Hepatitis B virus

Hepatitis B is an infectious disease caused by the hepatitis B virus (HBV) that affects the liver.

1. Hepatitis
B virus
A double stranded DNA virus, a
species of the genus
Orthohepadnavirus, and a
member of the Hepadnaviridae
family of viruses. This virus
causes the disease hepatitis B.
Included in oncogenic viruses
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2. The oldest
virus ever
found is
an STI
An international team of
scientists led by researchers at
the Max Planck Institute for the
Science of Human History and
the University of Kiel has
successfully reconstructed
genomes from Stone Age and
Medieval European strains of
the hepatitis B virus.
This unprecedented recovery of
ancient virus DNA indicates that
hepatitis B was circulating in
Europe at least 7000 years ago.
While the ancient virus is
similar to its modern
counterparts, the strains
represent a distinct lineage that
has likely gone extinct and is
most closely related to
chimpanzee and gorilla viruses.
May 10, 2018,
Source: Max Planck Institute for the Science of Human History

3. Structure

4. Structure
•HBV a member of the hepadnavirusgroup
•double-stranded DNA viruses which replicate by
reverse transcription.
•42-nm in size
•HBV express three main antigens:
1.HBsAg
2.HBcAg
3.HBeAg
•These antigens are recognized by antibody proteins
that bind specifically to one of these surface proteins

5. Structure/HBsAg
•Nucleocapsid is 27 nm in diameter surrounded by an
outer envelope of the surface protein (HBsAg)
embedded in membranous lipid derived from the
host cell
•also known as the Australia antigen. It indicates
current hepatitis B infection.
•Positive HBsAg tests can be due to recent vaccination
against HBV but this positivity is unlikely to persist
beyond 14 days post-vaccination
•It is present in the sera of patients with viral hepatitis
B (with or without clinical symptoms).

6. Structure/HBcAg
•HBcAg(core antigen) is a hepatitis B viral protein.
•It is an indicator of active viral replication
•This means the person infected with Hepatitis B can
likely transmit the virus on to another person.
•HBcAgis not secreted. HBcAgis considered
"particulate" and it does not circulate in the blood.
•it is readily detected in hepatocytes after biopsy
•The presence of both HBcAgand HBeAgproteins
together act as a marker of viral replication, and
antibodies to these antigens are a marker of
declining replication.

7. Structure/HBeAg
•It is an indicator of active viral replication; this means
the person infected with Hepatitis B can likely
transmit the virus on to another person.
•can be found between the icosahedral nucleocapsid
coreand the lipid envelope
•HBeAgis considered "nonparticulate" or "secretory".
•HBeAgis secreted and accumulates in serum as an
immunologically distinct soluble antigen.
•The presence of HBeAgin the serum of patients can
serve as a marker of active replication in chronic
hepatitis.

8. Multiplication

9. 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 mediated
by either clathrinor caveolin-1.
•HBV initially binds to heparin sulfate proteoglycan
•Following endocytosis, the virus membrane fuses with the
host cell's membrane, releasing the nucleocapsid into the
cytoplasm

10. Multiplication
•the viral genomic DNA has to be transferred to the cell nucleus.
•The core proteins dissociate from the partially double stranded viral
DNA, which is then made fully double stranded (by host DNA
polymerases) and transformed into 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
protein and the viral RNA-dependant-DNA-polymerase.

11. Hepatitis B
•Hepatitis B is an infectious disease caused by HBV that
affects the liver. It can cause both acute and chronic
infections.
•The virus may be detected within 30 to 60 days after
infection and can persist and develop into chronic
hepatitis B.
•The incubation period of the hepatitis B virus is 75 days
on average but can vary from 30 to 180 days.

12. Pathogenesis
•Hepatitis B virus primarily interferes with the functions of the
liver by replicating in hepatocytes.
•virions bind to the host cell via the viral surface antigenand
are subsequently internalized by endocytosis. HBV specific
receptors are expressed primarily on hepatocytes
•During HBV infection, the host immune response causes both
hepatocellular damage and viral clearance.
•Most liver injury is caused by cytotoxic T lymphocytes

13. Pathogenesis/Cancer
•HBV causes hepatocellular carcinoma
•An HBV protein traps protons and Cl−, and induces the expression of
collagen in the liver, which forms potent hydrogen bonds with
trapped protons.
•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

14. Symptoms
Acute Infection
•Symptoms of acute HBV infection are non-specific and include fatigue,
poor appetite, nausea, vomiting, abdominal pain, low-grade fever,
jaundice, and dark urine.
•itchy skin is a possible symptom of all hepatitis virus types
•liver tenderness, hepatomegaly, and splenomegaly
•it can lead to fulminant hepatic failure and may die or require emergent
liver transplantation.
•The infection may be entirely asymptomatic and may go unrecognized

15. Symptoms
Chronic Infection
•HBV infection is considered chronic when it persists longer than six months
•asymptomatic or may be associated with a chronic inflammation of the liver –Chronic
hepatitis
•Coinfection with human immunodeficiency virus (HIV) or hepatitis C virus can occur
•It can lead to liver cirrhosis
•increases the incidence of hepatocellular carcinoma (HCC; liver cancer)
•Acute necrotizing vasculitis, glomerulonephritis, jaundice, fever, skin rash, and
polyarteritis.
•Nephropathy, anemia

16. 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

17. Diagnosis
•evaluation of the patient's blood for
•HBsAg
•hepatitis B surface antibody (HBsAb)
•hepatitis B core antibody (HBcAb)
•presence of HBsAg indicates that the person is infectious
•presence of HBsAbindicates recovery and immunity from HBV
infection or successful immunization against HBV.
•HBcAbappears at the onset of acute HBV infection, but may
also indicate chronic HBV infection.

18. Diagnosis
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. 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-positive mothers: the
combination of vaccine plus hepatitis B
immunoglobulin is superior to vaccine alone
•Tenofovirgiven in the second or third trimester can
reduce the risk of mother to child transmission
•it is now believed that the hepatitis B vaccine
provides indefinite protection.

20. Treatment
•none of the available drugs can clear the infection
but can reduce virus load
•These include antiviral drugs
•lamivudine (Epivir)
•adefovir (Hepsera)
•tenofovir (Viread)
•telbivudine (Tyzeka)
•entecavir (Baraclude)
•the two immune system modulators
•interferon alpha-2a
•PEGylated interferon alpha-2a (Pegasys).