School of Pharmacy

Department of Clinical Pharmacy

JFK- Clinical Presentation

Topic: Hepatitis B Virus

Student Odaka M. Harris

December 6, 2023
1
 Objectives
• The aim of this presentation is for learners to
understand the prevalence, causes, risk,
effects, symptoms and management of
Hepatitis B Virus.

2
 Outline
• Introduction
• Definition
• Risk factors
• Clinical Pathophysiology
• Finding
• Investigation
• Management

3
 Introduction
• Hepatitis B is infectious disease caused by HBV
that affects the liver. It can cause both acute and
chronic infections.
• Range in severity from asymptomatic to
symptomatic, progressive disease.
• The virus may be detected within 30 to 60 days
after infection and can persist and develop in to
chronic hepatitis B.
• The incubation period is 75 days on average but
can vary from 30 to 180 days.
4
 Structure
• HBV a member of the hepadnavirus group
• Double-stranded DNA viruses which replicate by
reverse transcription.
• 42-nm in size
• HBV express three main antigen:
1. HBsAg – outer envelope of the surface protein
known as Australia antigen. It indicates current
hepatitis B infection.
2. Hubcap – (core antigen) a viral protein, it is an
indicator of active viral replication. It is not secreted
but ‘particulate’ and does not circulate in the blood.
5
• It is detected in hepatocytes after biopsy
• The presence of both Hubcap and HBeAg
proteins together acts as a marker of viral
replication and antibodies to these antigens are
a marker of declining replication.
3. HBeAg – it is an indicator of active viral
replication, can be transmitted on to another
person. It is considered as ‘nonparticulate’ or
‘secretory’.

6
7
 Epidemiology
• 2 billion people have evidence of past and
present infection with HBV.
• 240 million are chronic carriers of HBV surface
antigen (HBeAg).
• Acute hepatitis B – case fatality rate 0.5 – 1%
• Chronic hepatitis B – 650,000 people die each
year from the complications of CHB.
• Liberia prevalence rate of chronic HBV stands at
10% and 519 HBV related
• death according to the global hepatitis B virus
report on Liberia (Liberia 2019). 8
 Pathogenesis
• HBV primarily interferes with liver functions by
replicating in hepatocytes.
• Virons bind to the host cell via the viral surface
antigen and are subsequently internalized by
endocytosis. HBV specifce receptors are
expressed primarily on the hepatocytes.
• An HBV protein traps protons and Cl- , and
induces the expression of collagen in the liver,
which forms potent hydrogen bond with
trapped protons
9
• The presence of collagen in the liver marks the
progression to fibrosis
• Virus can cause inactivation tumor suppressor
genes, or activation of oncogenic genes like
cyclin A
• Translocation and chromosomal arrangements
also have been seen.

10
11
 Clinical presentation
Acute Infection
• Symptoms of acute HBV infection are non-
specific and include fatigue, poor appetite,
nausea, vomiting, abdominal pain, low-grade
fever, juandice, and dark urine.
• Itchy skin is a possible symptom of all hepatitis
virus types
• Liver tenderness, hepatomegaly, and
splenomegaly

12
Chronic Infection
• When it persists longer than six months
• Asymptomatic or may be associated with a
chronic inflammation of the liver – chronic
hepatitis
• It can lead to liver cirrhosis
• Nephropathy, anemia, jaundice, fever, skin rash
and polyarteritis.

