Hepatitis B And C Flashcards

1
Q

Hepatitis B epidemiology

A

33% have been infected at some point
- > 8% is seen in Asia Africa and western pacific regions

There is a 400 million population that has chronic HBV
- 10% of HIV patients have chronic HBV

Children have significantly higher carrier rates than adults

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2
Q

HBV facts

A

Also called “serum hepatitis”

Is a hepaDNAviridae virus

  • partially circular DsDNA virus
  • 3200 nucleotide genome (smallest DNA virus known to made)

Is 42nm with “Dane particles”
- Also has 22nm subviral particles attached to it

Is enveloped and complexed capsid

Encodes for a RT transcriptase even though its a DNA virus

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3
Q

How does HBV replicate

A

Replicates only in hepatocytes

Goes DNA -> RNA -> DNA again (unique)

  • uses reverse transcriptase to revert to an RNA intermediate and then uses host cell machinery to go back to DNA
  • also releases “decoy particles” to prevent finding
  • makes multiple mRNAs and the 3.5kb RNA template is the one that is converted back to DNA

targets sodium taurocholate co-transporter polypeptide receptor (NTCP) on hepatocytes

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4
Q

Pathogenesis of HBV

A

Symptoms are caused by cytotoxic cell-mediated responses to infections

90-95% of acute infections spontaneously resolve

  • if infant of immunocompromised is actually asymptomatic.
  • **symptoms are actually good in this case and it means your immune system is working!!

Transmission:

  • cutaneous or mucosal exposure to blood/body fluids (not found in urine/sweat/stool)
  • perinatal transmission (high chances)

*can go through horizontal (infected household contact -> child) or vertical (infected mother directly to infant)

Symptoms: (if any)

  • rashes
  • right quad pain
  • serum sickness symptoms
  • jaundice
  • renal damage (chronic only)
  • cirrhosis (chronic only)
  • hepatic cell carcinomas (chronic only)

antiboides to the surface capsid proteins (HBsAg) = immunity of disease

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5
Q

HBV serology

A

HBsAg = surface antigen

  • signals an active infection of HBV is present
  • presence alone DOESNT mean the patient is infectious
  • is the vaccination target**

HBcAg = core/capsid antigen

HBeAg = excreted antigen

  • signals active infection
  • alone can signal the patient is infectious**

HBV DNA
- found in PCR and can signal active or chronic infection of HBV

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6
Q

Antibodies for HBV

A

Anti-HBs

  • presence = acclimation of clearance or acute HBV infection has occurred
  • is NON-DETECTABLE while antigen is being produced
  • usually presents around 5 months in
  • **seroconversion and is protective

Anti-Hbe

  • presence = had an infection at one point
  • is NON-DETECTABLE while antigen is being produced
  • starts after a month into infection
  • **is non protective (can get infected again)

Anti-HBc

  • earliest detectable antibody and indicates an acute active HBV infection (IgM)
  • is non protective (can get infected again)
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7
Q

When during an HBV infection do you see elevated ALT/AST?

A

2-5 months after exposure

- correlates directly with increases of anti-HBC

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8
Q

What is the “eclipse period” in an HBV infection?

A

Time frame during a typical HBV infection where you cant detect antigen or antibodies to the virus

Usually shows around 4-5 months and 5-6 months

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9
Q

How to tell if a patient is in an acute or chronic HBV infection?

A

Acute = IgM and anti-HBc and HBsAg are present

Chronic = IgG and anti-HBc and Anti-HBs are present

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10
Q

Acute HBV infection symptoms

A

Long incubation period (1-6 months)

Symptoms:

  • ALT/AST >1
  • anorexia
  • malaise
  • nausea
  • right upper quadrant
  • fever/rash
  • jaundice/dark urine/pale stools (if liver failure)
  • arthritis

children have high risks of asymptomatic periods

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11
Q

What levels of HBV particles are required for Chronic HBV to be present?

A

> 10^5 IU/mL

Results in:

  • greater transmission
  • greater hepatocellular carcinoma

can degrade into extrahepatic vasculitis/arthritis/glomerulonephritis/ fulminant hepatitis

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12
Q

Can the HBV vaccine prevent hepatocellular carcinoma?

A

YESS
- 80% of these cancers are caused by HBV chronic infections and can be halted if a vaccine is given, even if already infected

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13
Q

HBV treatment options

A

HBV immunoglobulin and vaccine = acute/prophylaxis

Chronic HBV:

1) RT polymerase antivirals
- Lamivudine/entecavir/Tenofovir

2) nucleoside analogs
- adefovir/dipivoxil/famciclovir

3) high dose Pegylated interferon (IFN-a)

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14
Q

HBV vaccine

A

Is a recombination s. Cerevisidae antigen with attenuated HBsAG

  • the HBsAg self assembles into “pseudovirons” that replicate like normal HBV but cant induce infection properly
  • *Vaccine is recommended for everyone pretty much (except pregnant women if given alone!!)

***new Heplosav-B vaccine (experimental) can be given in adults)

pregnancy = HB immunoglobulin +HBV vaccine

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15
Q

HCV epidemiology

A

150 million worldwide with highest incidence in the Middle East

3.6 million in US

Is seen in 90% of HIV-infected IV drug users (strong correlation to both factors separately)
- as well tattoos

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16
Q

HCV facts

A

also called “non-A/non-B post transfusion hepatitis”

Is a part of the flaviviridae family

30-60 nm
- enveloped/icosahedral capsid

(+)ssRNA virus

  • possess two envelop glycoproteins E1/E2
  • possesses one capsid protein C

has high quasispecies and mutation rates since it encodes for a RNA-dependent RNA polymerase that is super error prone

17
Q

How does HCV replicated?

A

E2 interacts with the scavenger receptor class B type 1 (SCARB1) and CD81 tetraspanin receptors to enter host cells

This is translated in the cytoplasm and cleaved into structural and non-structural proteins
- buds through the ER after replication occurs

18
Q

HCV pathogenesis

A

Incubation = 4-20 weeks

mostly seen in IV drug users, less sexual activity and no fecal-oral

Acute infection is 85% asymptomatic
- does have a high percentage of cirrhosis risk (20%) due to viral heterogeneity from mutant strains

70% of infections are persistent infections

25% of patients will show classic hepatitis symptoms

19
Q

Chronic HCV specific sign/symptoms

A

NO jaundice is seen

Histological changes (best predictors) 
- more inflammation/fibrosis = likely to develop cirrhosis 

Usually has no early symptoms, but does have evidence of hypersplenisum/cryoglobulinemia

men and immunocompromised people are at highest rates of chronic HCV

20
Q

Diagnosis and treatment of HCV

A

1 = anti-HCV/HCV RNA presence via ELISA/PCR/RT-PCR

  • seroconversion usually is noted after 7-31 weeks (before this and you may not see these)
  • need to screen multiple times in order to tell acute from chronic however

Treatment:

  • limit alcohol consumption
  • preventive measures
  • pregulated IFN/ribivarin (watch for depression and serious flu-like symptoms, no longer recommended)
  • various other antiviral drug combinations