Hepatitis Viruses

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Hepatitis Viruses

• Etiology, epidemiology, pathogenesis,
  classification

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Hepatitis viruses (HV)-

• group of anthroponosis diseases with different
  mechanisms of transmition, which are accompanied
  by intoxication and disorders of liver function,
  quite often by an icterus.
• Distinguish HV-A, B, C, D, E, G, each of which
  has its own agents. The secondary hepatitis do
  not belong to this group, they are caused by the
  viruses of cytomegalo, herpes, Epstein-Barr and
  adenoviruses.

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Electronic microscopy ( negative contrast)
Hepatitis virus A (d27nm).
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Etiology of VHA

• Agent VHA was first discovered in 1973 by
  Feinstone. This is RNA - containing virus.
• VHA is sensitive to formaldehyde, may remain
  preserved for a period of few months or even
  years during temperature 4 C, some weeks -
  during room temperature. Complete inactivation
  of virus takes place during 85 C in a period of
  5 minutes. VHA is resistant to chlorine, in
  comparison with other viruses of this group and
  may enter through barriers of water cleaning
  stations.

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Electronic microscopy ( negative contrast)
.patient s serum with HV B .A-tubular part ?
Deyna part ? spheric part
A
B
C
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Etiology of VHB

• VHB in natural condition is revealed in sick
  people and carriers. This is DNA-containing virus
  is pathogenic for human and few types of
  primates. Causes acute and persistent infection,
  damages primarily liver.
• Virus consists on antigenic structure HBsAg -
  surface, HBcAg - internal (care), HBeAg -
  reflects infectiouness of virus.
• Towards these antigens in organism of patients
  antibodies are produced anti-HBs anti-HBc
  anti-HBe.

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Etiology of VHB

• HBsAg is revealed in majority of patients in
  incubation stage
• Presence of HBsAg in human organism testifies as
  presence of acute and latent proceeding infection
• Prolonged conservation HBsAg may testify
  about transformation of the process into
  chronic form
• HBcAg is practically not determined in blood and
  fixed in directly by DNA-polymerize reactions,
  falling positive in acute period of disease, as
  well as after many months and years in carriers
• HBeAg is revealed in early stages of disease,
  which is then changed by anti-HBe.

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Etiology of VHC

• Virion of virus of hepatitis C consists on
  nucleus and lipid external membrane. Genome is
  represented by single chain RNA. VHC is resistant
  in external medium, particularly in biological
  fluids such as preparations of blood, sperm and
  others. Sensitive to chloroform, other
  desinfective solutions and high temperatures
  (100 C and more).
• Antigenic structure of VHC is less studied.

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Etiology of VHD

• Virus represents defective virus particle,
  contains internal antigen (HDAg), made up of
  small circular RNA and surface covering, which is
  HBsAg VHB. It is considered that reproduction of
  virus is possible only during presence of HBsAg
  in organism of patient, therefore hepatitis D
  proceeds always as a coinfection or
  superinfection, joining with VHB.

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Etiology of VHE

• Virus of hepatitis E has been isolated from feces
  of patients with jaundice. Spherical particles
  similar to virus were able to discover due to the
  method of immune electronic microscopy.

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Epidemiology of VHA

• Viral hepatitis A - antroponosis. The source of
  disease is sick person in prejaundice period and
  in 15 - 20 days of acute period of the disease.
• Primary localization of virus is
  gastrointestinal tract. Mechanism of transmission
  is faecal-oral. Virus is excreted from the
  organism of sick person with feces.
• Specific final factors of transmission of
  hepatitis A virus are water and food. Spreading
  depends on conditions of water supply and its
  relation with fecal contamination. Important
  factors of transmission are flies, dirty hands.
• Susceptibility to the disease is high. Mainly
  children and adults up to 30 year fall sick.

