Hepatitis B Virus

Huzaifa Hamid Ahmad

Peshraw Karim Abdurrahman
Shanyar Kadir Hamakarim
Shkar Dilshad Abdulkarim
Shvan Omar Siddiq
 What is hepatitis?

Causes of Hepatitis:
drugs
toxins
alcohol
viral infections (A, B, C, D, E)
other infections (parasites, bacteria)
physical damage
 Liver

Functions
Stores sugar needed for energy
Absorbs good nutrients
Breaks down poisons (toxins) and drugs
Makes important proteins that help build new tissue and
repair broken tissue
Produces bile, which helps remove waste from the body
 Hepatitis Terms

Acute Hepatitis: Short-term hepatitis.

Body’s immune system clears the virus from the body
within 6 months

Chronic Hepatitis: Long-term hepatitis.

Infection lasts longer than 6 months because the body’s
immune system cannot clear the virus from the body
 Hepatitis B Virus

CDC website: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/hep_b/slide_1.htm

 Hepatitis B

What is it?
Hep B is a serious disease caused by a virus that infects
the liver

Can cause lifelong infection, cirrhosis (liver

scarring), liver cancer, liver failure and death
 Structure

Family: Hepadnaviridae
Hepa: for liver
Dna: for Deoxyribonucleic acid
Virion (aka Dane particle):
Outer lipid envelope
Icosahedral nucleocapsid core composed of protein
Outer envelope proteins:
Binding & entry into susceptible cells
Size: small, 42 nm in diameter
 Genome

Circular DNA
Unusual, partially double stranded
Long strand: 3020–3320 nucleotides
Short strand: 1700–2800 nucleotides

One end of the long strand is linked to the viral DNA

polymerase
Nomenclature for Hepatitis B Virus
components
Hepatitis B Virion, Dane particle and HBsAG
 HBV: Replication

Reverse transcription: one of the mRNAs is replicated

with a reverse transcriptase making the DNA that will
eventually be the core of the progeny virion
RNA intermediate: HBV replicates through an RNA
intermediate and produces and release antigenic decoy
particles.
Integration: Some DNA integrates into host genome
causing carrier state
 Clinical outcomes of Hepatitis B
infections

From Murray et. al., Medical Microbiology 5th edition, 2005, Chapter 62, published by Mosby Philadelphia,,
Determinants or acute and chronic HBV
infection

From Murray et. al., Medical

Microbiology 5th
edition, 2005, Chapter
66, published by Mosby
Philadelphia,,
 Transmission of HBV
Perinatal transmission Horizontal transmission

Perinatal
• 90% of • 6% of
infected Mother Host
people
infants infected over
become the age of 5
chronically become
infected chronically
infected
Infant
Recipient
Child-to-child
Contaminated needles
Sexual contacts
Healthcare worker
CDC. Available at: http://www.cdc.gov/hepatitis. Accessed December 2006. Blood transfusion
Lee WM. N Engl J Med. 1997;337:1733-1745.
Lavanchy D. J Viral Hepat. 2004;11:97-107.
What are some common myths and
misconceptions about Hepatitis B?

Hepatitis B is NOT transmitted through food/water.

Hepatitis B is NOT transmitted through casual contact

such as hugging or shaking hands.

Hepatitis B is NOT transmitted through kissing, sneezing

or coughing.

Hepatitis B is NOT transmitted through breastfeeding.

 Diagnostic tests
HBsAg HBcAb HBcAb HbsA
HBeAg Windo
HBV-DNA IgM IgG b IgG
w
period
Acute
infection + + - - only
HBc Ab
is +
Prior
infection - - + +
Chronic
infection- + + + -
carrier
Immunizat
ion - - - +
 Hepatitis B acute infection

Note:
Pattern of
serological
markers
varies
depending
on
whether
the
infection if
acute or
chronic

CDC website: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/hep_b/slide_3.htm

 Chronic Hepatitis B infection

Notes:
In patients with chronic
HBV infection, both HBsAg
and IgG anti-HBc remain
persistently
detectable, generally for
life. HBeAg is variably
present in these patients.
The presence of HBsAg for
6 months or more is
generally indicative of
chronic infection. In
addition, a negative test for
IgM anti-HBc together with
a positive test for HBsAg in
a single serum specimen
usually indicates that an
individual has chronic HBV
infection.

http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/hep_b/slide_4.htm
 Who is at highest risk?