13
 Transmission
• Exposure to infectious blood or body fluids
containing blood
• Possible forms of transmission include sexual
contact and blood transfusions
• Re-use of contaminated needles and syringes and
vertical transmission from mother to child during
childbirth
• Can be transmitted between family members
within households, possibly by contact of non-
intact skin or mucous membrane with secretions
or saliva containing HBV.
14
 Multiplication
• One of a few known non-retroviral viruses which
use reverse transcription.
• The virus gains entry into the cell by binding to
receptors on the surface of the cell and entering
it by endocytosis meddiated by either clathrin or
caveolin-1
• Following endocytosis, the virus membrane fuses
with the host cell’s membrane, releasing the
nucleocapsid in to the cytoplasm

15
• The core proteins dissociate from the partially
double stranded viral DNA, which then made
fully double stranded (by host DNA
polymerases) and transformed in to covalently
closed circular DNA (cccDNA) that serves as a
template for transcription of four viral mRNAs.
• The largest mRNA, (which is longer than the
viral genome), is used to make the new copies
of the genome and to make the capsid core
protien and the viral RNA-dependent-DNA-
polymeras.

16
17
 Diagnosis
• Evaluation of the patient’s blood for : HBsAg,
hepatitis B surface antibody (HBsAb), and
hepatitis B core antibody (HBcAb)
• Presence of HBsAg indicates that the person is
infectious
• Presence of HBsAb indicates recovery and
immunity from HBV infection or successful
immunization against HBV.
• HBcAb appears at the onset of acute HBV
infection, but may also indicate chronic HBV
infection. 18
Serum transaminases
• Once an individual has been diagnosed with
chronic HBV infection, follow-up testing must be
performed for alanine aminotransferase (ALT), a
marker of liver cell inflammation.
HBV-DNA
• The presence of HBV-DNA in serum or plasma
denotes active HBV infection and depending on
the viral load, correlates with the infectivity of
the patient.

19
 Risk groups for Hepatitis B
• Children of immigrants from areas where there
is high prevalence of hepatitis B.
• Infection drug abuse
• Infants born to infected mothers.
• History of sexually transmitted diseases,
multiple sex partners, homosexual relations
• Household contacts of chronically infected
individuals.
• Healthcare & public safety workers
• Hemodialysis patients
20
 Prevention
Vaccines
Most vaccines are given in three doses over a course
of months
The first dose is recommended within 24 hours of
birth with either two or three more doses given
after that
For newborns of HBsAg-postive mothers: the
combination of vaccine plus hepatitis B
immunoglobulin is superior to vaccine alone
Tenofovir give in the second or third trimester can
reduce the risks of mother to child transmission21
 Goals of treatment
• Suppression of HBV replication to
undetectable levels
• Decrease hepatic necroinflammation and
fibrosis
• Prevent progression to cirrhosis, liver failure
and HCC

22
 Treatment
• None of the available drugs can clear the infection but can
reduce virus load
These include antiviral drugs (Nucleoside/Nucleotide
Analogues)
• Lamivudine (Epivir) LAM
• Adefovir (Hepsera) ADV
• Tenofovir (Viread) disoproxil fumarate (TDF)
• Tenofovir alafenamide (TAF)
• Telbivudine (Tyzeka) TBV, (2nd line treatment)
• Entecavir (Baraclude) ETV
• Emtricitabine
MOA: mainly act by inhibition of HBV-DNA polymerase
enzyme activity resulting in decrease of viral replication. 23
 Injectables in HBV treatment
The two immune system modulators
(Alpha-interferon (IFN)
• Interferon alpha-2a
• PEGylated interferon alpha-2a (Pegasys)
MOA:
• Enhances phagocytic activity of macrophages
• Inhibits viral replication in virus-infected cells
• Increases cytotoxicity of lymphocytes for target
cells

24
25
26
27
28
29
30
 References
• Jia Q et al; Predictive effect of five hepatitis B
markers on re-vaccination time of hepatitis B
vaccine. Experimental and therapeutic medicine.
2017
• Johan Westin, et al; Management of hepatitis B
virus infection, updated Swedish guidelines 2019
• Gilead Sciences. VIREAD (tenofovir disoproxil
fumarate) package insert.
https//www.accessdata.fda.gov/drugsatfda_docs
/label/2012/021356s042,022577s002lbl.pdf.
Accessed June 20, 2017.
31