure of the HBs antigen. It contains a common antigen that causes cross (between subtypes) immunity and four type-specific antigenic determinants and, accordingly, four subtypesHBs Ag(andHBV).

Given the complex antigenic structure of the hepatitis B virus, a number of infection markers are used in the diagnosis of this infection, incl. antigens (HBs Ag, HBc Ag, HBe Ag) and their corresponding antibodies (anti - HBs, anti - HBc and anti - HBe).

Important for determining the prognosis and tactics of treating patients with hepatitis B is the allocation of two qualitatively different biological phases of the development of HBV - replicative and integrative. During the replicative phase (i.e. mass reproduction of the virus), the viral DNA polymerase replicates the HBV DNA and all viral subcomponents and proteins are copied in large quantities. During the integrative phase of development (i.e., when viral particles do not undergo further replication), the HBV genome is integrated into the hepatocyte genome. In the process of integration, the main role is played by the fragment carrying the gene encoding the HBs antigen; therefore, during this phase, HBs Ag is predominantly formed. Therefore, the biological stages of HBV differ in the spectrum of detection of infection markers. The replication stage is characterized by the identification DNAHBV, HBe Agand (or) anti-HBc - IgM, possibly - HBs Ag. In the integration stage, HBs Ag, anti - HBe, anti - HBc - IgG predominate.

epidemiological features.

The hepatitis B virus is spread by evolutionary natural and by artificial means distribution. For effective infection, the introduction of 0.0000007 ml of infected blood is sufficient (artificial parenteral routes of infection - through medical manipulations). Among the natural ways - vertical (from mother to offspring), sexual and contact (family) - "hemocontact" (L.M. Shlyakhtenko et al., 1990, 1998). The transmission of the pathogen is ensured by resistance in the external environment, the virus is transmitted by contact with blood and other body fluids (saliva, semen, contents of the nasopharynx, vagina, etc.). Transmission factors can be various personal hygiene items (toothbrushes, shaving and manicure devices, washcloths, combs, etc.). In recent years, the importance of drug addiction and sexual transmission has increased.

Clinical and pathogenetic features.

The target organ for the hepatitis B virus is the liver. The defeat of hepatocytes is not directly related to the direct action of the virus (there is no cytopathic effect), but to the host's immune (autoaggressive) reactions associated with the modification of cell membranes by viral proteins. Autoaggression is realized by T - cytotoxic lymphocytes and other killer cells, the production of autoantibodies against liver tissues. Liver damage can be in the form of acute and chronic forms of varying severity.

Post-infectious immunity prolonged, directed against the main protective HBs antigen, caused by virus-neutralizing anti-HBs antibodies.

Diagnostic methods.

Laboratory diagnostics is based on ELISA and PCR.

HBsantigen- the main and first marker of HBV infection. Its elimination and the appearance of anti - HBs - antibodies is an indispensable condition for recovery. Anti HBs - antibodies - an indicator of past infection.

HBcantigen- core antigen, nucleocapsid protein, detected only in the nuclei of hepatocytes, but absent in pure form in the blood. Blood tests are of great diagnostic value. anti-HBc - IgM. These antibodies in acute hepatitis are detected earlier than antibodies to other viral antigens. AntiHBc-IgM is detected in 100% of patients with acute hepatitis B, both HBs-positive and HBs-negative. Anti HBc antibodies can be the only marker of hepatitis B virus in the “window” phase, when neither HBs antigen nor antibodies to it can be detected in the blood.

The detection of anti-HBc-IgM is combined with the detection of virus DNA and DNA polymerase activity (ie, indicators of ongoing virus replication) and the activity of the pathological process in the liver. Anti HBc-IgG is a marker of past HBV infection.

HBe Ag - infectivity antigen, circulates only in the presence of HBs antigen. Its presence in the blood serum correlates with the detection of virus DNA, polymerase activity, and with the production of complete viral particles, i.e. with active viral replication. The duration of circulation of the HBe antigen is an important prognostic sign. Its detection two months after the onset of the disease is a sign of the likely development of chronic hepatitis. In most cases, HBe Ag is replaced by anti-HBe antibodies, which is a marker of the completed replication of the hepatitis B virus.

Provides important diagnostic information DNA detection methodsHBV. In some cases, in the absence of the HBs antigen in the blood, as well as serological markers of viral replication (HBe Ag, antiHBcor - IgM) , the continued reproduction of the virus in the liver can be judged by the results of molecular nucleic acid hybridization (MHNA) and PCR. Using the PCR technique, the subtype of the HBs antigen can also be determined.

Specific prophylaxis is currently carried out using recombinant vaccines (Engierix B, Recombivax B, etc.) obtained by genetic engineering methods on Saccharomyces cerevisae yeast cultures. The recombinant yeast clone produces the HBV surface antigen. Efficiency - 95%, duration - not less than 5 - 6 years. Three-fold immunization is provided - immediately after birth, after 1 - 2 months, until the end of the first year of a child's life. For emergency prophylaxis, donor immunoglobulin containing antibodies to HBV can be used for contact.

The specified period does not include the day of taking the biomaterial

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At least 3 hours after the last meal. You can drink water without gas.

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Research method: PCR

Viral hepatitis Delta (HDV) is a liver disease caused by an RNA-containing viroid (an imperfect virus) belonging to the Deltavirus family. The virus is able to replicate only in the presence of HBV. The pathogen transmission mechanism is parenteral. Infection can occur in the form of co-infection (simultaneous infection with HBV) and superinfection (accession after infection with HBV).

The hepatitis D virus during co- and superinfection suppresses the replication of the hepatitis B virus; therefore, HBV DNA and HBeAg are not detected in persons infected with HBV and HDD. Identification of HD determines the course of the disease and the tactics of antiviral therapy.

HDV RNA, a marker of HDV infection, appears in the blood 2-3 weeks earlier than antibodies to the virus. The study is carried out in patients with acute and chronic hepatitis B.

INDICATIONS FOR THE STUDY:

  • Patients with OGV;
  • HBV carriers;
  • Patients with CHB;
  • Patients with HD during and after antiviral treatment.

INTERPRETATION OF THE RESULTS:

Reference values ​​(norm option):

Analytical sensitivity of hepatitis D virus RNA - 300 copies/ml.

The detection of HDV RNA unambiguously indicates HDV infection.

We draw your attention to the fact that the interpretation of the results of studies, the establishment of a diagnosis, as well as the appointment of treatment, in accordance with Federal Law No. 323-FZ "On the Fundamentals of Protecting the Health of Citizens in the Russian Federation" dated November 21, 2011, must be carried out by a doctor of the appropriate specialization.

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Viral hepatitis D(delta hepatitis) is an infectious lesion of the liver, coinfection or superinfection of viral hepatitis B, which significantly worsens its course and prognosis. Viral hepatitis D belongs to the group of transfusion hepatitis, a prerequisite for infection with hepatitis D is the presence of an active form of hepatitis B. The detection of hepatitis D virus is carried out by PCR. A study of the liver is mandatory: biochemical tests, ultrasound, MRI, rheohepatography. The treatment of viral hepatitis D is similar to the treatment of hepatitis B, but requires larger doses of drugs and a longer duration of treatment. In most cases, chronic disease is observed with subsequent outcome in cirrhosis of the liver.