Injection drug users

Sex partners of those with Hep B
Sex with more than one partner
Men who have sex with men
Living with someone with chronic Hep B
Contact with blood
Transfusions, travel, dialysis
 Prevention

Prevent perinatal HBV transmission

Routine vaccination of all infants

Vaccination of children in high-risk groups

Vaccination of adolescents

Vaccination of adults in high-risk groups

 Hepatitis B Vaccine

Composition Recombinant HBsAg

Efficacy 95% (Range, 80%-100%)

Duration of
Immunity 20 years or more

Schedule 3 Doses

Booster doses not routinely recommended

 Symptoms

Nausea
Loss of appetite
Vomiting
Fatigue
Fever
Dark urine
Pale stool
Jaundice
Stomach pain
Side pain

A person may have all, some or none of these

 Treatment options

FDA approved
Interferon Alfa
Lamivudine – reverse transcriptase inhibitor
Adefovir – nucleotide analogue that inhibits viral
polymerase
Investigational
Tenofovir – adenine nucleotide analogue
Approved for HIV
Entecavir – guanosine analogue, highly selective for the
HBV polymerase
 Hepatitis B epidemiology

1/3 of world’s population

has been infected
350 million with chronic
disease
15-25% of these die due to
liver related diseases
1 million deaths annually
United States
1.25 million chronic carriers
5000 deaths annually

Figure 66-9. Worldwide prevalence of hepatitis B

carriers and primary hepatocellular carcinoma.
(Courtesy Centers for Disease Control and
Prevention, Atlanta.)
 CDC website: http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/hep_d/slide_1.htm
Notes:
HDV infection can be acquired either as a co-infection with HBV or as a superinfection of persons with chronic HBV
infection. Persons with HBV-HDV co-infection may have more severe acute disease and a higher risk of fulminant
hepatitis (2%-20%) compared with those infected with HBV alone; however, chronic HBV infection appears to occur
less frequently in persons with HBV-HDV co-infection. Chronic HBV carriers who acquire HDV superinfection usually
develop chronic HDV infection. In long-term studies of chronic HBV carriers with HDV superinfection, 70%-80%
have developed evidence of chronic liver diseases with cirrhosis compared with 15%-30% of patients with chronic
HBV infection alone.
Key features of Hepatitis Delta Virus

•Single stranded, self complementary RNA,

encapsidated in HbsAg

•Small, amorphous particle

•RNA encodes one protein: delta antigen

•Replicates via RNA directed RNA synthesis,

catalyzed by host RNA polymerase II
 Key features of Hepatitis Delta Virus

•Delta antigen required for replication, role unknown

•Dependent on HBV as a “helper”

•HBV provides HbsAg

•May be acquired as co-infection with HBV, or

superinfection of HBV infection

•Exacerbates HBV induced disease

 Hepatitis Delta Virion

From Murray et. al., Medical

Microbiology 5th edition, 2005,
Chapter 66, published by Mosby
Philadelphia,,
Figure 66-14
 Consequences of hepatitis B and delta virus infection

Figure 66-15. Consequences of deltavirus infection. Deltavirus (d) requires the presence of
hepatitis B virus (HBV) infection. Superinfection of a person already infected with HBV
(carrier) causes more rapid, severe progression than co-infection (shorter arrow).

From Murray et. al., Medical Microbiology 5th edition, 2005, Chapter 66, published by Mosby Philadelphia.
Thank You 