1) HBV is a partially double-stranded DNA virus that was discovered in the 1960s and can cause both acute and chronic hepatitis B infections. 2) It is transmitted through bodily fluids and can be diagnosed through serological and molecular testing for antigens and antibodies. 3) Vaccination provides effective immunization against HBV infection and treatment options for chronic infection include immunomodulators and nucleoside/nucleotide analogs.

1. HBV in Transfusion
Medicine
Dr. Sujay Bhowmik
Resident
Dept of IH&BT
AFMC,PUNE

2. Contents
History
Classification
Structure & Genetics
Epidemiology
Transmission
Clinical outcome
Lab diagnosis
Immunization
Treatment

3. HISTORY
outbreak of jaundice 2-8
mths after smallpox
vaccine
1885
larger outbreak of jaundice
after yellow fever vaccine
1937
surface protein of HBV
discovered by BLUMBERG
was called Australian Ag
1965
Dane Cameron and Briggs
visualized the HBV virion-
Dane particle
1970
HBsAg testing of donated
blood begins
1971
HBsAg testing begins in
India
1975
Indirect Tests for HBV
anti- HBc and ALT
implemented
1987

4. AUSTRALIAN ANTIGEN

5.  Family: Hepadnaviridae
 Genus: Orthohepadnavirus
 Species: Hepatitis B virus
CLASSIFICATION

6. STRUCTURE AND
GENETICS

7. STRUCTURE
• Partially double stranded DNAvirus.
• Composed of a 27nm nucleocapsid core (HBcAg)
• Surrounded by an outer lipoprotein coat also called envelope, containing the
surface antigen (HBsAg)
• Contain DNA dependent polymerase which repair the gap in DNA template and
have reverse transcriptaseactivity.

9. MORPHOLOGY OF VIRUS
• Ultra structure shows three distinct morphology :
• Small, spherical, noninfectious particles, 17 to 25 nm in diameter.
• Tubular, filamentous form of various length.
• Complex, spherical, double shelled particle of 42 nm which is the Hepatitis B virion.

11. GENOME
• CircularDNA :
Partially double stranded
Long strand: 3020–3320nucleotides
Short strand: 1700–2800nucleotides
• Oneendof the long strand islinked to the viral DNA polymerase
• 4ORFs
• 7Proteins

15. EPIDEMIOLOGY
 Ubiquitous virus with global distribution.
 More than one third of the world’s population has been infected.
 About 5% of the world population are chronic carrier
 In endemic area of Africa and Asia infant and children are more affected
than adult
 while in low endemic area it’s reverse

17. Prevalence of chronic HBV infection
Early in life Adolescent /young
adult
Adults, welldefined
risk groups
Asia, Middle East,
Pacific islands,
Africa 6/29/2014
India, Japan
Sunil Pandey- Medical Microbiology
US, Canada

18. Risks of Transmission by Transfusion

23. AFMC BLOOD BANK JUL 18 – JUN 19
TTI POSITIVE
HIV 24
HBV 80
HCV 22
MALARIA -
SYPHILIS -

24. MODES OF TRANSMISSION
Percutaneous
I.V drug abuse
Occupational (needle stick, non-intact skin)
Therapeutic (contaminated equipment , unsafeinjections)
Transfusions and transplants from infectiousdonors
Permucosal
Sexual contact with infectedpartner
Infected mother (perinatal)

26. PHASES OF HEPATITIS B

27. Clinicaloutcomes

28. DIAGNOSIS
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29. LABORATORY DIAGNOSIS
1. SEROLOGICAL METHODS
• ELISA
• Rapid test
2. MOLECULAR METHODS (NAT/PCR)
• Detection in window period
• Fulminant hepatitis
• HBsAg –ve
• Response