General information

Viral hepatitis D(delta hepatitis) is an infectious lesion of the liver, coinfection or superinfection of viral hepatitis B, which significantly worsens its course and prognosis. Viral hepatitis D belongs to the group of transfusion hepatitis.

Exciter characteristic

Hepatitis D is caused by an RNA-containing virus, which is the only currently known representative of the “wandering” genus Deltavirus, which is distinguished by its inability to independently form a protein for replication and uses a protein produced by the hepatitis B virus for this. Thus, the causative agent of hepatitis D is a satellite virus and occurs only in combination with the hepatitis B virus.

The hepatitis D virus is extremely stable in the external environment. Heating, freezing and thawing, exposure to acids, nucleases and glycosidases do not significantly affect its activity. The reservoir and source of infection are patients with a combined form of hepatitis B and D. Contagiousness is especially pronounced in the acute phase of the disease, but patients pose an epidemic danger throughout the entire period of circulation of the virus in the blood.

The mechanism of transmission of viral hepatitis D is parenteral, a prerequisite for the transmission of the virus is the presence of an active hepatitis B virus. The hepatitis D virus integrates into its genome and enhances the ability to replicate. The disease can be a co-infection, when the hepatitis D virus is transmitted simultaneously with B, or a superinfection, when the pathogen enters the body already infected with the hepatitis B virus. The most significant risk of infection during blood transfusion from infected donors, surgical interventions, traumatic medical manipulation (for example, in dentistry).

The hepatitis D virus is able to overcome the placental barrier, can be sexually transmitted (the spread of this infection among persons prone to promiscuity, homosexuals is high), which in some cases has a familial spread of the virus suggests the possibility of its transmission through household contact. Patients with viral hepatitis B, as well as carriers of the virus, are susceptible to viral hepatitis D. In particular, the susceptibility of persons who are chronic carriers of HBsAg is high.

Symptoms of viral hepatitis D

Viral hepatitis D complements and aggravates the course of hepatitis B. The incubation period of coinfection is significantly reduced, 4-5 days. Superinfection incubation lasts 3-7 weeks. The preicteric period of hepatitis B proceeds similarly to that of hepatitis B, but has a shorter duration and a more rapid course. Superinfection may be characterized by the early development of edematous-ascitic syndrome. The icteric period proceeds in the same way as in hepatitis B, but bilirubinemia is more pronounced, signs of hemorrhage often appear. Intoxication in the icteric period of hepatitis D is significant, prone to progression.

Co-infection proceeds in two phases, the interval between the peaks of clinical symptoms of which is 15-32 days. Superinfection is often difficult to differential diagnosis, since its course is similar to that of hepatitis B. A characteristic difference is the rate of development of the clinical picture, the rapid chronization of the process, hepatosplenomegaly, a disorder of protein synthesis in the liver. Recovery takes much longer than in the case of hepatitis B, residual asthenia may persist for several months.

Diagnosis of viral hepatitis D

In the acute phase of the disease, specific IgM antibodies are noted in the blood, over the next few months only IgG are detected. In wide practice, diagnosis is carried out using the PCR method, which makes it possible to isolate and identify the RNA virus.

To study the state of the liver in viral hepatitis D, ultrasound of the liver, rheohepatography, MRI of the liver and biliary tract are performed. In some cases, to clarify the diagnosis, a puncture biopsy of the liver can be performed. Nonspecific diagnostic measures are similar to those for hepatitis of a different etiology and are aimed at dynamic control of the functional state of the liver.

Treatment of viral hepatitis D

Treatment of hepatitis D is carried out by a gastroenterologist according to the same principles as the treatment of viral hepatitis B. Since the hepatitis D virus is more resistant to interferon, the basic antiviral therapy is adjusted towards increasing dosages, and the duration of the course is 3 months. If there is no effect, the dosages are doubled, the course is extended to 12 months. Since the hepatitis D virus has a direct cytopathic effect, drugs of the corticosteroid hormone group are contraindicated in this infection.

Forecast and prevention of viral hepatitis D

The prognosis in the case of mild to moderate co-infection is more favorable, since a complete cure is observed much more often than with superinfection. However, co-infection with hepatitis B and D viruses often proceeds in a severe form with the development of life-threatening complications. Chronic coinfection develops in 1-3% of cases, while superinfection develops into a chronic form in 70-80% of patients. Chronic viral hepatitis D leads to the development of cirrhosis. Recovery from superinfection is extremely rare.

Prevention of viral hepatitis D is similar to that of viral hepatitis B. Preventive measures are of particular importance for people with hepatitis B who are positive for the presence of the HBsAg antigen. Specific vaccination against viral hepatitis B effectively protects against delta hepatitis.

Viral hepatitis- this is a group of common and dangerous infectious diseases for humans, which differ quite significantly from each other, are caused by different viruses, but still have one thing in common - this is a disease that primarily affects the human liver and causes inflammation. Therefore, viral hepatitis of different types are often grouped together under the name "jaundice" - one of the most common symptoms of hepatitis.

Epidemics of jaundice have been described as early as the 5th century BC. Hippocrates, but the causative agents of hepatitis were discovered only in the middle of the last century. In addition, it should be noted that the concept of hepatitis in modern medicine can mean not only independent diseases, but also one of the components of a generalized, that is, affecting the body as a whole, pathological process.

Hepatitis (a, b, c, d), i.e. inflammatory liver disease, is possible as a symptom of yellow fever, rubella, herpes, AIDS and some other diseases. There is also toxic hepatitis, which includes, for example, liver damage due to alcoholism.

We will talk about independent infections - viral hepatitis. They differ in origin (etiology) and course, however, some symptoms of various types of this disease are somewhat similar to each other.

Classification of viral hepatitis

Classification of viral hepatitis is possible on many grounds:

The danger of viral hepatitis

Especially dangerous for human health hepatitis viruses B and C. The ability to exist in the body for a long time without noticeable manifestations leads to severe complications due to the gradual destruction of liver cells.

Another characteristic feature of viral hepatitis is that anyone can get infected. Of course, in the presence of factors such as blood transfusion or work with it, drug addiction, promiscuity, the risk of contracting not only hepatitis, but also HIV increases. Therefore, for example, healthcare workers should regularly donate blood for markers of hepatitis.

But you can also become infected after a blood transfusion, an injection with a non-sterile syringe, after an operation, a visit to the dentist, in a beauty parlor or for a manicure. Therefore, a blood test for viral hepatitis is recommended for anyone exposed to any of these risk factors.

Hepatitis C can also cause extrahepatic manifestations such as autoimmune diseases. The constant fight against the virus can lead to a perverse reaction of the immune system to the body's own tissues, resulting in glomerulonephritis, skin lesions, etc.

Important: in no case should the disease be left untreated, since in this case the risk of its transition to a chronic form or rapid damage to the liver is higher.

Therefore, the only available way to protect yourself from the consequences of hepatitis infection is to rely on early diagnosis with the help of tests and subsequent visits to a doctor.

Forms of hepatitis

Acute hepatitis

The acute form of the disease is the most typical for all viral hepatitis. Patients have:

  • deterioration of well-being;
  • severe intoxication of the body;
  • liver dysfunction;
  • development of jaundice;
  • an increase in the amount of bilirubin and transaminase in the blood.

