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Hepatitis G: symptoms, signs, treatment and prevention

Hepatitis is one of the most dangerous and common inflammatory diseases of the liver. Along with the already known viruses A, B and C in the mid-90s, there were several new strains - among them, hepatitis G virus is a type of strain C.

The exact name for the GB virus is hepatitis C, the “younger brother of hepatitis C,” as the English call it. It does not cause such pathological changes in the patient’s body as the original virus C, but is a good basis for more dangerous hepatitis C.

About the causative agent of hepatitis G

Hepatitis G virus has several names: hepatitis G virus - HGV, GBV-C (GB virus C), HPgV - pegyvirus A. However, the latter name has not yet been approved by the International Committee on Taxonomy of Viruses.
It has in its structure RNA. Belongs to the Flaviviridae family, which includes hepatitis C virus (HCV).

Due to the similarity of the genome and, accordingly, some properties, hepatitis G is also called the "younger brother of hepatitis C".

Currently, there are data on six genotypes and several subtypes of the virus. However, some authors do not quite agree with this division.

Discovery story

The first mention of the pathogen was made in 1966. British surgeon George Barker (initials - GB) suffered an infectious liver disease that was not identified with any of the then known causative agents of viral hepatitis. After another 9 years, several scientists found that serum with the causative agent of the disease at the doctor GB when administered to monkeys of the genus tamarins causes acute hepatitis in them. Subsequently, as new research methods emerged, hepatitis A, B, C viruses were excluded as the cause of the disease.

In 1995-1996, two groups of scientists independently studied the molecular properties of the RNA genome of this pathogen and established its similarity with the genome of HCV and some other viruses from the Flaviviridae family. So a new hepatitis virus was identified.

Transmission ways

The mechanism of transmission of hepatitis G virus is parenteral. The source of infection is a patient with manifestations of infection or an asymptomatic virus carrier.
The studies revealed a relatively high detection rate of this virus in people who have undergone a transfusion of blood and its components - more than 50%. Also, the virus was isolated in patients undergoing hemodialysis. In people who have undergone organ transplantation, immunosuppressive therapy contributes to chronic virus carriage.

In the study of blood samples prepared for blood transfusion in different countries, HGV was detected in 5–45% of cases.
A sufficiently high detection of the virus in injecting drug addicts is up to 25–35% according to various sources.

Sexual transmission is important, but occupies a far from leading position in the mechanism of infection. It accounts for only 10% of all cases of infection. In the study of transmission of viral infection from mother to child, it was found that the vertical (intrauterine) pathway plays a very small role in the infection of the fetus. More often, infection occurs during or immediately after birth through the natural birth canal. During delivery by caesarean section, the frequency of infection of newborns decreases markedly.

Very often, HGV is defined in a “company” with other types of hepatotropic viruses. Most often combined with hepatitis C, then with B and D. However, there is no information about the aggravation of the course of these types of hepatitis during their co-infection with HGV.

Up to 10% of cases of determining the RNA of the pathogen in patients with autoimmune and alcoholic hepatitis are described, which is probably associated with immunosuppression.
Further studies are underway to study the transmission of this infection.

Pathogen prevalence

HGV is more common than hepatitis C. According to some reports, up to one sixth of the world's population are infected or have had infection in the past. Such a widespread prevalence is confirmed, for example, by an experiment conducted in the USA. When examining blood donors, it turned out that about 2% were determined by RNA, and almost 15% - antibodies to HGV, which were indicators of past infection.

Hepatitis G virus is found everywhere in the world, however, unevenly. For example, in the Russian Federation, the detectability of HGV in Moscow and the region is about 2%, and in Yakutia - up to 8%.

Pathogenetic features of the course of the disease

It was found that HGV begins to be identified in the blood a week after the transfusion of infected blood.
Long-term observations have shown that the causative agent of infection can be in the blood of a patient with a virus carrier for a rather long time - cases of 16 years or more have been described. During this time, there were fluctuations in the amount of HGV RNA in the blood from an increase of several orders of magnitude to a temporary complete disappearance. With hepatocellular carcinoma, the frequency of detection of virus RNA in the body during monoinfection is very small.

Unfortunately, despite the active study of this infectious agent, there are still a lot of questions and ambiguities regarding its “abilities”. Until now, there is no accurate information about the true place of replication (reproduction) of the virus. It can be detected, for example, in the lymphatic system and not detected in the blood.

Some scientists question the ability of this pathogen to cause acute hepatitis or contribute to its chronicity. On the one hand, HGV is diagnosed in the blood of patients with acute or chronic liver damage in the absence of serological markers of other hepatitis viruses. But on the other hand, there is still no absolute evidence of its hepatotropy (for example, there is evidence that almost half of those infected have neither clinical nor serological symptoms of liver damage).

HGV - a “cure” for HIV infection?

An interesting property of HGV has recently been discovered in combination with its presence with HIV infection. In antiviral therapy for viral hepatitis C and G in patients with HIV infection, elimination of HGV RNA from the blood led to their earlier death in the AIDS stage and a decrease in overall life expectancy.

