Hepatitis A virus

 1.     HEPATITIS A VIRUS

·       HAV causes infectious hepatitis

·       Spread by the fecal-oral route.

·       Result from consumption of contaminated water, shellfish, or other food.

·       Picornavirus - a new genus Heparnavirus

·       Long incubation period - 15 to 40 days.

Mode of Transmission

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·       Contaminated water, food, and unclean hands are common means of virus transmission.

·       The virus is excreted in significant quantities through feces and is primarily disseminated through the fecal-oral route.

·       Shellfish, particularly clams, oysters, and mussels, serve as significant sources of the virus.

·       Hepatitis A virus (HAV) demonstrates resilience to detergents, highly acidic environments (pH of 1), and temperatures as high as 60°C, remaining viable for several months in both freshwater and saltwater.

·       Untreated or inadequately treated sewage has the potential to pollute the water supply and subsequently contaminate shellfish.

Structure

·       Size 27nm, naked – non-enveloped, icosahedral capsid

·       Positive-sense, single-stranded RNA genome consisting of approximately 7470 nucleotides.

·       The capsid is even more stable than other picornaviruses to acid and other treatments.

·       There is only one serotype of HAV.

 

Replication

·       HAV replicates like other picornaviruses.

·       Interacts specifically HAVCR-1 expressed on liver cells and T cells.

·       The structure of HAVCR-1 can vary for different individuals, and specific forms correlate with severity of disease.

·       Unlike other picornaviruses, however, HAV is not cytolytic and is released by exocytosis.

·       Laboratory isolates of HAV have been adapted to grow in primary and continuous monkey kidney cell lines, but clinical isolates are difficult to grow in cell culture.

Pathogenesis

·       HAV is ingested and probably enters the bloodstream through the epithelial lining of the oropharynx or the intestines to reach its target, the parenchymal cells of the liver.

·       The virus replicates in hepatocytes and Kupffer cells.

·       Virus is produced in these cells and is released into the bile and from there into the stool.

·       Virus is shed in large quantity into the stool approximately 10 days before symptoms of jaundice appear or antibody can be detected.

·       HAV replicates slowly in the liver without producing apparent cytopathic effects.

·       Although interferon limits viral replication, natural killer cells and cytotoxic T cells are required to eliminate infected cells.

·       Antibody, complement, and antibody-dependent cellular cytotoxicity also facilitate clearance of the virus and induction of immunopathology.

·       Icterus, resulting from damage to the liver, occurs when cell-mediated immune responses and antibody to the virus can be detected.

·       Antibody protection against reinfection is lifelong.

·       The liver pathology caused by HAV infection is indistinguishable histologically from that caused by HBV.

·       It is most likely caused by immunopathology and not virus induced cytopathology.

·       However, unlike HBV, HAV cannot initiate a chronic infection and is not associated with hepatic cancer.

 

 

Clinical Syndromes

·       The symptoms caused by HAV are very similar to those caused by HBV.

·       Disease in children is generally milder than that in adults and is usually asymptomatic.

·       The symptoms occur abruptly 15 to 50 days after exposure.

·       Initial symptoms include

o   Fever,

o   Fatigue,

o   Nausea,

o   Loss of appetite,

o   Abdominal pain,

o   Dark urine (bilirubinuria),

o   Pale stool,

o   Jaundice,

o   Itch.

·       Jaundice is observed in 70% to 80% of adults but in only 10% of children (<6 years of age).

·       Symptoms generally decrease during the jaundice period.

·       Complete recovery occurs 99% of the time within 2 to 4 weeks of onset.

·       Fulminant hepatitis in HAV infection occurs in one to three persons per 1000 and is associated with an 80% mortality rate.

Laboratory Diagnosis

·       Specific serologic tests demonstrate anti-HAV IgM

·       Enzyme linked immunosorbent assay (ELISA) 

·       Radioimmunoassay

Treatment, Prevention, and Control

·       Immune serum globulin

·       Killed HAV vaccines approved by U.S. – FDA for Children.

·       The spread of HAV is reduced by interrupting the fecaloral spread of the virus.

·       This is accomplished by avoiding potentially contaminated water or food, especially uncooked shellfish.

·       Proper hand washing

·       Chlorine treatment of drinking water.