With adequate and timely treatment, acute hepatitis ends complete recovery of the patient.

chronic hepatitis

If the disease lasts more than 6 months, then the patient is diagnosed with chronic hepatitis. This form is accompanied by severe symptoms (asthenovegetative disorders, enlargement of the liver and spleen, metabolic disorders) and often leads to cirrhosis of the liver, the development of malignant tumors.

Human life is in danger when chronic hepatitis, the symptoms of which indicate damage to vital organs, is aggravated by improper treatment, reduced immunity, and alcohol addiction.

General symptoms of hepatitis

jaundice appears with hepatitis as a result of bilirubin, which is not processed in the liver, enters the bloodstream. But it is not uncommon for the absence of this symptom in hepatitis.


Usually hepatitis in the initial period of the disease manifests flu symptoms. It notes:

  • temperature increase;
  • body aches;
  • headache;
  • general malaise.

As a result of the inflammatory process, the patient's liver increases and its membrane stretches, and at the same time a pathological process may occur in the gallbladder and pancreas. All this is accompanied pain in the right hypochondrium. Pain often have a long course, aching or dull character. But they can be sharp, intense, paroxysmal and give to the right shoulder blade or shoulder.

Descriptions of symptoms of viral hepatitis

Hepatitis A

Hepatitis A or Botkin's disease is the most common form of viral hepatitis. Its incubation period (from the moment of infection to the appearance of the first signs of the disease) is from 7 to 50 days.

Causes of Hepatitis A

Hepatitis A is most widespread in the countries of the "third world" with their low sanitary and hygienic standard of living, however, isolated cases or outbreaks of hepatitis A are possible even in the most developed countries of Europe and America.

The most common mode of transmission of the virus is through close household contact between people and ingestion of food or water contaminated with faecal material. Hepatitis A is also transmitted through dirty hands, so children most often fall ill with it.

Symptoms of Hepatitis A

The duration of hepatitis A disease can vary from 1 week to 1.5-2 months, and the recovery period following the disease sometimes stretches up to six months.

The diagnosis of viral hepatitis A is made taking into account the symptoms of the disease, anamnesis (that is, the possibility of the onset of the disease due to contact with patients with hepatitis A is taken into account), as well as diagnostic data.

Hepatitis A treatment

Of all forms, viral hepatitis A is considered the most favorable in terms of prognosis, it does not cause severe consequences and often ends spontaneously, without requiring active treatment.

If necessary, hepatitis A is treated successfully, usually in a hospital setting. During illness, bed rest is recommended for patients, a special diet and hepatoprotectors are prescribed - drugs that protect the liver.

Prevention of hepatitis A

The main measure for the prevention of hepatitis A is the observance of hygiene standards. In addition, children are recommended to be vaccinated against this type of viral hepatitis.

Hepatitis B

Hepatitis B or serum hepatitis is a much more dangerous disease characterized by severe liver damage. The causative agent of hepatitis B is a virus containing DNA. The outer shell of the virus contains a surface antigen - HbsAg, which causes the formation of antibodies to it in the body. Diagnosis of viral hepatitis B is based on the detection of specific antibodies in the blood serum.

Viral hepatitis b remains infective in the blood serum at 30–32 degrees Celsius for 6 months, at minus 20 degrees Celsius - 15 years, after warming up to plus 60 degrees Celsius - for an hour, and only with 20 minutes of boiling she disappears completely. That is why viral hepatitis B is so common in nature.

How is hepatitis B transmitted?

Infection with hepatitis B can occur through the blood, as well as through sexual contact and vertically - from mother to fetus.

Symptoms of Hepatitis B

In typical cases, hepatitis B, like Botkin's disease, begins with the following symptoms:

  • temperature increase;
  • weaknesses;
  • pain in the joints;
  • nausea and vomiting.

Symptoms such as dark urine and discoloration of feces are also possible.

Other symptoms of viral hepatitis B may also appear:

  • rashes;
  • enlargement of the liver and spleen.

Jaundice for hepatitis B is uncharacteristic. Liver damage can be extremely severe and, in severe cases, lead to cirrhosis and liver cancer.

Hepatitis B treatment

Treatment of hepatitis B requires an integrated approach and depends on the stage and severity of the disease. In the treatment, immune preparations, hormones, hepatoprotectors, antibiotics are used.

To prevent the disease, vaccination is used, which is carried out, as a rule, in the first year of life. It is believed that the duration of post-vaccination immunity to hepatitis B is at least 7 years.

Hepatitis C

The most severe form of viral hepatitis is hepatitis C or post-transfusion hepatitis. Hepatitis C virus infection can affect anyone and is more common in younger people. The incidence is on the rise.

This disease is called post-transfusion hepatitis due to the fact that infection with viral hepatitis C most often occurs through the blood - during blood transfusion or through non-sterile syringes. Currently, all donated blood must be tested for the hepatitis C virus. Sexual transmission of the virus or vertical transmission from mother to fetus is less common.

How is hepatitis C transmitted?

There are two ways of transmission of the virus (as with viral hepatitis B): hematogenous (i.e. through the blood) and sexual. The most common route is hematogenous.

How infection occurs

At blood transfusion and its components. This used to be the main mode of infection. However, with the advent of the method of laboratory diagnosis of viral hepatitis C and its introduction into the mandatory list of donor examinations, this path has faded into the background.
The most common way at present is infection with tattooing and piercing. The use of poorly sterilized, and sometimes not treated instruments at all, has led to a sharp surge in the incidence.
Often, infection occurs when visiting dentist, manicure rooms.
Using common needles for intravenous drug use. Hepatitis C is extremely common among drug addicts.
Using general with a sick person of toothbrushes, razors, nail scissors.
The virus can be transmitted from mother to child at the time of birth.
At sexual contact: this route is not so relevant for hepatitis C. Only 3-5% of cases of unprotected sex can become infected.
Injection with infected needles: this mode of infection is not uncommon among medical workers.

In about 10% of patients with hepatitis C, the source remains unexplained.


Hepatitis C Symptoms

There are two forms of the course of viral hepatitis C - acute (relatively short period, severe) and chronic (prolonged course of the disease). Most people, even in the acute phase, do not notice any symptoms, however, in 25-35% of cases, signs similar to other acute hepatitis appear.

Symptoms of hepatitis usually appear after 4-12 weeks after infection (however, this period can be within 2-24 weeks).

Symptoms of acute hepatitis C

  • Loss of appetite.
  • Abdominal pain.
  • Dark urine.
  • Light chair.

Symptoms of chronic hepatitis C

As with the acute form, people with chronic hepatitis C often do not experience any symptoms in the early or even late stages of the disease. Therefore, it is not uncommon for a person to be surprised to learn that he is sick after a random blood test, for example, when going to the doctor in connection with a common cold.

Important: you can be infected for years and not know it, which is why hepatitis C is sometimes called the "silent killer".

If the symptoms still appear, then they are likely to be as follows:

  • Pain, swelling, discomfort in the area of ​​the liver (in the right side).
  • Fever.
  • Muscle pain, joint pain.
  • Decreased appetite.
  • Weight loss.
  • Depression.
  • Jaundice (yellow tint to the skin and sclera of the eyes).
  • Chronic fatigue, rapid fatigue.
  • Vascular "asterisks" on the skin.

In some cases, as a result of the immune response of the body, damage can develop not only to the liver, but also to other organs. For example, kidney damage called cryoglobulinemia may develop.

