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Introduction:
 Picornavirus (RNA).
 Hepatitis A is an infectious disease of the liver caused
by Hepatovirus A.
 Many cases have few or no symptoms, especially in the young.
 The hepatitis A virus (HAV) is a common infectious etiology of
acute hepatitis worldwide.
 HAV does not cause chronic liver disease unlike hepatitis B or C.
 According to the World Health Organization (WHO), infection
rates in developed countries are low.
 The time between infection and symptoms, in those who develop
them, is 2–6 weeks.
 Epidemic jaundice described by Hippocrates.
Classification of Hepatitis Virus:
• 4 Genotypes
• One stable serotype only
• Naked RNA virus
• Stable at low pH
• Inactivated by high temperature
• Non-enveloped 27-nm
• Heat resistant.
• Virion contains four capsid polypeptides,
designated (VP1 to VP4).
Properties
Structure
Transmission:
 Close personal contact.
(e.g., household contact, sex contact, child day-care
centers).
 Contaminated food, water.
(e.g., infected food handlers).
 Blood exposure (rare).
(e.g., injection drug use, rarely by transfusion).
Life Cycle:
 The virus exits the host cell by lysis and viroporins.
 Virions are secreted into the bile and released in stool.
 HAV is excreted in large numbers about 11 days prior to the
appearance of symptoms or anti-HAV IgM antibodies in the
blood.
 The incubation period is 15–50 days and risk of death in those
infected is less than 0.5%.
Life Cycle:
Pathogenesis:
• HAV is typically acquired through ingestion (through fecal-oral transmission) and
replicates in the liver.
• After 10 to 12 days, virus is present in blood and is excreted via the biliary
system into the feces.
• Peak titers occur during the 2 weeks before onset of illness.
• Although virus is present in serum, its concentration is several orders of
magnitude less than in feces.
• Virus excretion begins to decline at the onset of clinical illness and decreases
significantly by 7 to 10 days after onset of symptoms.
• Most infected persons no longer excrete virus in the feces by the third week of
illness.
Pathogenesis:
Clinical Findings
• Dark urine appears first (bilirubinuria).
• Pale stool soon follows
• Jaundice -(70-85%) adults.
• Abdominal pain (40%).
• Itch
• Skin rash
• Hepatomegaly is common.
• Patients may have a fever with temperatures of up to 40°C.
Lab Diagnosis:
 Acute infection is diagnosed by the detection of
HAV-IgM.
 Past Infection i.e. immunity is determined by the
detection of HAV-IgG.
 Cell culture – difficult and take up to 4 weeks, not
routinely performed
 Direct Detection – PCR of faeces.
Can detect illness earlier than serology but rarely
performed.
Hepatitis A Virus (HAV).pptx

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Hepatitis A Virus (HAV).pptx

  • 1.
  • 2. Introduction:  Picornavirus (RNA).  Hepatitis A is an infectious disease of the liver caused by Hepatovirus A.  Many cases have few or no symptoms, especially in the young.  The hepatitis A virus (HAV) is a common infectious etiology of acute hepatitis worldwide.  HAV does not cause chronic liver disease unlike hepatitis B or C.  According to the World Health Organization (WHO), infection rates in developed countries are low.  The time between infection and symptoms, in those who develop them, is 2–6 weeks.  Epidemic jaundice described by Hippocrates.
  • 4. • 4 Genotypes • One stable serotype only • Naked RNA virus • Stable at low pH • Inactivated by high temperature • Non-enveloped 27-nm • Heat resistant. • Virion contains four capsid polypeptides, designated (VP1 to VP4). Properties
  • 6. Transmission:  Close personal contact. (e.g., household contact, sex contact, child day-care centers).  Contaminated food, water. (e.g., infected food handlers).  Blood exposure (rare). (e.g., injection drug use, rarely by transfusion).
  • 8.  The virus exits the host cell by lysis and viroporins.  Virions are secreted into the bile and released in stool.  HAV is excreted in large numbers about 11 days prior to the appearance of symptoms or anti-HAV IgM antibodies in the blood.  The incubation period is 15–50 days and risk of death in those infected is less than 0.5%. Life Cycle:
  • 9. Pathogenesis: • HAV is typically acquired through ingestion (through fecal-oral transmission) and replicates in the liver. • After 10 to 12 days, virus is present in blood and is excreted via the biliary system into the feces. • Peak titers occur during the 2 weeks before onset of illness. • Although virus is present in serum, its concentration is several orders of magnitude less than in feces. • Virus excretion begins to decline at the onset of clinical illness and decreases significantly by 7 to 10 days after onset of symptoms. • Most infected persons no longer excrete virus in the feces by the third week of illness.
  • 11. Clinical Findings • Dark urine appears first (bilirubinuria). • Pale stool soon follows • Jaundice -(70-85%) adults. • Abdominal pain (40%). • Itch • Skin rash • Hepatomegaly is common. • Patients may have a fever with temperatures of up to 40°C.
  • 12. Lab Diagnosis:  Acute infection is diagnosed by the detection of HAV-IgM.  Past Infection i.e. immunity is determined by the detection of HAV-IgG.  Cell culture – difficult and take up to 4 weeks, not routinely performed  Direct Detection – PCR of faeces. Can detect illness earlier than serology but rarely performed.