Hepatitis A and B

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Questions and Answers

If a patient tests positive for anti-HCV antibodies and exhibits elevated levels of ALAT alongside asthenia, which specific stage of Hepatitis C infection is most likely indicated?

  • Recovery phase, where the presence of anti-HCV antibodies indicates past infection and resolved liver damage.
  • Fulminant hepatic failure, marked by rapid liver deterioration and severe systemic complications, often necessitating transplantation.
  • Acute infection phase, characterized predominantly by asymptomatic presentation and minimal liver damage.
  • Chronic infection phase, potentially progressing towards asymptomatic cirrhosis due to persistent hepatic inflammation. (correct)

In the context of Hepatitis B diagnostics, what is the clinical significance of detecting both HBsAg and HBeAg in a patient's serum?

  • It indicates a resolved infection with no ongoing viral replication; HBsAg represents residual antigen from past exposure.
  • It implies a false-positive result, as these two antigens are mutually exclusive and cannot coexist during any stage of infection.
  • It suggests active viral replication and high infectivity, as HBeAg is associated with increased viral load and transmission risk. (correct)
  • It confirms immunity to Hepatitis B, as the presence of both antigens triggers a robust antibody response and long-term protection.

Considering the genomic structure and replication strategy of Hepatitis D virus (HDV), which of the following statements accurately reflects its unique dependence on Hepatitis B virus (HBV)?

  • HDV utilizes HBV's surface antigen (HBsAg) for virion assembly and entry into hepatocytes, as HDV lacks its own envelope proteins. (correct)
  • HDV directly integrates its genome into the host cell's DNA, eliminating the need for HBV co-infection.
  • HDV employs its own reverse transcriptase to replicate its RNA genome independently of HBV.
  • HDV encodes its own polymerase, which competes with HBV polymerase for nucleotide precursors, ultimately suppressing HBV replication.

Given the differing modes of transmission among hepatitis viruses, which scenario presents the highest risk for contracting Hepatitis E virus (HEV)?

<p>Consuming undercooked shellfish harvested from waters contaminated with fecal matter. (D)</p> Signup and view all the answers

If a novel antiviral drug effectively inhibits the RNA-dependent RNA polymerase of the Hepatitis C virus, what direct consequence would this have on the viral lifecycle?

<p>Blocking the replication of the viral RNA genome, thereby preventing the production of new viral particles. (D)</p> Signup and view all the answers

Considering the pathogenesis of Hepatitis B virus (HBV), which of the following mechanisms is MOST directly responsible for the hepatocellular damage observed in chronic HBV infection?

<p>Immune-mediated response targeting HBV-infected hepatocytes, resulting in inflammation and cell death. (C)</p> Signup and view all the answers

In the context of Hepatitis A virus (HAV) infection, what immunological marker provides the most reliable evidence of recent acute infection?

<p>The detection of IgM antibodies against HAV, which signify a recent or current acute infection. (C)</p> Signup and view all the answers

What is the rationale behind using inactivated vaccines for Hepatitis A, considering the virus's biological characteristics and the host's immune response?

<p>Inactivated vaccines elicit a strong neutralizing antibody response, preventing viral entry into hepatocytes and subsequent infection. (C)</p> Signup and view all the answers

Considering the various diagnostic approaches for detecting hepatitis viruses, which method offers the highest sensitivity and specificity for quantifying the viral load of Hepatitis B virus (HBV) in a patient's serum?

<p>Real-time polymerase chain reaction (PCR) assay, which quantifies HBV DNA levels with high precision and sensitivity. (C)</p> Signup and view all the answers

Given the complexities of hepatitis virus evolution and genetic diversity, what is the most significant implication of the high mutation rate observed in Hepatitis C virus (HCV) for vaccine development?

<p>The development of a broadly protective HCV vaccine is hindered by the virus's rapid evolution and the emergence of escape mutants. (B)</p> Signup and view all the answers

Flashcards

Hepatitis A Virus

Hepatitis A is caused by the Hepatovirus, which is part of the Picornaviridae family. It has a simple strand of RNA and is a small virus (30 nm)

Hepatitis B Virus

Hepatitis B is caused by the Orthohepadnavirus, belonging to the Hepadnaviridae family. It has circular DNA that is partially double-stranded.