In this condition, there are abnormal proteins in the blood that become solid when the temperature drops. Cryoglobulinemia can lead to consequences ranging from skin rashes to severe kidney failure.

Diagnosis of viral hepatitis C

Differential diagnosis is similar to that for hepatitis A and B. It should be borne in mind that the icteric form of hepatitis C, as a rule, occurs with mild intoxication. The only reliable confirmation of hepatitis C is the results of marker diagnostics.

Given the large number of anicteric forms of hepatitis C, it is necessary to carry out marker diagnostics of persons who systematically receive a large number of injections (primarily intravenous drug users).

Laboratory diagnosis of the acute phase of hepatitis C is based on the detection of viral RNA in PCR and specific IgM by various serological methods. If hepatitis C virus RNA is detected, genotyping is desirable.

The detection of serum IgG to antigens of viral hepatitis C indicates either a previous illness or the ongoing persistence of the virus.

Treatment of viral hepatitis C

Despite all the terrible complications that hepatitis C can lead to, in most cases the course of hepatitis C is favorable - for many years, the hepatitis C virus may not show up.

At this time, hepatitis C does not require special treatment - only careful medical monitoring. It is necessary to regularly check liver function, at the first signs of activation of the disease should be carried out antiviral therapy.

Currently, 2 antiviral drugs are used, which are most often combined:

  • interferon-alpha;
  • ribavirin.

Interferon-alpha is a protein that the body synthesizes on its own in response to a viral infection, i.e. it is actually a component of natural antiviral protection. In addition, interferon-alpha has antitumor activity.

Interferon-alpha has many side effects, especially when administered parenterally, i.e. in the form of injections, as it is usually used in the treatment of hepatitis C. Therefore, treatment should be carried out under mandatory medical supervision with the regular determination of a number of laboratory parameters and the appropriate dosage adjustment of the drug.

Ribavirin as an independent treatment has low efficiency, but when combined with interferon, it significantly increases its effectiveness.

Traditional treatment quite often leads to a complete recovery from chronic and acute forms of hepatitis C, or to a significant slowdown in the progression of the disease.

Approximately 70 to 80% of people with hepatitis C develop the chronic form of the disease, which is the greatest danger, as this disease can lead to the formation of a malignant tumor of the liver (that is, cancer) or cirrhosis of the liver.

When hepatitis C is combined with other forms of viral hepatitis, the patient's condition can deteriorate sharply, the course of the disease can become more complicated and lead to death.

The danger of viral hepatitis C is also in the fact that there is currently no effective vaccine that can protect a healthy person from infection, although scientists are making a lot of efforts in this direction of preventing viral hepatitis.

How long do people live with hepatitis C

Based on medical experience and research in this field, life with hepatitis C is possible and even long enough. A common disease, in other matters, like many others, has two stages of development: remission and exacerbation. Often hepatitis C does not progress, that is, does not lead to cirrhosis of the liver.

It must be said right away that lethal cases, as a rule, are not associated with the manifestation of the virus, but with the consequences of its effects on the body and general disturbances in the functioning of various organs. It is difficult to specify a specific period during which pathological changes incompatible with life occur in the patient's body.

Various factors influence the rate of progression of hepatitis C:

According to the statistics of the World Health Organization, there are more than 500 million people in whose blood a virus or pathogenic antibodies are found. These data will only go up every year. The number of cases of cirrhosis of the liver has increased by 12 percent worldwide over the past decade. The average age category is 50 years.

It should be noted that in 30% of cases the progression of the disease is very slow and lasts about 50 years. In some cases, fibrotic changes in the liver are quite insignificant or absent even if the infection lasts for several decades, so you can live with hepatitis C for quite a long time. So, with complex treatment, patients live 65-70 years.

Important: if appropriate therapy is not carried out, then life expectancy is reduced to an average of 15 years after infection.

Hepatitis D

Hepatitis D or delta hepatitis differs from all other forms of viral hepatitis in that its virus cannot multiply in the human body separately. To do this, he needs a "helper virus", which becomes the hepatitis B virus.

Therefore, delta hepatitis can be considered rather than as an independent disease, but as a complicating course of hepatitis B, a companion disease. When these two viruses coexist in the patient's body, a severe form of the disease occurs, which doctors call superinfection. The course of this disease resembles that of hepatitis B, but the complications characteristic of viral hepatitis B are more common and more severe.

Hepatitis E

Hepatitis E in its characteristics, it is similar to hepatitis A. However, unlike other types of viral hepatitis, in severe hepatitis E, there is a pronounced lesion not only of the liver, but also of the kidneys.

Hepatitis E, like hepatitis A, has a fecal-oral infection mechanism, is common in countries with a hot climate and poor water supply to the population, and the prognosis for recovery is favorable in most cases.

Important: the only group of patients for whom infection with hepatitis E can be fatal is women in the last trimester of pregnancy. In such cases, mortality can reach 9-40% of cases, and the fetus dies in almost all cases of hepatitis E in a pregnant woman.

Prevention of viral hepatitis in this group is similar to the prevention of hepatitis A.

Hepatitis G

Hepatitis G- the last representative of the family of viral hepatitis - in its symptoms and signs resembles viral hepatitis C. However, it is less dangerous, since the progression of the infectious process inherent in hepatitis C with the development of liver cirrhosis and liver cancer is not typical for hepatitis G. However, the combination of hepatitis C and G can lead to cirrhosis.

Medicines for hepatitis

Which doctors to contact with hepatitis

Tests for hepatitis

To confirm the diagnosis of hepatitis A, a biochemical blood test is sufficient to determine the concentration of liver enzymes, protein and bilirubin in the plasma. The concentration of all these fractions will be increased due to the destruction of liver cells.

Biochemical blood tests also help determine the activity of the course of hepatitis. It is by biochemical indicators that one can get an impression of how aggressively the virus behaves in relation to liver cells and how its activity changes over time and after treatment.

To determine infection with the other two types of virus, a blood test is performed for antigens and antibodies to hepatitis C and B. Blood tests for hepatitis can be taken quickly, without spending much time, but their results will allow the doctor to obtain detailed information.

By assessing the number and ratio of antigens and antibodies to the hepatitis virus, you can find out about the presence of infection, exacerbation or remission, as well as how the disease responds to treatment.

Based on the data of blood tests in dynamics, the doctor can adjust his appointments and make a forecast for the further development of the disease.

diet for hepatitis

The diet for hepatitis is as sparing as possible, since the liver, which is directly involved in digestion, is damaged. For hepatitis, frequent small meals.

Of course, one diet for the treatment of hepatitis is not enough, drug therapy is also necessary, but proper nutrition plays a very important role and favorably affects the well-being of patients.

Thanks to the diet, pain is reduced and the general condition improves. During an exacerbation of the disease, the diet becomes more strict, during periods of remission - more free.

In any case, it is impossible to neglect the diet, because it is the reduction in the load on the liver that can slow down and alleviate the course of the disease.

What can you eat with hepatitis

Foods that can be included in the diet with this diet:

  • lean meats and fish;
  • low-fat dairy products;
  • inedible flour products, lingering cookies, yesterday's bread;
  • eggs (only protein);
  • cereals;
  • boiled vegetables.