A deeper analysis of such cases was carried out, and it was found that the mortality rate of HIV-infected patients is much higher among those who do not have HGV in the blood. This was especially true for those patients in whom the existing virus disappeared as a result of treatment or spontaneously. The mechanism of this influence is still unclear. There are suggestions that HGV blocks HIV access to the cell. Research on this issue is ongoing.

Symptoms of viral hepatitis G

Hepatitis G can have an acute or chronic course. There is also asymptomatic carriage of the virus or the development of fulminant form (fulminant hepatitis G).
From the moment of infection to the development of symptoms of the disease usually takes 7-12 days.
Isolated cases of clinically pronounced acute liver damage are described. In this case, moderate manifestations of intoxication are noted - an increase in body temperature, weakness, fatigue. The icteric period lasts about three weeks.

Complications from the biliary tract are characteristic: gall bladder dysfunction, biliary sludge phenomenon up to cholecystolithiasis. There is an assumption of a specific lesion of the bile ducts of HGV followed by the formation of intrahepatic cholestasis syndrome.
The activity of hepatic aminotransferases increases moderately. Extrahepatic manifestations were not observed.

However, acute hepatitis G is usually asymptomatic. The activity of hepatic transaminases and other biochemical parameters may slightly change or even remain within the normal range.

Fulminate hepatitis G occurs with a relatively slow development of acute liver failure - from 16 to 45 days. Blood biochemical parameters can fluctuate over a wide range. Mortality remains high.
Some authors question the development of fulminant hepatitis G.

Acute viral hepatitis G may result in:

  1. Recovery with the disappearance of RNA in the blood and determination of antibodies E2 HGV.
  2. Transition to a chronic form of infection with a long-term determination of RNA in the blood (up to several years), followed by recovery and determination of E2 HGV antibodies.
  3. The formation of long-term “healthy” HGV carriage.

Chronic hepatitis G is asymptomatic and more often in the form of “healthy” HGV carriage. The occurrence of severe liver damage (cirrhosis, hepatocellular carcinoma) as a consequence of the course of chronic hepatitis is unlikely.

Diagnostics

Clinical manifestations, if present, are usually of little value in diagnosis. It is necessary to carefully determine the history in order to determine the possible route of transmission (transfusion of blood and its components, drug addiction, etc.).
Blood biochemical parameters are determined, in particular, the activity of hepatic transaminases, the level of bilirubin, etc.

Specific diagnosis

Determination of HGV RNA in the blood by PCR is evidence of infection. However, as already mentioned above, the virus can periodically disappear from the peripheral blood for reasons that are still unknown. Also, virus RNA can be detected in organs other than the liver, for example, in lymphoid tissue.

Using ELISA, antibodies to the pathogen are determined: anti-E2 HGV. Antibodies appear, as a rule, after the disappearance of the RNA of the pathogen from the blood or shortly before. Therefore, the definition of anti-E2 HGV in the blood indicates the recovery of the body.

Treatment

Usually has difficulties, given the high frequency of combination of HGV with other types of hepatitis.
For specific antiviral therapy, alpha-interferon preparations are used. In almost half of patients, the virus is eliminated. However, the full effect of therapy is observed in only 18–20% of patients.
There is an assumption of a weaker response to antiviral treatment in patients with a combination of HGV + HCV than with hepatitis C monoinfection.

Forecast

Given the frequent low-symptom course of both acute and chronic liver damage, we can draw certain conclusions about the relative favorable prognosis for the patient. But do not forget that HGV in the vast majority of cases is in the body together with any other virus and this affects the prognosis of the disease.

It should be emphasized once again that the hepatitis G virus and the liver damage it causes are still at the stage of active research.

Moreover, some scientists generally question the very existence of HGV, as a pathogen with a hepatotropic effect.

Infection mechanism

According to studies, most often this type of hepatitis is found in people who have undergone a blood transfusion procedure or its components. This category of people accounts for more than half of all cases of G hepatitis.

It can also affect people undergoing hemodialysis. And people who have undergone a liver transplant and are on immunosuppressive treatment can become chronic carriers of the virus.

Hepatitis G virus is transmitted parenterally. You can get infected from the carrier of the infection, which has no symptoms of pathology, or from a patient with clinical signs of the disease.

In different countries of the world, studies of blood samples prepared for transfusion were conducted, as a result of which HGV was detected in about 5-45%. Also, the virus was found in 25-35% of drug addicts who inject drugs.

In addition, you can get infected with this type of hepatitis in the following ways:

  • When transplanting any organ.
  • With unprotected sexual contact (up to 10% of the total volume of infections).
  • During childbirth (in a natural process, the frequency of infection is higher than in cesarean section).
  • The intrauterine method for transmission of infection from mother to fetus (the percentage of such cases is very small).

HGV often develops along with other hepatotropic pathologies. In most cases, this virus is in combination with hepatitis C, and more rarely with hepatitis B and D. But to date, there is no accurate evidence that the presence of these hepatitis somehow complicates the course of HGV.

However, due to the fact that about 10% of infections occur in people with alcoholic and autoimmune liver damage, it can be concluded that immunosuppression affects the frequency of infection.

Other methods of transmission of hepatitis G are still being studied by scientists around the world.

