Hepatitis Viruses Flashcards
Types of Hepatitis
Viral hepatitis
Alcoholic hepatitis
Non alcoholic steatohepatitis
Autoimmune hepatitis
Neonatal hepatitis
Genome of Hepatitis viruses
Only HBV - DNA
Others - RNA
HAV belongs to which family
Picornaviridae (Enterovirus 72)
HBV belongs to which family
Hepadnaviridae
HCV belongs to which family
Flaviviridae
HDV belongs to which family
Deltaviridae
Relies on HBV
HEV belongs to which family
Caliciviridae Now Herpeviridae
Mode of infection and incubation period of HAV and HEV
Feco- oral
IP - 15-50 Days
Mode of infection and incubation period in HBV
IP - 50-150 days
Mode - Parenteral, Sexual, Vertical
Mode of Transmission and incubation period of HCV
IP - 15-150 Days
Transmission - Parenteral, iv Blood transfusion
Which Hepatitis viruses are enveloped
HBV
HCV
HDV
Which Hepatitis virus is cultivable
HAV
Vaccines available against which hepatitis viruses
HAV
HBV
HEV
Which hepatitis virus is most common cause of Fulminant hepatitis
HDV - 5-20%
HAV - 0.1%
Which hepatitis is most common cause of Fulminant hepatitis in Pregnancy
HEV - 25%
Which hepatitis virus infection leads to Chronicity
HBV and HCV
Hepatitis G affects
Doesn’t cause human infection
Affects monocular cells
Route of transmission - blood transfusion
Can protects against HIV
Sizes of Hepatitis viruses
Hepatitis A - 27nm
Hepatitis B - 42nm
Hepatitis C - 60nm
Hepatitis E - 30nm
Genotypes and Serotypes of HAV
Serotype 1
Genotypes - 6, In humans, 1,2,3
Which genotype of HAV is M/C in world and in India
In world - Type 1
In India - 3
HAV is susceptible to
Boiling, chlorine, autoclave, Formalin
Clinical features of HAV
Fever, anorexia
Nausea/Vomiting
Jaundice
Dark urine
Pale feces
HAV Shedding in stools can be seen for how long
2 weeks prior to 2 weeks after symptoms onset
When IgM and IgG appears in case of HAV infection
IgM appears with onset of Jaundice
2-4 weeks later IgG seen
When IgM appears in case of HAV infection
IgM appears with onset of Jaundice
On Liver biopsy, Hepatitis A and Hepatitis E shows
Hepatitis A - Shows increase in Plasma cells
Hepatitis E - Shows Cholestasis (Bile plugs)
Vaccines against Hepatitis A
Formaldehyde inactivated vaccine im
Live attenuated vaccine
Formaldehyde inactivated vaccine for HAV given after age of and doses
More than 12 months
2 doses apart 6 months gap
Strains of Live attenuated vaccine
OH2
And OLA1 Strain
For postexposure prophylaxis of HAV
Immunoglobulins - within <2 weeks of exposure
Protection for 1-3 months
Vaccine against HEV
Recombinant capsid protein (China)
Genotypes of HBV
8 genotypes (A to H)
Serotypes of HBV
aYw
adr
Which genotype of HBV is most prevalent in India
D genotype
HBV is double stranded or single stranded DNA virus
HBV - Partial dsDNA virus - 2 linear strands of DNA - 1) Complete strand or minus strand 2) Incomplete or Plus strand
All DNA Viruses are have dsDNA except
ssDNA - Parvovirus
Partial dsDNA - HBV
Antigen present in HBV Viruses
P antigen - Largest, DNA polymerase, Reverse transcriptase, RNAase
C - Core Antigen
S- Surface antigen (HBSAg) - S,M,L
X - HbX - carcinogenesis
Which antigen is also known as Australia antigen
S - Surface antigen (HBSAg)
Which antigen is also known as Australia antigen
S - Surface antigen (HBSAg)
Which Antigen of HBV is responsible for carcinogenesis
X - HbX - carcinogenesis - HCC
Infectious particles of HBV
Spherical particles - 42nm
Full virions - DANE particles
Genome +, Infection +
Non infections particles of HBV
Spheres/tubular
Filaments
Genome - , Infection -
Mode of infection of HBV
Blood products
Sexual intercourse
Percutaneous
Mother to child
Needle stick injury (HBV-30%)
Pathogenesis of HBV
HBV virion entry - endocytosis - Uncoating (partial dsDNA) - cccDNA (Covalently closed Circular DNA) - then converted to complete DNA - Converted to pgRNA via translation - PgRNA is converted to Minus strand DNA with the help of Reverse transcriptase - Then minus strand DNA converted to Plus strand with the help of DNA Polymerase - Assemble in ER - Release
1st virological marker of HBV in blood
HBV DNA
1st antigen to appear in case of HBV and when it appears and disappears