What not to eat with hepatitis

The following foods should be excluded from your diet:

  • fatty meats, duck, goose, liver, smoked meats, sausages, canned food;
  • cream, fermented baked milk, salty and fatty cheeses;
  • fresh bread, puff and pastry, fried pies;
  • fried and hard-boiled eggs;
  • pickled vegetables;
  • fresh onions, garlic, radishes, sorrel, tomatoes, cauliflower;
  • butter, lard, cooking fats;
  • strong tea and coffee, chocolate;
  • alcoholic and carbonated drinks.

Prevention of hepatitis

Hepatitis A and hepatitis E, which are transmitted by the fecal-oral route, are quite easy to prevent if basic hygiene rules are followed:

  • wash hands before eating and after going to the toilet;
  • do not eat unwashed vegetables and fruits;
  • do not drink raw water from unknown sources.

For children and adults at risk, there is hepatitis A vaccination, but it is not included in the mandatory vaccination calendar. Vaccination is carried out in case of an epidemic situation in terms of the prevalence of hepatitis A, before traveling to areas unfavorable for hepatitis. It is recommended to vaccinate against hepatitis A for workers of preschool institutions and physicians.

As for hepatitis B, D, C and G, transmitted through the infected blood of a patient, their prevention is somewhat different from the prevention of hepatitis A. First of all, contact with the blood of an infected person should be avoided, and since hepatitis is enough to transmit the hepatitis virus the minimum amount of blood, then infection can occur when using one razor, nail scissors, etc. All these devices must be individual.

As for the sexual transmission of the virus, it is less likely, but still possible, so sexual contact with unverified partners should take place only using a condom. Increases the risk of contracting hepatitis intercourse during menstruation, defloration, or other situations in which sexual contact is associated with the release of blood.

The most effective protection against hepatitis B infection today is considered to be vaccination. In 1997, hepatitis B vaccination was included in the mandatory vaccination calendar. Three vaccinations against hepatitis B are carried out in the first year of a child's life, and the first vaccination is given in the maternity hospital, a few hours after the birth of the baby.

Adolescents and adults are vaccinated against hepatitis B on a voluntary basis, and experts strongly recommend such a vaccination to representatives of the risk group.

Recall that the risk group includes the following categories of citizens:

  • employees of medical institutions;
  • patients who received blood transfusions;
  • drug addicts.

In addition, people who live or travel in areas with a high prevalence of hepatitis B virus, or who have family contact with people with hepatitis B or carriers of the hepatitis B virus.

Unfortunately, vaccines to prevent hepatitis C are currently does not exist. Therefore, its prevention is reduced to the prevention of drug addiction, mandatory testing of donor blood, explanatory work among adolescents and young people, etc.

Questions and answers on the topic "Viral hepatitis"

Question:Hello, what is a healthy carrier of hepatitis C?

Answer: A hepatitis C carrier is a person who has the virus in their blood and does not show any symptoms. This condition can last for years while the immune system keeps the disease at bay. Carriers, being a source of infection, must constantly take care of the safety of their loved ones and, if they wish to become parents, carefully approach the issue of family planning.

Question:How do I know if I have hepatitis?

Answer: Get a blood test for hepatitis.

Question:Hello! I am 18 years old, hepatitis B and C negative, what does this mean?

Answer: The analysis showed the absence of hepatitis B and C.

Question:Hello! My husband has hepatitis B. I recently had my last hepatitis B vaccine. A week ago, my husband's lip cracked, now it doesn't bleed, but the crack hasn't healed yet. Is it better to stop kissing until it heals completely?

Answer: Hello! It is better to cancel, and you to pass anti-hbs, hbcorab total, PCR quality for him.

Question:Hello! I did a trimmed manicure in the salon, my skin was injured, now I’m worried, after what time should I be tested for all infections?

Answer: Hello! Contact an infectious disease specialist to decide on an emergency vaccination. After 14 days, you can take a blood test for RNA and DNA of hepatitis C and B viruses.

Question:Hello, please help: I ​​was recently diagnosed with chronic hepatitis b with low activity (hbsag +; dna pcr +; dna 1.8 * 10 in 3 tbsp. IU / ml; alt and ast are normal, other indicators in the biochemical analysis are normal ; hbeag - ; anti-hbeag +). The doctor said that no treatment is required, no diet is needed, however, I have repeatedly come across information on various sites that all chronic hepatitis is treated, and there is even a small percentage of complete recovery. So maybe you should start treatment? And yet, for more than a year I have been using a hormonal drug prescribed by a doctor. This drug adversely affects the liver. But it is impossible to cancel it, what to do in this case?

Answer: Hello! Observe regularly, follow a diet, exclude alcohol, it is possible to prescribe hepatoprotectors. HTP is currently not required.

Question:Hello, I am 23 years old. Recently, I had to take tests for a medical examination, and this is what was found out: the analysis for hepatitis B is deviating from the norm. Do I have a chance to pass a medical examination for contract service with such results? I was vaccinated against hepatitis B in 2007. I have never observed any symptoms related to the liver. Jaundice did not hurt. Nothing bothered. Last year, for six months I took SOTRET 20 mg per day (there were problems with the skin of the face), nothing more special.

Answer: Hello! Probably transferred viral hepatitis B with recovery. The chance depends on the diagnosis made by the hepatological commission.

Question:Maybe the question is in the wrong place, tell me who to contact. The child is 1 year and 3 months old. We want to vaccinate him against infectious hepatitis. How can this be done and are there any contraindications.

Answer:

Question:What should other family members do if the father has hepatitis C?

Answer: Viral hepatitis C refers to the "blood infections" of a person with a parenteral mechanism of infection - during medical procedures, blood transfusions, during sexual intercourse. Therefore, at the household level in family foci for other family members, there is no danger of infection.

Question:Maybe the question is in the wrong place, tell me who to contact. baby is 1 year and 3 months old. We want to vaccinate him against infectious hepatitis. How can this be done and are there any contraindications.

Answer: Today it is possible to vaccinate a child (as well as an adult) against viral hepatitis A (infectious), against viral hepatitis B (parenteral or "blood") or by a combined vaccination (hepatitis A + hepatitis B). Vaccination against hepatitis A is single, against hepatitis B - three times at intervals of 1 and 5 months. Contraindications are standard.

Question:I have a son (25 years old) and a daughter-in-law (22 years old) with hepatitis G, they live with me. In addition to the eldest son, I have two more sons of 16 years old. Is hepatitis ji contagious to others? Can they have children and how this infection will affect the health of the child.

Answer: Viral hepatitis G is not transmitted by contact and is not dangerous for your younger sons. A woman infected with hepatitis G can give birth to a healthy child in 70-75% of cases. Since this is generally a fairly rare type of hepatitis, and even more so - in two spouses at the same time, to exclude a laboratory error, I recommend repeating this analysis again, but in a different laboratory.

Question:How effective is the hepatitis B vaccine? What are the side effects of this vaccine? What should be the vaccination plan if a woman is going to become pregnant in a year? What are the contraindications?

Answer: Vaccination against viral hepatitis B (performed three times - 0, 1 and 6 months) is highly effective, cannot lead to jaundice on its own and has no side effects. There are practically no contraindications. Women who are planning a pregnancy and have not had rubella and chickenpox, in addition to hepatitis B, must also be vaccinated against rubella and chickenpox, but no later than 3 months before pregnancy.

Question:What to do about hepatitis C? To treat or not to treat?

