HEPATITIS D
GROUP 4 PRESENTATION
• Hepatitis D virus is a defective virus; cannot replicate by itself; depends on
Hepatitis B virus for its survival
• Hepatitis D virus is taxonomically unclassified though resembles viroids(small
single-stranded, circular RNAs that are infectious pathogens.[1][2]
Unlike viruses,
they have no protein coating) hepatitis d has core proteins.
• It is also called delta antigen since it contains HDAg surrounded by the HBsAg
• The morphology:
• Circular, negative sense ssRNA
• • Protein coat made up of single protein called hepatitis D antigen (HDAg)
• • Surrounded by envelope protein derived from HBsAg from hepatitis B virus;
hence it is called defective virus
PATHOGENESIS
• Transmission is similar to that of HBV and HCV. Parenteral route is the most common
mode; followed by sexual and vertical routes.
• HDV and HBV Association
• The association of HDV with HBV is of two types :
• • Co-infection: It occurs when a person is exposed simultaneously to serum containing both
HDV and HBV. • Hepatitis B virus infection sets in first so that HBsAg becomes available for
HDV. • This is usually a transient and self-limited condition; clinically indistinguishable from
acute hepatitis B infection . • It rarely progresses to chronic stage; at a rate similar to that o
f HBV infection alone(hepatitis B is suppressed by hepatitis d probably due to the use of its
antigen by hepatitis d). • Vaccination against hepatitis B prevent against HDV.
• • Super-infection: It occurs when a chronic carrier o f HBV is exposed to serum containing
HDV. This results in disease 30-50 days later which may have two phases :
• Acute phase in which HDV replicates actively with high transaminase
levels with suppression of HBV .
• • ChroniC phase in which HDV replication decreases, HBV replication
increases, transaminase levels fluctuate, and the disease progresses
to cirrhosis and hepatocellular carcinoma ( Mortality rate is above
20%)- activation of chronic hepatits B.
• Nb: transaminases regarded here are the alanine transaminase that
are markers of liver damage.
LABORATORY DIAGNOSIS
• serology
• Anti HBc antibody is the key to differentiate between co-infection and
super-infection. lgM anti HBc + lgM anti-HDV: Indicates coinfection.
lgG anti HBc + mixture of lgM and lgG anti-HDV: Indicates super-
infection.
• Molecular methods eg PCR
• HDV RNA is detectable in the blood and liver just before and in the
early days of acute phase of both co-infection and super-infection.
epidemiology
• Two epidemiologic patterns have been identified:
• 1. In endemic areas, such as Mediterranean countries (NorrhernAfrica,Southern
Europe. And Middle East) H DV is endemic among persons with hepatitis Band is
transmitted predominantly by non-percutaneous means, especially by close
personal contact
• 2. In non-endemic areas, such as the USA and Northern Europe, HDV infection is
confined to persons frequently exposed to blood and blood products, primarily
injection drug users and hemophiliacs who are infected with HBV. H DV infection
can be introduced into a non endemic population through IV drug users or by
migration of persons from endemic to nonendemic areas. • lntroduction of HDV
into non-endemic areas where HBV infection is common may lead to explosive
outbreaks of severe hepatitis with high mortality.
• Patients with HDV infection can be treated with IFN-GAMMA
Treatment
• for HBV should be continued as described earlier
• Vaccination for HBV can also prevent HDV infection. General
prophylactic measures are essentially same as That for HBV.
• THE END

HEPATITIS D and pthogenesis associated.pptx

  • 1.
    HEPATITIS D GROUP 4PRESENTATION
  • 2.
    • Hepatitis Dvirus is a defective virus; cannot replicate by itself; depends on Hepatitis B virus for its survival • Hepatitis D virus is taxonomically unclassified though resembles viroids(small single-stranded, circular RNAs that are infectious pathogens.[1][2] Unlike viruses, they have no protein coating) hepatitis d has core proteins. • It is also called delta antigen since it contains HDAg surrounded by the HBsAg • The morphology: • Circular, negative sense ssRNA • • Protein coat made up of single protein called hepatitis D antigen (HDAg) • • Surrounded by envelope protein derived from HBsAg from hepatitis B virus; hence it is called defective virus
  • 4.
    PATHOGENESIS • Transmission issimilar to that of HBV and HCV. Parenteral route is the most common mode; followed by sexual and vertical routes. • HDV and HBV Association • The association of HDV with HBV is of two types : • • Co-infection: It occurs when a person is exposed simultaneously to serum containing both HDV and HBV. • Hepatitis B virus infection sets in first so that HBsAg becomes available for HDV. • This is usually a transient and self-limited condition; clinically indistinguishable from acute hepatitis B infection . • It rarely progresses to chronic stage; at a rate similar to that o f HBV infection alone(hepatitis B is suppressed by hepatitis d probably due to the use of its antigen by hepatitis d). • Vaccination against hepatitis B prevent against HDV. • • Super-infection: It occurs when a chronic carrier o f HBV is exposed to serum containing HDV. This results in disease 30-50 days later which may have two phases :
  • 5.
    • Acute phasein which HDV replicates actively with high transaminase levels with suppression of HBV . • • ChroniC phase in which HDV replication decreases, HBV replication increases, transaminase levels fluctuate, and the disease progresses to cirrhosis and hepatocellular carcinoma ( Mortality rate is above 20%)- activation of chronic hepatits B. • Nb: transaminases regarded here are the alanine transaminase that are markers of liver damage.
  • 6.
    LABORATORY DIAGNOSIS • serology •Anti HBc antibody is the key to differentiate between co-infection and super-infection. lgM anti HBc + lgM anti-HDV: Indicates coinfection. lgG anti HBc + mixture of lgM and lgG anti-HDV: Indicates super- infection. • Molecular methods eg PCR • HDV RNA is detectable in the blood and liver just before and in the early days of acute phase of both co-infection and super-infection.
  • 7.
    epidemiology • Two epidemiologicpatterns have been identified: • 1. In endemic areas, such as Mediterranean countries (NorrhernAfrica,Southern Europe. And Middle East) H DV is endemic among persons with hepatitis Band is transmitted predominantly by non-percutaneous means, especially by close personal contact • 2. In non-endemic areas, such as the USA and Northern Europe, HDV infection is confined to persons frequently exposed to blood and blood products, primarily injection drug users and hemophiliacs who are infected with HBV. H DV infection can be introduced into a non endemic population through IV drug users or by migration of persons from endemic to nonendemic areas. • lntroduction of HDV into non-endemic areas where HBV infection is common may lead to explosive outbreaks of severe hepatitis with high mortality.
  • 8.
    • Patients withHDV infection can be treated with IFN-GAMMA Treatment • for HBV should be continued as described earlier • Vaccination for HBV can also prevent HDV infection. General prophylactic measures are essentially same as That for HBV.
  • 9.