30. SEROLOGICAL METHODS
Three clinically useful antigen-antibody systems :
• Hepatitis surface antigen(HBsAg) and antibody to it (anti-HBsAg)
• Antibody (anti-HBc IgM and anti-HBc IgG) to core antigen (HBcAg)
• Hepatitis e antigen (HBeAg) and antibody to it (anti-HBeAg)

31. 31
HBsAg- anti-HBs system:
 HBsAg appears 1-2 weeks (late up to 11-12 weeks) after exposure,
 persists for 1-6 weeks( even 5 months) in acute hepatitis B.
 In chronic patients or carrier, HBsAg persist many years
 HBsAg is the marker of infectivity
 Found in blood and secretions: saliva, urine, semen, tears, sweat and breast milk
 Anti-HBs Ab appear after HBsAg disappear
 Anti-HBs is protective antibody, can persist for many years

32. HBcAg—anti-HBc system
 HBcAg can be found in the nuclei of liver cells, no free HBcAg in serum
 HBcAg is the marker of replication of HBV
 Anti-HBc IgM is a marker of acute infection and acute attack of chronic infection .
 Anti-HBc IgG is the marker of past infection, high titer means low level replication .
32

33. HBeAg—anti-HBe system
33
 HBeAg is a soluble antigen
 HBeAg is a reliable indicator of active replication of HBV
 Anti-HBe is a marker of reduced infectivity.

34. Hepatitis B acute infection

35. Chronic Hepatitis Binfection

37. MOLECULAR METHODS
PCR/ NAT
• Can detect levels as low as 0.001pg (200to 400 genomic equivalents)

38. Reduction in window period
SEROLOGICAL METHODS :
3RD GEN ELISA : 50 Days
4TH GEN ELISA: 30 Days
MOLECULAR METHODS :
NAT MP: 30 Days
NAT ID : 25 Days

39. IMMUNIZATION
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40. HEPATITIS B VACCINE
• Hepatitis B vaccines available since early 1980’s.
• 1982 (plasma), 1986 (recombinant)
• Third generation vaccines( mammalian cell recombinant vaccines)
• First recommended for high risk groups only
• In 1991, the Global Advisory Group of EPI (Expanded Program on Immunization)
integrating the hepatitis B vaccination into national immunization programs
• Monovalent or in combination with other vaccines
• High immunogenicity (three dose, 95-99%) , Long-term protection

41. PRE EXPOSURE IMMUNIZATION
1. Infants (Universal immunization)
2. Infants and adolescents not vaccinated previously (catch-up vaccination)
3. Person with occupational risk
4. Haemodialysis patients
5. Recipients of blood and blood products
6. Susceptible drug abusers.
7. Sexually active men or women
8. Jail inmates
9. Household contacts and partners of HBV carriers
10. Population with a high incidence of disease
11. Travellers to area of high HBV endemicity
12. Transplant candidates.

42. PREVENTION & IMMUNOPROPHYLAXIS
Hepatitis B immunoglobulin (HBIG) :
• Effective for passive immunization if given prophylactically within hours
of infection.
• Hepatitis vaccine should always be given with HBIG.
• Indicated for sexual contacts , babies born to HBsAg+ mothers and parenteral
exposure (needle stick).
• 0.06ml/Kg HBIG plus first dose of Hepatitis B Vaccine and continue vaccine course.

43. MANAGEMENT
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44. MANAGEMENT–ACUTEHEPATITISB
• In healthy adults who present with clinically apparent acute hepatitis,
recovery occurs in ~ 99%
• Antiviral therapy is not required.
• In rare instances of severe acute hepatitis B, institution of antiviral therapy
with a nucleoside analogue (entecavir or tenofovir)

45. MANAGEMENT OF CHB
The currently approved treatment options include :
• Immunomodulatory Therapies : Conventional interferon alpha( IFNα), Pegylated
Interferon α
• Nucleoside Analogs (NA’s): Lamivudine, Entecavir, Telbivudine and Emtricitabine
• Nucleotide Analogs : Adefovir and Tenofovir

46. THANK YOU