How common is the virus

Hepatitis G is a more common virus than hepatitis C. It is believed that earlier the number of infected reached 1/6 of the population of the whole world. This prevalence of infection has been confirmed by an experiment in the United States.

Blood donors were examined, in 2% of which RNA of this virus was detected. In addition, antibodies to this pathology were found in about 15% of donors, which is evidence of a disease that has already passed.

There are people infected with hepatitis G worldwide, but it is more common in some countries. For example, its prevalence in Yakutia is 8%, and in Moscow and Moscow Region - only 2%.

Virus features

So all the same, what is this “hepatitis G virus”, and how does it proceed? HGV can be determined as early as a week after infection through the blood, especially when infected during transfusion. According to studies, the causative agent of the virus can be active in the blood of the carrier for a long period of time.

There are cases when it was stored in the blood for more than 15 years. During this period, the RNA level changed and even completely disappeared, but then returned again.

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This infection has been actively studied in recent decades, but, despite this, there are still many unclear points. For example, the location of the reproduction of the infection is still not known, since it can be detected both in the blood and in the lymphatic system.

According to some scientists, the causative agent of this virus cannot cause the development of acute hepatitis. HGV can occur in people with chronic or acute liver disease, but who do not have markers of other hepatitis. But at the same time, there is no direct evidence of hepatotropy of the pathogen. Very rarely, HGV is found in people with hepatocellular carcinoma.

HGV and HIV

Not so long ago, the ability of the hepatitis G pathogen to interact with HIV infection was identified. If such a patient was prescribed antiviral treatment to get rid of hepatitis C or G, in which the virus RNA was extracted from the blood, then the patient died earlier.

A more thorough study of this phenomenon revealed that the death rate in patients who do not have HGV in their blood is higher. This was especially observed in patients in whom the virus disappeared spontaneously or after therapy. The reasons for this effect have not yet been elucidated, so studies are still ongoing.

Symptoms of the virus

Symptoms of hepatitis G vary depending on its course. It is acute and chronic. Also, a person may simply be an asymptomatic virus carrier. In addition, there is the likelihood of a very rapid development of the disease - the fulminant form. From infection to the onset of the first signs of the virus, an average of 7 to 12 days passes.

Severe liver damage caused by this pathology is extremely rare. However, it can cause intoxication, the signs of which are weakness, fever and fatigue. Within 3 weeks, the patient may manifest jaundice.

Complications with the biliary system are also possible:

  • gallbladder dysfunction,
  • biliary sludge,
  • cholecystolithiasis.

In addition, HGV is thought to affect the bile ducts, thereby causing the development of intrahepatic cholestasis syndrome.

But with the acute form of hepatitis G, the symptoms are not pronounced. Liver transaminases and other indicators can either remain the same or increase slightly.

The duration of a typical form of hepatitis G is longer - 16-45 days. During this period, the infected person may develop acute liver failure. In this case, the indicators of the biochemical analysis of blood can significantly differ from each other. This form is characterized by a high percentage of deaths.

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The further prognosis for patients with acute hepatitis G may be different:

  • complete cure, the disappearance of the RNA of the virus from the blood and the production of antibodies,
  • degeneration of the disease into a chronic form with cure and antibody production only after a few years,
  • transition to the stage of virus carrier.

The course of hepatitis G in chronic form is most often asymptomatic or even in the form of a carriage of the virus. Serious complications such as hepatocellular carcinoma or cirrhosis are very rare.

Diagnostic Methods

The presence of clinical signs of the disease in a patient is not so important for diagnosis. To identify a possible mechanism of infection (drug abuse, blood transfusion, etc.), an anamnesis is determined. A biochemical blood test is also prescribed, based on which the level of bilirubin, the activity of transaminases and other necessary indicators are determined.

  • PCR procedure used to detect RNA of the virus in the blood. But at the same time, one should not forget that the infection periodically disappears from the blood. HGV RNA can also be found not only in the liver, but also in other organs.
  • IFA procedure for determining antibodies. They can appear shortly before the disappearance of the pathogen of the virus from the blood or after that.

Therapy

Hepatitis G treatment may be difficult due to frequent cases of complex infection with this virus and other types of hepatitis. An antiviral agent, Alpha Interferon, is usually prescribed.. Moreover, in every second patient, the disappearance of the RNA of the virus from the blood is observed. Nevertheless, complete cure occurs only in 18-20% of patients.

Hepatitis G: treatment and prevention of the disease, signs of an ailment, how to treat pathology with folk remedies

Hepatitis G is a consequence of infection of the human body with the HBV virus. The causative agent of the disease causes a malfunction of the liver and bile ducts.

Viral hepatitis G is common in all countries, but its location in the region often depends on living conditions and the quality of medical care.

So, for the states of North America, the largest number of diseases with this disease is registered in less developed Mexico.

An ailment is found more often in men aged 30 to 45 years. It is impossible to establish the prognosis of the disease precisely, since the virus progresses and changes its behavior in the human body.

The causative agent of HGV disease in its structure and characteristics resembles the HCV virus, which is the cause of hepatitis C.

The virus is transmitted through blood to a healthy person from people who are carriers of the disease in a chronic or acute form.

