Hepatitis B virus infection.

1. Hepatitis B Infection (HBV)
Uzzal chondra
Uzzal.chondra@gmail.com
Gono Bishwabidyalay,Dhaka,Bangladesh

2. HEPATITIS B
INFECTION
 Hepatitis B is a potentially life-threatening liver
infection caused by the hepatitis B virus, which
infects the liver of hominoidea, including humans. It
can cause chronic infection and puts people at high
risk of death from cirrhosis and liver cancer.

3. EPIDEMIOLOGY:
 >200 million carriers worldwide
 1 million people die each year from hepatitis B and its
complications
 Established cause of chronic hepatitis and
 cirrhosis
 Human carcinogen - cause of up to 80% of hepatocellular
carcinomas

4. GLOBAL HBV: MAJOR
GENOTYPES
A,B,C,D,G
B,C
G
A,B,C,D
D
A,D,E
F
A
D

5. HEPATITIS BVIRUS
 Hepatitis B virus is an hepadnavirus
 Has a circular genome composed of partially double-stranded
DNA
 The viruses replicate through an RNA
 intermediate form by reverse transcription
 Replication takes place in the liver
 Retains infectivity for at least 1 month at
 room temperature

6. STRUCTURE

7. CHARACTERISTICS
• Lipid envelope
• Icosahedral nucleocapsid
• Core composed of proteins
• Nucleocapsid enclosed viral
DNA
• DNA polymerase
• Outer envelope containing
embedded proteins
• Enveloped 42 nm virus

8. Hepatitis B may exist in 3 different forms:
• Spherical 22nm
• Tubular 22 nm varying length
• Double walled spherical 42 nm (Dane
particle)
no DNA in these forms
so they are not
infectious
MMMMM

9. DANE PARTICLE
 HBV virion is also referred to as Dane particle. Core antigens are
located in its center:
 HBsAg = surface (coat) protein ( 4 phenotypes : adw, adr,
ayw and ayr)
 HBcAg = inner core protein (a single serotype)
 HBeAg = secreted protein; function unknown
 HBxAg
 8 genotypes (A-H) according to overall
 nucleotide sequence variation of the genome

10. DANE PARTICLE

11. 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

12. RESISTANCE
 HBV is a relatively heat stable virus (viable
 room temperature for long periods)
 60° C for 10 hours (reduce infectivity 100- 1000 times)
 Susceptible to chemical agents(hypochlorine, gluteraldehyde)

13.  Parenteral:IV drug abusers,health workers
 are at increased risk
 Sexual:sex workers and homosexuals are at particular risk
 Perinatal (vertical): from mother (HBeAg+) to
 infant
 Though not transmissible by holding hands, sharing eating
utensils or drinking glasses, kissing, hugging, coughing,
sneezing, or breastfeeding
MODES OFTRANSMISSION

14. CONCENTRATION OF HBV IN
VARIOUS BODY FLUIDS
High Moderate Low
Blood Semen Urines
Serum Vaginal fluid Feces
Wound exudates Saliva Tears
Breast milk

15. PATHOGENESIS
• The incubation period is from 6 weeks to 6 months after
 artificial inoculation of infected blood and blood products
• HBV interferes with the functions of the liver by replicating in
hepatocytes
• HBV virions bind to the host cell via the preS domain of the
viral surface antigen and are subsequently internalized by
endocytosis
• PreS and IgA receptors interact with each other
• HBV-preS specific receptors are primarily expressed on
hepatocyte
• During HBV infection, the host immune response causes
both
 hepatocellular damage and viral clearance

16. SYMPTOMS
o Loss of appetite, nausea, vomiting, headache,
myalgia, body aches, mild fever, dark urine, and then
progresses to development of jaundice
o Itchy skin is a possible indication of all HV types
o At least 50% of infections are asymptomatic
o Tends to cause a more severe disease than Hepatitis
A
o Extrahepatic manifestations of hepatitis B are
present in 1–10% of HBV-infected patients and
include serum-sickness–like syndrome, acute
necrotizing vasculitis (polyarteritis
nodosa), membranous glomerulonephritis,
and papular acrodermatitis of childhood (Gianotti-
Crosti syndrome)

17. POSSIBLE
OUTCOMES

18. LABORATORY DIAGNOSIS
• Serum or blood tests (detect either viral antigens or antibodies)
• Hepatitis B surface antigen (HBsAg) is most frequently detected
• Hepatitis B core antigen (HBcAg)
• IgM antibodies to the hepatitis B core antigen anti-HBc IgM
• HBeAg in a host's serum means higher rates of viral replication and
enhanced infectivity
• A person negative for HBsAg but positive for anti-HBs has either
cleared an infection or has been vaccinated previously
• Individuals who remain HBsAg positive for at least six months are
considered to be hepatitis B carriers
• Carriers of the virus may have chronic hepatitis B, which would be
reflected by elevated serum alanine aminotransferase (ALT)
• PCR tests have been developed to detect and measure the amount
of HBV DNA

19. SEROLOGIC MARKERS FOR PHASES OF ACUTE AND
CHRONIC HBV INFECTION
HBsAg HBeAg IgM IgG Anti- Anti- HBV Interpretation
anti- anti- HBs HBe DNA
HBc HBc
Acute HBV Infection
+ + + + Early phase
+ ± Window phase
+ + + - Recovery phase
Chronic HBV Infection
+ + + + Replicative phase
+ + + - Low, nonreplicative
phase
+ ± + + Flare-up
+ + + Precore/core
promoter mutants

20. TREATMENT
• Acute hepatitis B infection does not usually require treatment
because most adults clear the infection spontaneously
• Treatment of chronic infection may be necessary to reduce the risk
of cirrhosis and liver cancer
• Although none of the available drugs can clear the infection, they
can stop the virus from replicating, thus minimizing liver damage
• Antiviral drugs:
• lamivudine (Epivir)
• adefovir (Hepsera)
• tenofovir (Viread)
• telbivudine (Tyzeka)
• entecavir (Baraclude)
• Immune system modulators: interferon alpha-2a and PEGylated
interferon alpha-2a (Pegasys)

21. HEPATITIS BVACCINE
 Composition Recombinant HBsAg
 Efficacy 95% (Range, 80%-100%)
 Duration of
 Immunity MORETHAN 15 years
 Schedule 3 Doses
 Booster doses not routinely recommended