Answer: Viral hepatitis C should be treated in the presence of three main indicators: 1) the presence of cytolysis syndrome - elevated levels of ALT in whole and diluted 1:10 blood serum; 2) a positive test result for antibodies of the immunoglobulin M class to the core antigen of the hepatitis C virus (anti-HCVcor-Ig M) and 3) detection of hepatitis C virus RNA in the blood by polymerase chain reaction (PCR). Although the final decision should still be made by the attending physician.

Question:Hepatitis A (jaundice) was diagnosed in our office. What should we do? 1. Should the office be disinfected? 2. When does it make sense for us to get tested for jaundice? 3. Should we limit contact with families now?

Answer: Disinfection in the office should be done. Analyzes can be taken immediately (blood for ALT, antibodies to HAV - hepatitis A virus classes of immunoglobulins M and G). It is desirable to limit contacts with children (before testing or up to 45 days after the discovery of a case of the disease). After clarifying the situation of healthy non-immune employees (negative test results for IgG antibodies to HAV), it is advisable to vaccinate against viral hepatitis A, as well as hepatitis B - in order to prevent similar crises in the future.

Question:How is the hepatitis virus transmitted? And how not to get sick.

Answer: Hepatitis A and E viruses are transmitted with food and drink (the so-called fecal-oral route of transmission). Hepatitis B, C, D, G, TTV are transmitted through medical procedures, injections (for example, among injecting drug users using one syringe, one needle and a common “shirk”), blood transfusions, during surgical operations with reusable instruments, as well as during sexual contacts (the so-called parenteral, blood transfusion and sexual transmission). Knowing the ways of transmission of viral hepatitis, a person can control the situation to a certain extent and reduce the risk of the disease. From hepatitis A and B in Ukraine, there have long been vaccines, vaccinations with which give a 100% guarantee against the onset of the disease.

Question:I have hepatitis C, genotype 1B. He was treated with reaferon + ursosan - without result. What drugs to take to prevent cirrhosis of the liver.

Answer: In hepatitis C, combined antiviral therapy is most effective: recombinant alpha 2-interferon (3 million per day) + ribavirin (or in combination with other drugs - nucleoside analogues). The treatment process is long, sometimes more than 12 months under the control of ELISA, PCR and indicators of cytolysis syndrome (AlT in whole and diluted 1:10 blood serum), as well as at the final stage - puncture liver biopsy. Therefore, it is desirable to be observed and undergo a laboratory examination by one attending physician - it is necessary to understand the definition of “no result” (dosages, duration of the first course, laboratory results in the dynamics of the use of drugs, etc.).

Question:Hepatitis C! A 9-year-old child has had a fever for all 9 years. How to treat? What's new in this area? Will the right way be found soon? Thank you in advance.

Answer: Temperature is not the main sign of chronic hepatitis C. Therefore: 1) it is necessary to exclude other causes of fever; 2) determine the activity of viral hepatitis C according to three main criteria: a) ALT activity in whole and diluted 1:10 blood serum; b) serological profile - Ig G antibodies to HCV proteins of classes NS4, NS5 and Ig M to the HCV nuclear antigen; 3) test the presence or absence of HCV RNA in the blood by polymerase chain reaction (PCR), and determine the genotype of the detected virus. Only after that it will be possible to talk about the need to treat hepatitis C. There are quite advanced drugs in this area today.

Question:Is it possible to breastfeed a child if the mother has hepatitis C?

Answer: It is necessary to test the mother's milk and blood for hepatitis C virus RNA. If the result is negative, you can breastfeed the baby.

Question:My brother is 20 years old. Hepatitis B was discovered in 1999. He is now diagnosed with hepatitis C. I have a question. Does one virus pass into another? Can it be cured? Is it possible to have sex and have children? He also has 2 lymph nodes on the back of his head, can he be tested for HIV? Didn't take drugs. Please, please answer me. Thank you. Tanya

Answer: You know, Tanya, with a high degree of probability, infection with two viruses (HBV and HCV) occurs precisely when injecting drugs. Therefore, first of all, it is necessary to clarify this situation with the brother and, if necessary, recover from drug addiction. Drugs are a cofactor that accelerates the adverse course of hepatitis. It is advisable to be tested for HIV. One virus does not pass into another. Chronic viral hepatitis B and C are treated today and sometimes quite successfully. Sex life - with a condom. You can have children after treatment.

Question:How is the hepatitis A virus transmitted?

Answer: The hepatitis A virus is transmitted from person to person by the fecal-oral route. This means that a person with hepatitis A is shedding viruses in their stool that, if not properly hygienic, can get into food or water and infect another person. Hepatitis A is often referred to as "dirty hand disease".

Question:What are the symptoms of viral hepatitis A?

Answer: Often, viral hepatitis A is asymptomatic, or under the guise of another disease (for example, gastroenteritis, flu, colds), but, as a rule, some of the following symptoms may indicate the presence of hepatitis: weakness, fatigue, drowsiness, tearfulness and irritability in children; decreased or lack of appetite, nausea, vomiting, bitter belching; discolored feces; fever up to 39°C, chills, sweating; pain, feeling of heaviness, discomfort in the right hypochondrium; darkening of urine - occurs a few days after the first signs of hepatitis appear; jaundice (the appearance of a yellow color of the sclera of the eyes, body skin, oral mucosa), as a rule, appears a week after the onset of the disease, bringing some relief to the patient's condition. Often there are no signs of jaundice in hepatitis A at all.

Methodological instructions for students for practical lesson No. 11.

Subject: Laboratory diagnosis of viral hepatitis.

Target: Study of methods of laboratory diagnostics of viral hepatitis.

Module 3. General and special virology.

Special Virology.

Theme 11 : Laboratory diagnosis of viral hepatitis.

Relevance of the topic: Viral hepatitis in Ukraine accounts for approximately 20% of all viral diseases that lead to prolonged disability: acute liver necrosis, cirrhosis, primary liver cancer. The hepatitis A virus causes epidemic hepatitis (infectious epidemic jaundice, Botkin's disease). For morphological and physico-chemical characteristics similar to enteroviruses. Hepatitis B virus described in 1970 and named Dane particles. It is a complex virus that contains DNA. Causes serum hepatitis. In recent years, there has been an increase in the incidence of this form of hepatitis.

HEPATITIS A VIRUS.

Hepatitis A (Botkin's disease)- an infectious disease with a fecal-oral route of transmission, clinically and morphologically characterized by liver damage with the development of a symptom complex of acute hepatitis. The disease has been known since ancient times, its description is contained in the works of Hippocrates. The virus was first isolated by S. Feystone (1973).

HBsAg. First identified Ar of hepatitis B virus; it was first isolated by B. Blumberg (1965) from the blood of an Australian aborigine, therefore this Ar is also called Australian. HBsAg often forms defective morphological particles of the 1st type, devoid of infectious properties (side metabolites of the replication cycle). In the cytoplasm of infected cells, there is an excess of HBsAg associated with the cell membrane and endoplasmic reticulum. HBsAg appears in the blood 1.5 months after infection; constantly circulates in the serum of infected individuals, and its purified aggregates are part of the hepatitis B vaccine. HBsAg includes two polypeptide fragments: preS 1 has pronounced immunogenic properties (the recombinant product can be used to prepare vaccine preparations); preS 2 is a polyglobulin receptor leading to adsorption of the virus on hepatocytes.