How to diagnose

The most common way to determine the presence of hepatitis G virus in the human body is a biochemical blood test. The main indicators in this study that indicate disease are hepatic transaminase activity and bilirubin levels.

The HGV virus found in the blood is evidence of human infection, but it should be borne in mind that this marker may disappear and the patient’s biological material can not be detected.

This effect has not yet been sufficiently studied, therefore, biological material from lymphoid tissue can be used to diagnose hepatitis G.

An ELISA test is considered a good method of confirming infection with this virus, which allows you to detect antibodies designed to fight the causative agent of this disease. They appear until the complete disappearance of HGV and indicate a speedy recovery.

Preventive action

Compliance with the rules aimed at preventing human infection with the HGV virus allows you to maintain health and avoid other ailments. Disease prevention consists of the following recommendations:

  • a person should regularly maintain physical activity,
  • you need to balance your diet and drink enough normal water,
  • use contraceptives (condoms) for sexual contact,
  • in medical institutions, the instruments with which they penetrate the skin of a person should only be disposable,
  • tools used for manicuring and shaving men must be handled appropriately,
  • do not get involved in tattoos, any violation of the skin is fraught with infection,
  • a prerequisite for the prevention of the disease is a mandatory vaccination against hepatitis B,
  • medical personnel require special conditions, care and caution when working with the blood of infected patients,
  • regular preventive examinations with the delivery of biological material for laboratory and instrumental studies will identify the problem in the early stages and quickly stop unpleasant manifestations.

Consequences of the disease

Treatment of hepatitis G, not burdened by other diseases, goes without complications, but if this ailment develops against the background of infection of the body with viruses of type B or C, in the absence of proper therapy, the following undesirable consequences arise:

Complications of the liver

  • in addition to the liver, other internal organs often suffer,
  • the development of cholecystitis is possible,
  • in advanced cases, if the disease is not treated, there is a threat of cirrhosis of the liver,
  • there is a risk of the disease becoming chronic
  • possibly developing hepatic encephalopathy,
  • malignant neoplasms in the liver are recorded,
  • the patient may fall into a coma.

The defeat of the body exclusively by the HGV virus does not cause serious consequences.

If pathogens of hepatitis B and C are found in parallel with the disease, then the therapy is noticeably complicated, and the absence of treatment leads to death, therefore, regular preventive examinations and medical examination are necessary to maintain health and timely detection of the disease.

About the causative agent of hepatitis g

Hepatitis G virus has several names: hepatitis G virus - HGV, GBV-C (GB virus C), HPgV - pegyvirus A. However, the latter name has not yet been approved by the International Committee on Taxonomy of Viruses.
It has in its structure RNA. Belongs to the Flaviviridae family, which includes hepatitis C virus (HCV).

Due to the similarity of the genome and, accordingly, some properties, hepatitis G is also called the "younger brother of hepatitis C".

Currently, there are data on six genotypes and several subtypes of the virus. However, some authors do not quite agree with this division.

Hepatitis G virus

The biological properties of HGV are not well understood. It is established that they are RNA-containing viruses. They have no more than 30% identity with other viruses of this group. It is known that pathogens are often found in mixed infections with hepatitis B, C and D. HIV replication has a suppressive effect.

Infection pathways

In 60% of cases, this virus is transmitted through the blood.. The most common infection routes:

  • blood transfusion,
  • from mother to fetus during pregnancy. The risk increases if in the last stages a woman has had acute hepatitis or is infected with HIV. There is also a risk of infection during breastfeeding if a woman has nipples on her nipples and the baby’s mouth is damaged,
  • single needle injections (for drug addicts),
  • in tattoo parlors, during manicure, pedicure, ear piercing (when using non-sterile instruments and skin damage),
  • using other people's hygiene products (e.g. razors),
  • during sexual contact with the carrier in case of mucosal damage.

In 40%, the cause of the infection cannot be established.

Symptoms of the disease

For inactive symptoms, doctors called hepatitis G "silent disease". The incubation period of the virus is 2-24 weeks, after which the first signs of the disease may appear. They, as a rule, do not have an active nature of manifestation (often the disease is generally asymptomatic), which has negative consequences: the disease goes into a chronic form very imperceptibly.

With the clinical manifestation of the disease, the first signs of the virus resemble a flu disease and are characterized by:

  • loss of appetite
  • lethargy, weakness,
  • fatigue
  • headache
  • a gradual increase in temperature
  • mild bouts of fever
  • body aches.

Further classic jaundice symptoms may appear:

  • clouding of urine
  • whitening feces,
  • yellowing of the protein of the eyes,
  • yellowing of the skin,
  • intercostal pain on the right.

The appearance of several of these signs serves as a signal for visiting a doctor.

Symptoms of Hepatitis G

Symptoms of this virus primarily depend on the form of the course of the disease, which can be chronic or acute. The neglect of the disease is observed, which virtually eliminates the possibility of a full recovery. In the second case, this is acute intoxication of the body for three weeks (the bad thing is that it can pass and is completely asymptomatic). Very often at the acute stage icteric manifestations are observed.

Infected with hepatitis g, symptoms appear after an incubation period of 7-11 days after exposure to the virus.