Hepatitis C Virus

Hepatitis C is caused by the Hepatocivirus and belongs to the Flaviviridae family. It has a single strand of RNA and an average size of 55 nm.

Hepatitis D Virus

Hepatitis D is caused by the Deltavirus. It features a circular, single-stranded RNA and is enveloped, deriving its envelope from HBV.

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Hepatitis E Virus

Hepatitis E is caused by the Hepevirus, which belongs to the Hepeviridae family. It has a single strand of RNA and is a small, resilient virus (30 nm).

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Hepatitis A Transmission

HAV transmits through the fecal-oral route.

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Hepatitis B Transmission

HBV transmits through sexual contact, parenterally, and perinatally.

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Hepatitis C Transmission

HCV transmits via blood transfusions, IV drug use, and accidental exposures.

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Hepatitis D Transmission

HDV transmits through parenteral and sexual routes.

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Hepatitis E Transmission

HEV transmits via the fecal-oral route.

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Study Notes

  • There are 5 types of hepatitis: A, B, C, D (delta) and E

Hepatitis A

  • Family: Picornaviridae
  • Genus: Hepatovirus
  • Genome: single-stranded RNA, small virus (30 nm)
  • Envelope: non-enveloped capsid icosahedral (VP1, VP2, VP3 + VP4)
  • Pathogenesis:
    • Very resistant
    • Incubation: 30 days
    • Child: asymptomatic or pseudo-flu-like forms
    • Adult: more frequent jaundice forms, asthenia
    • Complications: fulminant hepatitis
  • Diagnosis:
    • Direct: detection of Ag or genome
    • Indirect: serology (total Ac and IgM)
    • Inactivated vaccine
  • Contamination: fecal-oral transmission

Hepatitis B

  • Family: Hepadnaviridae
  • Genus: Orthohepadnavirus
  • Genome: partially double-stranded circular DNA
    • Long strand
    • Short strand: + with terminal RNA sequence
  • Envelope: lipid envelope with HBs Ag
  • Capsid: icosahedral
  • Pathogenesis:
    • Incubation: 45 days to 3 months
    • Acute infection
      • Asymptomatic (80%) but may cause jaundice, elevated ALT, rare fulminant form: hemorrhagic risk or even hepatic insufficiency
    • Chronic:
      • Adult < child (90%)
      • HBs Ag > 6 months
  • Diagnosis:
    • Direct = molecular biology, antigenemia
    • Indirect = serology ++
    • HBS = viral carriage
    • HBe = viral replication
  • Contamination: sexual +++, parenteral, perinatal

Hepatitis C

  • Family: Flaviviridae
  • Genus: Hepatocivirus
  • Genome: single-stranded RNA, average size 55 nm
  • Envelope: lipid envelope with E1 and E2 proteins
  • Capsid: icosahedral
  • Pathogenesis:
    • Incubation: 4-12 weeks
    • Acute infection: asymptomatic, elevated ALT
    • Chronic infection:
      • 80% adults / 50% children
      • Asthenia + elevated ALT + anti-HCV Ac
      • Asymptomatic cirrhosis
  • Diagnosis:
    • Indirect = serology +++ ELISA test
    • Direct = molecular biology
  • Contamination: blood: transfusions, IV drugs, STDs...

Hepatitis D (delta)

  • Not classified
  • Genus: Deltavirus
  • Genome: single-stranded circular RNA, enveloped derived from VHB
  • Derived from HBV
  • No capsid
  • Ag HD
  • Pathogenesis:
    • Liver lesions
    • Only develops in HBV patients
    • Acute → symptomatic
    • Chronic → cirrhosis
  • Diagnosis:
    • Direct = HD Ag Detection
    • Indirect = serology
  • Contamination: parenteral +++, sexual

Hepatitis E

  • Family: Hepeviridae
  • Genus: Hepevirus
  • Genome: single-stranded RNA, small (30 nm), very resistant
  • Envelope: non-enveloped, icosahedral capsid
  • Pathogenesis:
    • Incubation: 40 days
    • Unimportant human-to-human
    • Classic jaundice form
    • Severe form in pregnant women
    • Asymptomatic form in children under 15 years of age
  • Diagnosis:
    • Direct = genome detection
    • Indirect = serology (IgM)
  • Contamination: fecal-oral transmission

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