HBcAg. Core HBcAg is represented by a single antigenic type; it is found only in the core of Dane particles. Ar marks viral replication in hepatocytes. It can be detected only during the morphological study of biopsy specimens or autopsy material of the liver. In the blood in a free form, it is not determined. Point mutations in the region encoding the synthesis of the precursor HBcAg HB c Ag producing mutants of the hepatitis B virus, originally isolated in fulminant forms of hepatitis. The transition from HvcAg + to HvcAg - - forms is observed in patients with chronic, relatively mild lesions.

HBeAg. It is not part of the Dane particles, but is associated with them, as it appears in the serum in the incubation period, immediately after the appearance of HBsAg. The formation of HBeAg is translated by RNA containing regions of the core Ar and its precursor. After translation is completed, the resulting HBeAg molecule is expelled from the cell. The functions of HBeAg are unknown, however, HBeAg can be regarded as the most sensitive diagnostic indicator of active infection. The detection of HBeAg in patients with chronic hepatitis indicates the activation of the process, which poses a high epidemic risk. Ar may be absent in infections caused by a mutant strain of the virus.

HBxAg- the least studied Ar. Presumably mediates malignant transformation of liver cells.

DNA appears in serum simultaneously with other Ar virus. Disappears from the bloodstream at the beginning of the second week of acute illness. Prolonged persistence is evidence of a chronic infection. In the diagnosis of acute hepatitis B, DNA determination is rarely used.

Epidemiology. The pathogen reservoir is an infected person. The mechanism of transmission of infection is blood-contact. The main routes of transmission of the hepatitis B virus are injection, blood transfusion and sexual. The possibility of vertical transmission of hepatitis B virus from mother to fetus has also been shown. 7-10% of those infected become chronic carriers. At least 50 people fall ill every year. In Russia, a 10-15% increase in the incidence is noted. The main risk groups are medical workers;

  • persons receiving blood transfusions or blood products;
  • intravenous drug addicts;
  • patients with hemophilia;
  • persons on hemodialysis;
  • children of HBsAg carrier mothers;
  • sexual partners of carriers of the virus.

Pathogenesis. The hepatitis B virus is hematogenously introduced into the liver and multiplies in hepatocytes. In the second half of the incubation period (40-180 days), the virus is isolated from blood, semen, urine, feces and nasopharyngeal secretions. Autoimmune humoral and cellular reactions play an important role in the pathogenesis of lesions, which confirms the relationship between the onset of clinical manifestations and the appearance of specific antibodies. The pathological process begins after recognition of virus-induced Ar on hepatocyte membranes by immunocompetent cells. Complications of the chronic form are caused by chronic inflammation and necrotic processes in the liver parenchyma, the main complications are cirrhosis and primary liver carcinoma.

Cirrhosis is commonly seen in people with acute chronic hepatitis, with more than 10,000 hepatitis B-related deaths each year.

Liver carcinoma. A clear relationship has been shown between malignant transformation of hepatocytes and past viral hepatitis B. Certain cofactors, many of which remain unknown, are involved in the development of the tumor process.

Principles of microbiological diagnostics. Hepatitis B virus replication markers - HBeAg. AT (IgM) to HBcAg, viral DNA and viral DNA polymerase. To identify HBsAg and HBeAg, ELISA and RNGA are used; studies are supplemented by the detection of hepatitis B virus DNA and viral DNA polymerase. Virus-specific antibodies to HBsAg, HBsAg, HBeAg are determined by ELISA and RNGA. The presence of a “fresh” infection is indicated by high titers of HBsAg, IgM to HBsAg and HBsAg. In patients with clinically manifested hepatitis, the HbsAg titer first increases, and then (as the immune reactions develop) decreases. Anti-HBsAg antibodies can be detected only after a few weeks, which is explained by their active binding into immune complexes. During this period (the so-called “window”), only antibodies to HBcAg can be detected.

AT to HBcAg. An important diagnostic marker of infection, especially when HBsAg is negative.

· IgM to HBsAg. One of the earliest serum markers of viral hepatitis B. In chronic hepatitis, virus replication and process activity in the liver are marked. Their disappearance is an indicator of either the sanitation of the body from the pathogen, or the development of the integrative phase of the infection.

· IgG to HBcAg. Stored for many years. Evidence of an existing or previously transferred infection.

AT to HBeAg. Serological marker of virus integration. In combination with IgG, HBsAg and HBsAg indicate the complete completion of the infectious process.

AT to HBsAg. Protective AT; also form after vaccination. In relation to chronic viral hepatitis, they may indicate the end of a viral infection. AT to preS 1 - - preS 2 fragments of HBsAg. They indicate the development of protective immunity at the end of the infectious process. AT to Pre-S 1 is detected simultaneously with AT to HBsAg, and AT to Pre-S 2 .

Treatment. Means of specific therapy are absent, treatment is mainly symptomatic. The use of DNA polymerase inhibitors (for example, lamivudine), α-IFN and its inducers has certain prospects. Despite the fact that less than 50% of patients respond to IFN therapy, a significant disappearance of all markers of infection (DNA of the hepatitis B virus, HBsAg and HBeAg) and an increase in antibody titers to HBsAg are shown.

Immunoprophylaxis. Passive immunization with specific Ig (HBIg) is indicated for persons who have been in contact with infected material and carriers of HBsAg (including sexual partners and children born to HBsAg-positive mothers). Two types of vaccines have been developed for active immunization. The former are prepared from patient plasma containing Ar. Hepatitis B virus in quantities sufficient to create vaccine preparations. The main condition is the complete inactivation of the hepatitis B virus. The second group consists of recombinant vaccines (for example, Recombivax B, Engerix B) obtained by genetic engineering on cultures of baker's yeast (Saccharomyces cerevisiae). Mass immunization is an essential component of infection control. Adults receive 2 doses within a month and a booster immunization 6 months later. Children receive the first dose immediately after birth, the next - after 1-2 months and by the end of the first year of life. If the mother is HBsAg-positive, then the child is given a specific Ig at the same time as the first vaccination.

HEPATITIS D VIRUS (DELTA HEPATITIS)

hepatitis D virus discovered M. Risetto et al. (1977) in hepatocyte nuclei during an unusually severe outbreak of serum hepatitis in Southern Europe. Later, it began to be found everywhere, especially often in North America and the countries of North-Western Europe.

Taxonomy, morphology, antigenic structure. The causative agent of delta hepatitis is a defective RNA-containing virus of the Deltavirus genus of the Togaviridae family. It is isolated only from patients infected with the hepatitis B virus. The defectiveness of the pathogen manifests itself in complete dependence on its transmission, reproduction and the presence of the hepatitis B virus. Accordingly, monoinfection with the hepatitis D virus is absolutely impossible. Hepatitis D virus virions are spherical, 35-37nm in diameter. The genome of the virus forms a single-stranded circular RNA molecule, which brings the hepatitis D virus closer to viroids. Its sequences do not have homology with the DNA of the hepatitis B pathogen, but the supercapsid of the D virus includes a significant amount of HBsAg of the hepatitis B virus. The reservoir of the pathogen is an infected person; the virus is transmitted parenterally. Vertical transmission of hepatitis D virus from mother to fetus is possible.