The main manifestations of hepatitis g include:

  • Impaired gallbladder function.
  • Impaired liver function, and in the most difficult cases - cirrhosis

Suspecting infection with this virus at the very beginning is very difficult, because it manifests itself like any other (resembling the same flu): temperature, headache, weakness, etc. Joint pain can occur, as well as skin rashes.

In the future, the development of the disease can be judged by:

  • characteristic pain in the right hypochondrium,
  • nausea and vomiting
  • loss of appetite
  • dark urine and light feces.

At this stage, changes in blood and internal organs characteristic of hepatitis are already clearly visible.

But the most dangerous is the chronic stage, which can be judged by severe fatigue and general ailments (the patient is practically unable to work physically).

Structure

Viruses have a spherical shape ranging in size from 20 to 60 nm in diameter. Nucleocapsid has an icosahedral type of structure. The supercapsid is covered with spines.

Fig. 2. The structure of the HGV (model). 1 - external viral envelope protein glycoprotein (E1). 2 - capsid shell glycoprotein (C). 3 - nucleic acid. 4 - lipids of the outer shell. 5 - external viral envelope protein glycoprotein (E2).

The genome and genotype of the virus

The virus genome is represented by a single-stranded linear non-segmented molecule + RNA containing 2800 amino acid residues. It consists of structural (E1 and E2) and non-structural (NS2 - NS5) sections.

Genes encoding structural proteins (cor and env) are concentrated in the 5th region, non-structural proteins (proteases, helicases, polymerases) in the 3rd region.

There are 3 genotypes and 5 subtypes of the genome. 1A and 1B subtypes are more common in African countries, 2A and 2 B in American countries, 3 in Southeast Asian countries. In the Russian Federation, Kazakhstan and Kyrgyzstan, genotype 2A dominates.

The HGV genome is less variable than the HCV genome.

Cultivation

In cell cultures, the virus is not cultured. HGVs persist in liver and kidney cells extracted from organisms of experimentally infected animals at the height of the disease.

Resistance and mutability of viruses is not well understood. Pathogens have pronounced carcinogenicity.

Fig. 3. Hepatitis G virus (figure).

Epidemiology of the disease

The epidemiology of hepatitis G is poorly understood. The epidemiological characteristics of HGV infection are very similar to those of other serum hepatitis, including HCV. Among individuals with acute viral hepatitis of unspecified etiology, HGV RNA findings range from 3 to 45%. Based on studies in the USA and Europe, HGV infection occurs in 20% of cases in patients with chronic HCV, in 10% of cases - chronic HBV, in 10% of cases in patients with autoimmune hepatitis, in 10% of cases in patients with alcoholic hepatitis. According to other data, the frequency of determination of HGV RNA in patients with HBV is 24%, HCV - 37%. It was found that HGV viruses do not aggravate the course of these diseases.

Disease prevalence

The prevalence of HGV infection is widespread and uneven. In the Russian Federation, the frequency of detection of RNA (hereditary material of the virus) ranges from 2% (Moscow) to 8% (Yakutia). A high prevalence of diseases is recorded in West African countries.

Viral hepatitis G is more often recorded among urban residents, 1.5-2 times more often in men than in women. High levels of HBV are recorded in regions with a high prevalence of HBV and HCV.

General information

Hepatitis G is a viral disease that predominantly affects the human hepatobiliary system. For the first time, the HGV virus was isolated in 1967 from the blood of an American surgeon J. Barker, who had hepatitis “neither A nor B”, however, the pathogen was identified only in 1995 due to the introduction of molecular genetic diagnostics. Most often, males, young adults (up to 45 years) are affected. In 91-98% of cases, patients have a concomitant disease with other parenteral hepatitis: the frequency of co-infection with acute hepatitis B and C is up to 37%, with chronic - up to 17%. Delta hepatitis co-infection occurs in 39.9% of patients. There is no clear seasonal affection for the infection.

Causes of Hepatitis G

The causative agent of the infection is an RNA-containing virus (HGV virus, GBV-C, HPgV virus), which belongs to the flavivirus family. Today, the virus includes three genotypes and several subtypes. In its properties, the pathogen is similar to the hepatitis C virus, but is able, in contrast to it, to reproduce the infection on inhuman monkeys (which could potentially reduce the cost and simplify the study of the pathogenesis of hepatitis C, the body's response to the antiviral drugs used). Infection occurs parenterally through contact with infected blood. Cases of infection with unprotected sex and transmission of the virus from mother to fetus are known.

Risk groups for the disease include patients with hemodialysis departments, recipients of internal organs, people who have undergone blood transfusions, patients with hemophilia, HIV infection, medical personnel, people who have numerous homosexual and bisexual contacts, who practice intravenous drug use. The prevalence of the disease is widespread; for West Africa, HGV infection is considered endemic. The virus is unstable in the environment, dies when boiled and exposed to standard doses of disinfectant solutions.

