Hepatitis A: a new look at an old problem (lecture)

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Hepatitis A is a serious medico-social problem in the health care system worldwide. In the Russian Federation, hepatitis A virus continues to be the major etiological agent of acute viral hepatitis. The features of Hepatitis A at the present are its frequent association with chronic alcohol intoxication, chronic hepatitis B and C, HIV infection, a tendency to a prolonged course with exacerbations and relapses, the presence of cholestatic syndrome and an autoimmune disorder, more frequent development of severe forms of the disease due to the incidence declined in children and increased in adults. Due to the lack of specific antiviral therapy, vaccination is currently recognized as the most effective measure to combat hepatitis A. Thus, hepatitis A vaccination is included in the National Immunization Program in at least 20 countries, including the United States, China and Brazil. Expansion of the National Immunization Program and inclusion of hepatitis A vaccination will significantly reduce the incidence of this disease in the Russian Federation. The article describes the features of the hepatitis A virus reproduction cycle, including a description of quasi-enveloped form of virions. Current data on the epidemiology and pathogenesis of hepatitis A are presented. Clinical manifestations of manifest forms of hepatitis A are considered. The main and most promising methods of laboratory diagnostics of hepatitis A, as well as methods of specific disease prevention are described.

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作者简介

Dmitrii Gladin

Saint Petersburg State Pediatric Medical University

编辑信件的主要联系方式.
Email: gladin1975@mail.ru
ORCID iD: 0000-0003-4957-7110
SPIN 代码: 8149-9885

MD, PhD, Head of the Department of Microbiology, Virology and Immunology

巴基斯坦, Saint Petersburg

Nadezhda Kozlova

North-Western State Medical University named after I.I. Mechnikov

Email: spbkns@gmail.com
ORCID iD: 0000-0002-6713-4156
SPIN 代码: 7914-4401

MD, PhD, Associate Professor of Department of Medical Microbiology

俄罗斯联邦, Saint Petersburg

Vladimir Marchenko

North-Western State Medical University named after I.I. Mechnikov

Email: vmarcenco@mail.ru
ORCID iD: 0000-0001-6870-3157
SPIN 代码: 4463-7720

MD, PhD, Associate Professor of Department of Medical Microbiology

俄罗斯联邦, Saint Petersburg

Ilya Baranov

North-Western State Medical University named after I.I. Mechnikov

Email: vodolaz74@yandex.ru
ORCID iD: 0000-0001-9741-0230
SPIN 代码: 9869-5443
俄罗斯联邦, Saint Petersburg

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2. Fig. 1. The structure of the virion and the structure of the genome of the hepatitis A virus. Оne large peptide is formed during translation, and is cleaved by proteolysis into three precursor proteins — P1, P2 and P3. Еhe first one, P1, forms four capsid proteins (VP1, VP2, VP3, VP4) through additional proteolysis. P2 consists of three non-structural proteins (2A, 2B and 2C) required for viral replication. P3 consists of the following proteins: 3A is necessary for anchoring P3 to the cell membrane, 3B is a VPg protein, 3C is a cysteine protease that cleaves precursor proteins (P1, P2 and P3) into individual structural and non-structural proteins, 3D is RNA-dependent RNA-polymerase. © O. Gholizadeh, et al. 2023. The figure is adapted from [17].

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3. Fig. 2. Genotypes and subtypes of the hepatitis А virus. © S.M. Lemon, et al. 2018. Distributed under CC-BY-NC-ND 4.0 license. Source: borrowed from [23].

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4. Fig. 3. Reproduction cycle of the hepatitis A virus. The virus interacts with receptors on the basolateral membrane of the hepatocyte, after which it penetrates into the cell as part of an endosome, followed by undressing and presentation of the genome in the cytoplasm. Translation leads to synthesis of one large precursor polyprotein, which after proteolysis is cleaved into structural and non-structural proteins, some of which required in transcription and translation. In final stages of infection, copies of genomic viral RNA are packaged into viral particles, which are integrated into multivesicular bodies to form quasi-enveloped virions (qHAV). The release of qHAV occurs through the apical or basolateral surface of the hepatocyte, respectively. HAV, hepatitis A virus; IRES, internal ribosome entry site. © O. Gholizadeh и соавт., 2023. The figure is adapted from [17].

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5. Fig. 4. Prevalence of viral hepatitis A in the world [28].

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6. Fig. 5. Release of quasi-enveloped and non-enveloped HAV virions from hepatocytes. Image adapted with modifications from [12]. © 2023. Springer Nature Limited.

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7. Fig. 6. Serological and some biochemical markers during HAV infection. Image adapted with modifications from [30]. © 2023. Springer Nature Limited.

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8. Fig. 7. Operating principle of a DNA biosensor. © 2012 Elsevier Ltd. Image adapted with modifications from [25].

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