Pathogenesis and clinical manifestations. Infection of HBsAg-positive individuals is accompanied by active reproduction of the hepatitis D virus in the liver and the development of chronic hepatitis - progressive or fulminant. It is clinically manifested only in persons infected with the hepatitis B virus. It can occur in two ways:

coinfection(simultaneous infection with hepatitis B and D viruses). A short prodromal period with high fever is noted;

  • often migrating pain in large joints;
  • increase in intoxication in the icteric period;
  • often pain syndrome (pain in the projection of the liver or epigastrium);
  • occurrence in 2-3 weeks from the onset of the disease or clinical and laboratory exacerbation. The course is relatively benign, but the recovery period takes a long time.

Superinfection infection with the hepatitis D virus in a person infected with the hepatitis B virus). Short incubation and preicteric periods (3-5 days) are noted with high fever, severe intoxication, repeated vomiting, pain syndrome, arthralgia. Characterized by severe jaundice, the development of edematous-ascitic syndrome, severe hepatosplenomegaly, repeated clinical and laboratory exacerbations. With this option, the development of a malignant (fulminant) form of the disease with a fatal outcome is possible.

Principles of microbiological diagnostics. For the diagnosis of acute and chronic viral hepatitis D, ELISA and RIA are widely used. Markers of virus replication - AT (IgM) to Ar of hepatitis D virus and viral RNA. Ar of hepatitis D virus appears in the blood 3 weeks after infection. Virus-specific IgM appear 10-15 days after the development of clinical manifestations. After 2-11 weeks, virus-specific IgG can be identified, constantly circulating in infected individuals.

Treatment and prevention. Means of specific chemotherapy and immunoprophylaxis are absent. Since the reproduction of the hepatitis D virus is impossible in the absence of the causative agent of hepatitis B, the main preventive measures should be aimed at preventing the development of hepatitis B.

HEPATITIS C VIRUS

Hepatitis C usually proceeds chronically and is characterized by the predominant development of chronic forms of hepatitis with an outcome in cirrhosis and primary liver carcinoma.

Hepatitis C virus is included in the genus of the Flaviviridae family. Virions are spherical, 35-50 nm in diameter, surrounded by a supercapsid. The genome is made up of single-stranded RNA. There are 6 serovars, each of which is “tied” to certain countries. For example, hepatitis C virus type 1 is common in the United States, and type 2 in Japan.

- an infected person. The main route of transmission of the virus- parenteral. The main difference from the epidemiology of the hepatitis B virus is the lower ability of the hepatitis C virus to transmit from a pregnant woman to a fetus and through sexual contact. The patient sheds the virus a few weeks before the onset of clinical signs and within 10 weeks after the onset of manifestations. The disease is more often registered in the USA (up to 90% of all transfusion hepatitis) and Africa (up to 25%). The clinical symptoms of viral hepatitis C are characterized by a change in the consistency and size of the liver. With an active process, the liver is usually enlarged and painful on palpation, its consistency is moderately dense. Other manifestations include splenomegaly, dyspeptic and asthenic syndromes, jaundice, arthralgia and myalgia, carditis, vasculitis, pulmonary lesions, anemia, etc. Complications of the chronic process are cirrhosis and primary liver carcinoma.

Principles of microbiological diagnostics. Virus replication markers - AT (IgM) to Ar hepatitis C virus RNA. Markers are detected by ELISA and PCR. An indication for the search for antibodies or RNA of the virus is any inflammatory liver disease. Virus-specific antibodies appear after an average of 3 months and indicate a possible infection with the hepatitis C virus or a past infection. In the seronegative period, hepatitis C virus RNA is detected. To confirm the results of ELISA, as well as when examining patients who do not belong to the main risk groups, the method of recombinant immunoblotting is used, which effectively eliminates false positive ELISA results.

Treatment and prevention. Means of etiotropic therapy are absent; in chronic infections, IFN-alpha can be used. During IFN therapy, 40-70% of patients notice a subsidence of the inflammatory process (as indicated by a decrease in the concentration of aminotransferases in serum), however, at the end of the course, 40-50% of patients experience a relapse of inflammation. Means of specific immunoprophylaxis have not been developed.

HEPATITIS E VIRUS

Hepatitis E- acute infectious liver disease, manifested by symptoms of intoxication and, less often, jaundice.

Pathogenesis and clinical picture. Hepatitis E virus is included in the Calicivirus genus of the Caliciviridae family. Virions are spherical, 27-38 nm in diameter. The genome is formed by a non-segmented +RNA molecule.

Pathogenesis and clinical picture. Exciter reservoir- Human. The epidemiology of the disease is largely similar to hepatitis A; the pathogen causes endemic outbreaks. Incubation period does not exceed 2-6 weeks. The disease is manifested by general malaise; jaundice is observed relatively rarely. In most cases, the prognosis of the disease is favorable, and patients recover completely. Infection of pregnant women, especially in the third trimester, can be fatal (mortality can reach 20%). Chronization of the process is not observed. Recovery is accompanied by the formation of persistent immunity to re-infection.

Principles of microbiological diagnostics. Virus replication markers - AT (IgM) to Ar hepatitis E virus and viral RNA. Virus-specific IgM is detected by ELISA, starting from 10-12 days after infection; diagnostic titers persist for 1-2 months. Abs of the IgG class to Ar of the hepatitis E virus appear one month after the disease. Virus RNA is detected in PCR reactions and molecular hybridization Virus RNA can be detected from the first day of infection; however, it is impossible to detect it in the icteric period.

Treatment. There are no means of etiotropic therapy and specific prophylaxis; carry out symptomatic treatment.

HEPATITIS G VIRUS

Taxonomy, morphology, antigenic structure. taxonomic position virus G remains unexplained. It is conventionally assigned to the Flaviviridae family. The genome is formed by a non-segmented +RNA molecule. The nucleocapsid is organized according to the type of cubic symmetry. Based on the set of Ar virions, it is suggested that there are at least three subtypes of the virus. The hepatitis G virus is presumably a defective virus and requires the presence of the hepatitis C virus in order to reproduce.

Pathogenesis and clinical picture. Exciter reservoir- Patients with acute or chronic hepatitis G and carriers of the hepatitis G virus. Often the registration of the disease is relatively low. In Russia, the detection rate of hepatitis G virus RNA ranges from 2% in Moscow to 8% in Yakutia. At the same time, in the blood serum of donors, the frequency of detection of hepatitis G virus RNA was 1.4%. More often markers of hepatitis G virus infection are detected in individuals receiving multiple transfusions of whole blood or its preparations, as well as among patients with transplants. A special risk group is made up of drug addicts (among those who inject drugs intravenously), the frequency of detection of hepatitis G virus RNA reaches 33-35%. Violations of the immune status contributes to the development of long-term carriage of the virus. The possibility of vertical transmission of the hepatitis G virus from an infected mother to the fetus has been proven. Hepatitis G in most cases proceeds as a mixed infection with viral hepatitis C, not significantly affecting the nature of the development of the underlying process.

Principles of microbiological diagnostics. Virus replication markers - AT(IgM) to Hepatitis G virus Ar and viral RNA. Virus-specific IgM is detected by ELISA, starting from 10-12 days after infection; diagnostic titers persist for 1-2 months. Abs of the IgG class to Ar of the hepatitis E virus appear one month after the disease. Virus RNA is detected in PCR reactions and molecular hybridization. Virus RNA can be detected from the first day of infection; however, it is impossible to detect it in the icteric period.