Methods of infection

When it comes to hepatitis g, the transmission of the disease is closely related to blood. Denote the most probable transmission routes of the virus (from the most to the least common):

  • Failure to comply with the mandatory hygiene rules when handling blood. Most often, people who use drugs and do not care about personal safety become infected (for example, when one injection needle is used).
  • Blood transfusions from hepatitis g virus donors (all medical institutions are required to strictly check donor blood for viruses).
  • Infection by a woman in childbirth during childbirth (in cases of not acute form of the course of the virus, there is a very real possibility of excluding infection).
  • Unprotected sexual contact with the carrier of the virus.
  • Any other blood related manipulations (ear piercing, tattoos, etc.)

Pathogenesis

The pathogenesis of hepatitis G is not well understood. It is believed that the virus does not have primary hepatotropic properties, but has an affinity for mononuclear cells, spleen cells, bone marrow, and also acts as a suppressor of human immunodeficiency virus replication. When it penetrates the human body, the pathogen infects lymphocytes, with a blood stream it enters various organs and systems, persisting for a long time in the lymph. Getting into the liver occurs passively, together with lymphocytic cells, while inflammatory changes are expressed only in the intrahepatic bile ducts and biliary system. The virus probably has a specific damaging effect on the bile ducts, since the occurrence of cholangitis with the phenomenon of biliary sludge is described. There are also studies to determine the trigger role of the HGV virus in autoimmune liver lesions and the formation of pathologies such as aplastic anemia, thalassemia, and Tarda porphyria, however, a clear description of the mechanism of influence was not obtained due to the small number of observations.

Characteristics of the main routes of transmission of hepatitis G

  1. HBV can be transmitted through syringes contaminated with virus-containing blood and medical instruments, through non-sterile instruments used during cosmetic procedures (shaving, pedicures, manicures, etc.), piercings, and tattoos.
  2. HGV RNA is found in individuals receiving multiple blood transfusions. In hemophilia patients, HGV RNAs are found in 24 to 57% of cases. Detection of hepatitis G virus in the blood is determined only with the use of an expensive PCR diagnostic method, so its mass introduction today seems impossible. An examination of blood donors for the presence of hepatitis B and C markers (anti-HBV and HbsAg), surrogate markers of hepatitis G, can be considered as prevention of the disease.
  3. The detection rate of serum HBV RNA in patients with a transplanted heart, kidney, and liver reaches 43%. Immunosuppressive therapy contributes to the development of chronic HGV carriage. At risk are hemophilia patients and patients with hemodialysis units.
  4. Helps transmit HGV using syringes contaminated with infected blood. HBV RNA is detected in the blood of injecting drug addicts in 30 to 35% of cases.
  5. There is a sexual transmission of infection, both in the family (husband and wife), and in promiscuous sexual intercourse. A high infection rate is observed in males. At risk are prostitutes, homosexuals and bisexuals. The risk of infection is higher, the greater the person has sexual partners.
  6. Mother-to-child transmission of HGV is considered proven (vertical transmission). Based on studies in Germany, Australia, and France, children are infected with HGV from mother mothers in 50% of cases.
  7. Cases of intra-family transmission of HGV have been reported.

Fig. 4. Blood contact is the main mechanism of transmission of infection.

Classification

The clinic of HGV infection is similar to the symptoms of HCV infection, but cirrhotic changes in the liver tissue, extrahepatic manifestations are practically not found, however this statement is true only for monoinfection. In the presence of simultaneously more than two viruses affecting the liver tissue, a mutual aggravation of pathological processes in the body occurs. There are acute and primary chronic course of the disease, as well as two clinical forms:

  • Anicteric. The most common picture of the disease. Patients complain of intoxication symptoms and a sharp malaise, laboratory tests may reveal antibodies to the virus, a moderate increase in liver enzymes.
  • Jaundice. It is manifested by icteric staining of mucous membranes, skin, dark urine (similar in color to tea leaves), and itchy skin.

Prevention

A special vaccine against hepatitis G has not yet been developed due to the lack of knowledge and unpredictability of the strain.

The main preventive measures are individual safety measures:

  • visit only well-established beauty salons and tattoo parlors,
  • make sure that the disposable syringe is removed from the individual packaging before the procedure,
  • if blood transfusion is necessary, ask for blood substitutes,
  • use only your personal hygiene products,
  • refuse unprotected sex.

It is worth remembering that the virus, even in a dried state, is able to remain alive for several weeks, but it does not tolerate high temperatures (as when boiling).

Hepatitis G strain is considered relatively benign, but not he himself is terrible, but his possible co-infection with virus C and the consequences of this combination for the patient and his environment. Observing simple rules of prevention, you can avoid this dangerous disease and maintain health.

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Hepatitis and pregnancy

The issue of hepatitis G and pregnancy is very complex, especially because of its little knowledge. Since during pregnancy or childbirth there is a chance of a mother becoming infected with the child, additional burden is placed on the doctors. Fortunately, the chances of not only minimizing the risk of infection, but also significantly increasing the chances of a child recovering, even in the event of such, are quite high. The necessary activities are planned and implemented in each individual case.

