Hepatitis Viruses I Flashcards

1
Q

Hepatitis means…

A

…inflammation of the liver.

  • The causes of hepatitis are varied and include viruses, bacteria, protozoa and toxins.
  • Viral hepatitis accounts for significant cases of hepatitis
  • Some hepatitis may result in cirrhosis of liver and hepatocellular carcinoma (HCC)
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2
Q

Other Viruses that can cause liver inflammation…

A
  • Epstein–Barr virus (Herpesviridae)
  • Cytomegalovirus (Herpesviridae)
  • Varicella–zoster virus (Herpesviridae)
  • Yellow fever virus (Flaviviridae)
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3
Q

Hepatitis A Virus

A
  • Hepatitis A Virus genus of the Picornaviridae family
  • ( + ) ss RNA icosohedral naked
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4
Q

Hepatitis A Structure

A
  • small, icosahedral l (+) single stranded RNA (7.48 kb)
  • 4 structural proteins
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5
Q

Hepatitis A Replication

A
  • replicates in the cytoplasm
  • the mRNA is encoded as a polyprotein that is further cleaved to various mature proteins
  • virus assembly in the cytoplasm lvirus release as a result of cell lysis
  • difficult to propagate in vitro lseveral HAV strains
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6
Q

HAV Clinical Disease

A

•Worldwide - Higher incidence in lower socioeconomic population

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7
Q

HAV Transmission

A

•fecal–oral transmission, shellfish (oysters, clams), water, contaminated food, vegetables

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8
Q

HAV Incubation

A
  • Virus replicates initially in the enteric mucosa (incubation period 15 – 45 days, mean 25)
  • Virus can be found in feces 10-14 days before the onset, replication in intestine, followed by a period of viremia with spread to the liver lmost infections are asymptomatic
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9
Q

HAV

A

lacute hepatitis: replicate in small intestine, ldevelopment of viremia, spreads to liver

  • replicates in the liver and causes necrosis of liver lonset is sudden after 14–40 days incubation
  • The response to replication in the liver consists of lymphoid cell infiltration, necrosis of liver parenchymal cells, and proliferation of Kupffer cells. A variable degree of biliary stasis may be present
  • Cytotoxic T lymphocytes (CTLs) damage the hepatocytes
  • Initial immune response is the development of HAVspecific IgM antibody followed by appearance of IgG after a few weeks
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10
Q

HAV Symptoms

A
  • fever, poor appetite, nausea, headache, malaise, vomiting, abdominal pain, jaundice (may not develop in children), dark urine, clay-colored stool, enlarged liver
  • usually self–limiting (complete recovery), immunity is complete
  • In rare cases (~0.1%) fulminant hepatitis is associated with extensive liver necrosis
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11
Q

HAV Prevention

A
  • Immune serum globulin administered before or during incubation period. (Household members, travelers going to endemic areas)
  • Inactivated Hepatitis A Vaccine: Havrix and VAQTA Inactivated Hepatitis A virus strain HM175
  • Booster: 6-12 month after the initial dose
  • Active immunization is as effective as ISG, if given shortly after exposure.
  • 92% decline in HAV since vaccination (1995)
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12
Q

Hepatitis B Virus

A
  • Hepatitis B Virus genus of the Hepadnaviridae family
  • partially ds DNA icosohedral enveloped
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13
Q

Hepatitis B Structure

A
  • Small (42 nm), circular, smallest DNA virus
  • Partially double stranded DNA 3200 nucleotides associated with viral DNA polymerase
  • HBcAg (core antigen) encloses DNA
  • HBeAg (encoded by core gene), glycoprotein
  • HBsAg (surface antigen) surrounds the core, envelope
  • 4 subtypes of HBsAg (adw, ayw, adr, ayr)
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14
Q

HBV Replication

A
  • Full length (+)RNA is inserted into core
  • Reverse transcriptase synthesizes a full length (–)DNA strand using the (+)RNA template
  • (–)DNA template is used to make a variable short piece of (+)DNA l RNA degrades in the core
  • Virus assembly in the cytoplasm
  • Acquires envelope from Golgi or ER membranes
  • Released from the cells
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15
Q

HBV Epidemiology

A
  • Worldwide, in the United States 0.1 to 0.5% of the population are chronic carriers
  • 50% infections in U.S. are sexually transmitted
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16
Q

HBV Pathogenesis

A
  • Immunologic responses
  • Serum-sickness like rash and arthritis, jaundice
  • Circulating immune complexes activate complement system
  • CTL kills infected cells causing damage to liver, type IV hypersensitivity
  • Insufficient T-cell function increase the risk of chronicity
17
Q

HBV Clinical Disease

A
  • acute hepatitis B (similar to Hepatitis A) but differs in longer incubation period (mean 60-90 days)
  • onset tends to be slow
  • mode of transmission is usually through body fluid (blood, saliva, semen, cervical secretions, blood products)
  • vertical transmission to infants tends to be more severe
  • chronic carriers arise in about 10% of infections
18
Q

Chronic HBV

A
  • 10-20% adult cases become chronic
  • ~90% chronicity in newborns after transmission
  • main reservoirs of infection - liver
  • Virus replicates in the liver
  • Integrated HBV DNA may be present
  • Covalently closed circular DNA (cccDNA) in the nucleus forms the mini-chromosome and provides stability to HBV DNA for persistence
  • demonstrate HBsAg in serum (for life)
  • Anti-HBc and HBeAg are also seen in chronicity
  • Cirrhosis of liver
  • Hepatocellular carcinoma (HCC) (200–fold increased risk)
  • HBV DNA found in nearly all HCC cases
  • Mechanisms of role of HBV in HCC is unclear
19
Q

HBV Diagnosis Acute Hepatitis B

A
20
Q

HBV Diagnosis Chronic Hepatitis B

A
21
Q

HBV Treatment

A

•Interferon-alpha, Lamivudine (3TC), nucleoside and nucleotide analogs are active

22
Q

HBV Prevention

A
  • hyperimmune globulin (passive)
  • HBV Vaccine: HBsAg from carriers (fixed) ,HBsAg synthesized in yeasts, humoral immunity