This document discusses hepatitis A virus (HAV) which causes hepatitis A, an infectious liver disease. HAV is a picornavirus with a single serotype that is transmitted primarily through the fecal-oral route. It does not cause chronic infection like hepatitis B or C. While many cases are asymptomatic, symptomatic cases typically have an incubation period of 2-6 weeks followed by jaundice, abdominal pain, and fever. HAV infection is diagnosed through detection of IgM antibodies and past infection through IgG antibodies.

1. 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.

2. Classification of Hepatitis Virus:

3. • 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

4. Structure

5. 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).

6. Life Cycle:

7.  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:

8. 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.

9. Pathogenesis:

10. 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.

11. 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.