Features of the course of the disease

  • Hepatitis G virus is associated with damage to liver cells. However, when examining infected patients, it was found that in most of them the level of transaminases remained within normal limits.
  • Hepatitis G is often asymptomatic. Subclinical and anicteric forms are characteristic of the disease.
  • The acute period of HBV is asymptomatic or asymptomatic.
  • The transition to the chronic form occurs imperceptibly, with a frequency of 2 - 9%, more often with mixed infection.
  • The progression of the disease with the subsequent development of chronic hepatitis, liver cirrhosis and hepatocellular carcinoma, which are so characteristic of hepatitis C, are not characteristic of HBV.
  • The chronic form of the disease often proceeds as a healthy carrier state.

Complications

HGV monoinfection with timely detection practically does not cause complications, most often the formation of chronic lesions of the gallbladder and biliary tract (cholecystitis, cholangitis, cholelithiasis). In fulminant course, the appearance of acute liver failure, DIC, acute liver encephalopathy. If necessary, invasive diagnostic, therapeutic procedures (injections, catheterization, fine-needle biopsy, and others) are highly likely to cause bacterial complications ranging from local to multisystem lesions and sepsis.

Etiology

The taxonometry of the pathogen is not fully defined. He was conditionally assigned to the flavivirus family. Genetic material is represented by a single-stranded RNA molecule.

It is believed that there are three types of G viruses. Frequent detection of it in patients with hepatitis C makes it possible to assume that it is a defective virus, and for its reproduction, the presence of an assistant, virus C, is necessary.

Acute phase of the disease

The acute phase of HBV occurs in a clinically mild form or is asymptomatic. ALT is moderately elevated, indicating a small degree of cytolysis (destruction) of liver cells. In a number of cases, during monoinfection, signs of intrahepatic cholestasis are recorded: the activity of GGT (gamma-glutamyltranspeptidase) and alkaline phosphatase increases, which indicates a possible damage to the bile ducts.

The acute phase imperceptibly passes into a chronic form, proceeding in the form of a virus carrier. Extrahepatic manifestations of the disease are not marked.

Clinic

The incubation period is up to 30 days. But it is possible a long carrier of the virus up to 8 years without the onset of symptoms of the disease. In such cases, the detection of the virus will be an accidental find during the examination.

Complaints are not specific to this disease. This is a feeling of general malaise and weakness, increased fatigue. The temperature may rise slightly. In case of monoinfection, jaundice may be absent. If there is a combination with B or C hepatitis, then the appearance of jaundice will be necessary. In parallel, there will be pains in the liver, the color of the feces will change, the urine will darken.

With an asymptomatic course of complaints, there will not be a long time, a person acts as a virus carrier. In a typical form, the severity of the clinic will depend on the manifestation of an additional infection.

The disease can occur lightning fast. Then there will be a rise in temperature, severe symptoms of intoxication, liver damage. Such development is possible in the presence of hepatitis B or C.

Changes in laboratory parameters will be typical for patients with hepatitis:

  • an increase in bilirubin,
  • rise in cholesterol, alkaline phosphatase,
  • ALT increased.

Viral hepatitis G

Viral hepatitis G is an inflammatory infectious disease caused by the HBV virus, which is characterized by a progressive dysfunction of the liver and biliary system.

The disease is spread throughout the globe and makes up 3 - 24% of all cases of viral hepatitis. Such an uneven frequency of occurrence of pathology depends on living conditions and living standards of the population of certain regions.

So in the countries of North America in the frequency of occurrence of viral hepatitis G in the first place is Mexico. In the countries of South America - Chile, Peru, Brazil. In the countries of Europe - Moldova, Ukraine, Belarus, the European part of Russia. In Asian countries - Kazakhstan, China, Tibet, the Asian part of Russia, Iraq, Iran.

In Africa - the countries of the northern and central parts.

More often viral hepatitis occurs in middle-aged people (30 - 45 years old), the male gender is more predisposed.

The prognosis of the disease is doubtful, since the pathological process is constantly progressing, and cases of complete cure are isolated.

Causes

The source of the spread of viral hepatitis G is patients with an acute and chronic form of the disease, as well as virus carriers - persons in whose blood the virus is detected, and the symptoms of the disease are completely absent.

HGV virus is transmitted from a sick person to a healthy parenteral route (through the blood), this is done when:

  • surgical interventions
  • blood transfusion (donated blood transfusion),
  • hemodialysis (connecting the body to an artificial kidney apparatus),
  • frequent use of non-sterile medical needles for injections.

There is a risk group for the occurrence of this disease, it includes:

  • Persons suffering from persistent violation or weakening of the immune system:
  • HIV infected
  • AIDS patients (acquired immunodeficiency syndrome),
  • persons receiving immunosuppressants (patients with cancer, the postoperative period after organ transplantation),
  • persons suffering from endocrine pathology (diabetes mellitus, hypothyroidism),
  • donation
  • drug addicts
  • Doctors and nurses.