HBsAg - onset of infectivity
Appears 2-6 weeks before onset of symptoms
Disappears 1-2 month after onset of jaundice
Epidemiological marker of HBV
Anti HBs - comes after gap
When HBeAg appears and what it indicates
Appears shortly after HBsAg
Indicate active infections and high infectivity
AntiHBe indicates
It indicates decrease in infectivity
Core Ag/HBcAg and AntiHBc antibodies
Not detected in blood
AntiHbc antibody - IgM (Marker of window period) and IgG
Interpretation of lab diagnosis findings in case of Acute Hepatitis B - high infectivity
HBsAg +
Anti HBs -
Anti HBc - IgM
HBeAg +
Anti HBe -
Interpretation of lab diagnosis markers in Chronic Hepatitis B - High infectivity
HBsAg +
Anti HBs -
Anti HBc - IgG
HBeAg +
Interpretation of lab diagnosis markers in HBV Recovery phase
Antibodies +ve
Anti HBs +
Anti HBc - IgM + IgG
Anti HBe +
Lab diagnosis findings in case of HBV vaccination/immunity
Anti HBs +ve
Lab diagnosis finding in case of HBV window period
Anti HBc IgM +ve
How much risk of transmission of HBV to baby if mother is HBeAg +ve
90% risk of transmission
Risk of transmission of HBV to baby if mother is HBe antibody +ve
10-15% risk of transmission
Prophylaxis of neonate born to HBV +ve mother
One arm immunoglobulins
Other arm HB vaccine (0,1,6 months)
Hepatitis B vaccine and it’s schedule
Prepared in Yeastv(Saccharomyces cerevicae)
Recombinant killed vaccine
Schedule - 0,1, 6 months
Prophylaxis of HBV in case of Needle stick injury in unvaccinated healthcare worker on basis of different sources
If HBsAg +ve : Ig + 0,1,6 vaccine
If HBsAg -ve : 0.1,6 vaccine
If Source unknown: 0,1,6 vaccine
Prophylaxis of HBV in case of Needle stick injury in vaccinated and responder healthcare worker on basis of different sources
Responder - Anti HBs >10IU/ml
No Prophylaxis needed
Prophylaxis of HBV in case of Needle stick injury in vaccinated and non responder healthcare worker on basis of different sources
Non responder - Anti HBs <10IU/ml
If HBsAg + : Ig + 0,1,6 vaccine
No Prophylaxis if HBsAg -ve or if source unknown
Carriers of HBV are classified into
If HBsAg +ve beyond 6 months
Simple carriers
Super carriers
HBV simple carriers Lab findings
HBsAg +ve
HBeAg -ve
Low DNA Polymerase
HBV Super carriers lab findings
HBsAg +ve
HBeAg +ve
High DNA Polymerase
Increased liver enzymes
Escape mutants means
No HBsAg, So anti HBs antibodies will not able to neutralize the escape mutant
Most common cause of Fulminant hepatitis
Hepatitis D
HDV Coinfection means
HBV + HDV infection together
In Iv drug users mostly leads to Fulminancy
HDV Superinfection means
Patient is already infected with HBV gets Superadded infection with HDV
Causes fulminant hepatitis
Which hepatitis virus is highly mutable and it’s most mutable protein
Hepatitis C
Most mutable protein - E2
Lab diagnosis findings of HCV
IgM HCV
Hep C Tridot testing
HCV RNA PCR - Diagnosis of choice
Morphological changes in Acute hepatitis
Bodies - Councilman bodies (Hep.C)
Spotty necrosis - Dropout necrosis
Kupffer cell hyperplasia (Macrophages)
Morphological changes of Chronic hepatitis
Ito/Stellate cells - Fibrosis
Histological finding of Hepatitis B infection
Ground glass hepatocyte (diffusely pink cells) - contains surface antigen in ER
Histological findings in case of Hepatitis C
Macrovascular steatosis (fatty changes)
Lymphoid follicles (prominent)
Histological findings of Hepatitis D infection
Microvascular steatosis
Most common cause of Sporadic Acute hepatitis in India
Hepatitis E
Most common of Fulminant viral hepatitis
HDV
Most common cause of Fulminant viral hepatitis in Pregnancy
HEV
Most common cause of transfusion related hepatitis
HBV
Most common cause of Chronic hepatitis
HBV
Which hepatitis virus have Maximum risk of potential of chronicity
HCV
Most common cause of carrier state
HBV
Most common cause of viral Hepatocellular carcinoma
HBV
Which hepatitis virus have strong association with Hepatocellular carcinoma
HCV
Extra hepatic manifestations of Hepatitis B
Polyarteritis Nodosa
Membranous glomerulopathy
Extra hepatic manifestations of Hepatitis C
Mixed Cryoglobulinemia (M/C)
Lichen planus
MPGN