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Epidemiology of VHB

• The source of VHB is sick person with acute or
  chronic form, healthy carrier.
• Mechanism contact (wound).
• Ways of transmission parenteral, sexual, through
  placenta from sick mother to fetus (vertical or
  transplacentar).
• Factors blood, sperm, vaginal secret, milk of
  mother
• Susceptibility to the disease is high.
• Risk group drug addicts, homosexualists,
  prostitutes, medical personnal

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Anatomic pathology

• Morphological changes take place in all tissual
  components of liver - parenchyma, connective
  tissue, reticuloendothelium, in bile pathways.
• Dystrophic and single necrotic changes, massive
  and submassive necroses of liver parenchyma.
• Three variants of changes mesenhymal
  inflammation, cholestatic and cytolitic

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Macro-preparation massive hepatonecrosis
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Pathogenesis

• Entrance gates
• The agent approaches regional lymphatic glands,
  where its massive reproduction takes place
• Organism replies on this negative influence by
  immunological reaction of reticular tissue of the
  lymphatic gland (primary virusemia)
• Virus continue to enter from lymphatic glands
  into blood in a large quantities (clinical
  period)
• Secondary virusemia

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Pathogenesis of VHB

• explained from viral-immunogenetic position,
  because it is known that power of immune response
  is genetically determinated
• Immune reaction may be strong (in fulminate form
  of hepatitis), flabby and adequate. Only adequate
  immune reaction promotes cyclic course and
  favorable outcomes of the disease

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Classification hepatitis viruses (IDC XX WHO)

• Hepatitis viruses (?15-?19)
• Conclusions cytomegalovirus (?25.1)
• herpes viral (herpes simplex) hepatitis (?00.8)
• out comes of viral hepatitis (?94.2)
• ?15 Acute hepatitis
• ?15.0 Hepatitis A with hepatic coma
• ?15.9 Hepatitis A without hepatic coma
• ?16 Acute hepatitis ?
• ?16.0 Acute hepatitis ? with delta-agent
  (co-infections) and hepatic coma
• ?16.1 Acute hepatitis ? with delta-agent
  (co-infections) without hepatic coma
• ?16.2 Acute hepatitis ? without delta-agent
  accompanied by hepatic coma
• ?16.9 Acute hepatitis ? without delta-agent and
  without hepatic coma

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• ?17 Other acute viral hepatitis
• ? 17.0 Acute delta (super infection) infection
  in hepatitis B
• ?17.1 Acute hepatitis C
• ? 17.2 Acute hepatitis E
• ?17.8 Other confirmed acute viral hepatitis
• ?18 Chronic viral hepatitis B
• B18.0 Chronic viral hepatitis B with delta-agent
• ?18.1 Chronic viral hepatitis B without
  delta-agent
• ?18.2 Chronic viral hepatitis ?
• ?18.8 Other chronic viral hepatitis
• ?18.9 Chronic viral hepatitis, without
  confirmation
• ?19 Unconfirmed viral hepatitis
• ?19.0 Unconfirmed viral hepatitis with coma
• ?19.9 Unconfirmed viral hepatitis without hepatic
  coma

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Classification of viral hepatitis (Hepatites
virosae) (?15-?19)

• According to infectious agent ? (?15), ?
  (?16), ? (?17.1), D (?17.0), ? (?17.2), G
  (?17.8), not confirmed (?19).
• Clinical forms jaundice, cholestatic, without
  jaundice, sub-clinical (asymptomatic), fulminant.
  
• Duration Acute, prolonged, chronic (?18).
• Degree of severity mild degree, moderate degree,
  severe degree, very severe degree.

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• Complications Acute hepatic encephalopathy (?,
  ??, ???, ?V stages) (?15.0 ?16,0 ?16.2 ?19.0),
  exacerbation (clinical, fermented), functional
  and general diseases of biliary tracts.
• Results recovery, remaining symptoms
  ( astenovegitativ syndrom,
  hepatomegaly), difficult recovery,
  hyperbilirubinemia, chronic hepatitis (?18),
  liver cirrhosis, primary liver cancer.