Laboratory research methods

Nonspecific examinations, which give an idea of ​​the presence of a pathological process in the liver:

  • general blood test, in which an increase in leukocytes will be detected, more than 11 * 109 / l, a shift of the leukocyte formula to the left and an increase in ESR (erythrocyte sedimentation rate) more than 30 mm / h,
  • general urinalysis, which is characterized by the presence of traces of protein (normally negative protein) and squamous epithelium more than 20 in the field of view, in rare cases, the appearance of red blood cells in the urine - blood cells,
  • liver tests:

Indicator Normal value Hepatitis G value

Total protein64 - 83 g / l60 - 65 g / l and below
Total bilirubin8.6 - 20.5 μmol / L25.5 - 40.0 μm / L and higher
Direct bilirubin8.6 μmol / L9.0 - 12.5 μmol / L and higher
ALT (alanine aminotransferase)5 - 30 IU / L30 - 60 IU / L and higher
AST (aspartate aminotransferase)7 - 40 IU / L40 - 55 IU / L and higher
Alkaline phosphatase50 - 120 IU / L120 - 260 IU / L and higher
LDH (lactate dehydrogenase)0.8 - 4.0 pyruvate / ml-h4.0 pyruvate / ml-h and above
Albumen35 - 50 g / l34 - 45 g / l and below
Thymol test1 - 4 units2 - 4 units. and more

Serological research methods

These are specific methods for the diagnosis of viral hepatitis G, which make it possible to make a final diagnosis and prescribe treatment appropriate to the disease:

  • ELISA (enzyme immunoassay)
  • XRD (X-ray fluorescence analysis),
  • RSK (complement fixation reaction),
  • PCR (polymerase chain reaction).

When carrying out these tests in the blood, the titer of the HGV virus is determined, which not only determines the disease, but also indicates the phase of the process (exacerbation, remission), form (acute, chronic) and reveals virus carriers.

Drug treatment

Etiotropic therapy - aimed at weakening or complete destruction of the hepatitis G virus:

  • 3-6 million IU of interferon is injected into each nasal passage 3 times a week. The course of treatment is 6-12 months.

Symptomatic therapy - aimed at reducing the inflammatory process in the liver parenchyma and alleviating the course of the disease:

  • rheosorbylact 200.0 ml intravenously 1 time per day,
  • Ringer's solution or saline 200.0 ml intravenously drip 1 time per day.

  • polysorb 1 tablespoon, previously dissolved in ½ cup cool boiled water 3 times a day with honey meals,
  • dufalac or normase 30 to 40 mg (depending on body weight) 3 times a day for 15 to 20 minutes before eating.

  • Creon 20 000 - 25 000 IU 3 times a day with food,
  • Mezim-Forte 20,000 units 3 times a day with meals.

  • Holosas 1 tablespoon 3 times a day,
  • allohol 2 tablets 3 times a day.

Antispasmodics for pain:

  • nospa or baralgin 1 tablet 3 times a day.

Fortifying and vitamin therapy:

  • stimol 1 sachet 3 times a day,
  • B vitamins (B1, B6, B12) - neurorubin-forte-lactab or neurobion 1 tablet 1 to 2 times a day,
  • vitamin C 1 tablet (500 mg) 2 times a day or a complex of multivitamins and minerals.

Alternative treatment

  • Take in equal proportions the grass of horsetail, St. John's wort, tansy, yarrow, chamomile flowers, burdock root, rose hips, sage leaves, elecampane root, burdock leaves and scallop grass. Grind the resulting mixture with a blender. 4 tablespoons of the resulting mixture, pour in a thermos and pour 1 liter of boiling water. Let it brew for 4 to 6 hours. Take ½ cup 3 times a day 1 to 1.5 hours after eating.
  • Take ½ cup of extra virgin olive oil and put a heating compress or heating pad on the right hypochondrium. Olive oil can be replaced with 2 tablespoons of sorbitol dissolved in heated water. Contraindication to this method of treatment is the presence of stones in the gallbladder.
  • Grind 1 kg of washed cranberries through a meat grinder and add ½ cup honey. The mixture is taken 1 tablespoon 3 times a day 1 hour after a meal. Cranberries can be replaced with viburnum.

Diet facilitating the course of the disease

With viral hepatitis G, you should strictly adhere to a diet.

Allowed Products:

  • vegetable soups on the water,
  • boiled, not fatty meat of chicken and beef,
  • boiled fish not fatty varieties,
  • porridge (preference is given to rice, oat and semolina),
  • vegetable stew,
  • fruits (bananas, baked apples),
  • dried apricots, raisins,
  • dairy products (not fatty cheese, a small amount of butter in the morning),
  • dried white bread
  • fruit drinks, compotes, rose hips, black and green tea.

Foods to be excluded from the diet:

  • borscht, cabbage soup, hodgepodge, soups on meat broths,
  • fatty, fried meat, poultry or fish,
  • pasta,
  • pickled, pickled vegetables and other pickles,
  • eggs
  • Fresh vegetables and fruits
  • whole milk, cream, sour cream,
  • alcoholic drinks, sweet soda, coffee.

The outcome of acute hepatitis G

  • Recovery (complete disappearance of HGV RNA from blood serum and the appearance of specific antibodies).
  • The formation of a chronic form of the disease (HGV RNAs are detected for a long time, disappear for several years and then virus-specific antibodies appear in the blood serum).
  • Prolonged carriage of HGV.

Fig. 5. A severe form of the disease develops with co-infection and often results in death.

Watch the video: What is Hepatitis C and Why Should You Care? (February 2020).

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