HEPATITIS C. United States 3-4 M Americas 12-15 M Africa 30-40 M Southeast Asia 30-35 M Australia 0.2 M WesternEurope 5 M 170-200 Million (M) Carriers.

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Presentation transcript:

HEPATITIS C

United States 3-4 M Americas M Africa M Southeast Asia M Australia 0.2 M WesternEurope 5 M Million (M) Carriers Worldwide Hepatitis C: A Global Health Problem EasternEurope 10 M Far East Asia 60 M

VirusHepatitis C FamilyFlaviviridae GenusHepacivirus Virion60 nm spherical EnvelopeYes GenomessRNA Genome size9,4 kb StabilityEther-sensitive, acid-sensitive TransmissionParenteral PrevalenceModerate Fulminant diseaseRare Chronic diseaseOften OncogenicYes Characteristics of hepatitis C viruses

HEPATITIS C PATHOGENESIS

HEPATITIS D

VirusHepatitis D FamilyUnclassified GenusDeltavirus Virion35 nm spherical EnvelopeYes (HBsAg) GenomessRNA Genome size1,7 kb StabilityAcid-sensitive TransmissionParenteral PrevalenceLow, regional Fulminant diseaseFrequent Chronic diseaseOften Oncogenic? Characteristics of hepatitis D viruses

HDV INFECTION PATTERNS  COINFECTION  ACUTE SIMULTANEOUS INFECTION WITH HBV AND HDV  OFTEN RESULTS IN FULMINANT INFECTION (70% CIRRHOSIS)  SURVIVORS RARELY DEVELOP CHRONIC INFECTION (< 5%)

HDV INFECTION PATTERNS  SUPERINFECTION  RESULTS IN HDV SUPERINFECTION IN AN HBsAg CARRIER (CHRONIC HBV)  CAN OCCUR ANYTIME DURING CHRONIC DISEASE  USUALLY RESULTS IN RAPIDLY PROGRESSIVE SUBACUTE OR CHRONIC HEPATITIS

HDV Transmission: OralNo PercutaneousCommon SexualYes, rare PerinatalNo Incubation period days JaundiceUnknown Fulminant2 – 7.5% Diagnostic tests: Acute infectionIgM anti-HDV Chronic infectionIgG anti-HDV, HBsAg + ImmunityNot applicable Case-fatality rate1 – 2% Chronic infection: Superinfection80% Coinfection< 5%

HEPATITIS E

VirusHepatitis E FamilyCaliciviridae GenusUnnamed Virion30-32 nm, icosahedral EnvelopeNo GenomessRNA LINEAR Genome size7,6kb StabilityHeat-stable TransmissionFecal-oral PrevalenceRegional Fulminant diseaseIn pregnancy Chronic diseaseChronic and acute OncogenicNo HEPATITIS E VIRUS

Feco oral transmission Primary replication in the GI tract Liver replication releases the virus in the bile and stool as well as in the blood Non cytopathic damage immune mediated Cholestatic hepatitis is often present PATHOGENESIS

 Contaminated water supplies in tropical or subtropical developing countries  Mainly young adults  Can infect primates, swine, sheep, rats  Swine may be reservoir of infection in North America (attenuated virus)  Maternal-infant transmission occurs and is often fatal mortality might reach up to 20 %  Contaminated water supplies in tropical or subtropical developing countries  Mainly young adults  Can infect primates, swine, sheep, rats  Swine may be reservoir of infection in North America (attenuated virus)  Maternal-infant transmission occurs and is often fatal mortality might reach up to 20 % Epidemiology

Clinical features Incubation period 2-8 weeks Typically self limiting disease resolving without sequelae Clinical manifestation similar to HAV just with higher mortality 1% vs 0.2% Severe infections during pregnancy mortality up to 20% Bilateral involvement of cervical nerve roots and/or plexus, elevated liver function tests, and abnormal CSF are typical features of HEV-associated Neurologic amyotrophy. The pathogenesis involves possible immune-mediated mechanisms.

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