3. • In the family Hepadnaviridae; common name:
Hepadnavirus
• Known as the smallest DNA virus
• Double stranded, circular 42 nm DNA
genome;Virion also called Dane particle
• Normal virions consist of icosahedral
nucleocapsid surrounded by a 27nm HBcAg and
enveloped containing HBsAg (AKA enveloped
Ag)-originally termed Australia Ag or Hepatitis
asstd Ag (HAA).

5. 1. Infectious Hepatitis particles (Hepatitis B
virion)- The virion has three forms of HBsAg
(S,M,L) and nucleocapsid contains at least
one HBcAg, polymerase protein, HBV
genome
2. Non-Infectious Hepatitis particles
i.
Hepatitis B sphere- composed of the small and
middle HBsAg
ii. Hepatitis B filament-large HBsAg

Both particles have a diameter of 22nm and are
composed solely of hepatitis B surface proteins. The
absence of the hepatitis B core, polymerase, and
genome reflects these particles' non-infectious nature

10. • Exposure to ether, acid (pH 2.4 for at least 6
h), and heat (98°C for 1 min; 60°C for 10 h)
does not destroy immunogenicity or
antigenicity; incomplete inactivation due to
high [virus]
• Antigenicity and probably infectivity are
destroyed after exposure of HBsAg to 0.25%
sodium hypochlorite for 3 min
• Infectivity is lost after autoclaving at 121°C for
20 min or dry heat treatment at 160°C for 1 h

11. *HUMANS ARE RESERVOIR AND A VECTOR
1. BLOOD BORNE
– BLOOD CONTAMINATED NEEDLES

12. – BLOOD CONTAMINTED OBJECTS

13. 2. SEXUAL-via oral, anal & vaginal
– VAGINAL FLUID
– SEMENAL FLUID
3. PRENATAL
HIGH RISK INDIVIDUALS:
 HEMOPHILIACS
 DIALYSIS PATIENTS
 IV DRUG ABUSERS
 HEALTH CARE PERSONNEL
 HOMOSEXUALLY ACTIVE MALES
 HETEROSEXUALLY WITH MULTIPLE PARTNERS
 INFANT OF INFECTED MOTHER

15. • Can enter into small tissue tears
• Hepatitis B has a long incubation period of four weeks
to six months during which time HBV infects the liver
but is not cytolytic
• Oncogenic-gene has a potential to cause cancer
• Site of latency: Liver
• Disease:
– Acute infection with resolution (90%);
– fulminant hepatitis most co-infected with delta virus (1%);
– chronic hepatitis,persistence of HBSAg (9%) followed by
resolution (disappearance of HBSAg),asymptomatic carrier
state, chronic persistent (systemic disease without
progressive liver disease),or chronic active disease
(progressive liver damage

16. 1. Acute HBV infection is characterized by the
presence of HBsAg and immunoglobulin M (IgM)
antibody to the core antigen, HBcAg. During the initial
phase of infection, patients are also seropositive for
HBeAg(Antigenic determinant).
2. Chronic infection is characterized by the persistence
(>6 months) of HBsAg (with or without concurrent
HBeAg). Persistence of HBsAg is the principal
marker of risk for developing chronic liver disease and
hepatocellullar carcinoma (HCC) later in life.
3. The presence of HBeAg indicates that the blood and
body fluids of the infected individual are highly
contagious

17. Assay result
HBsAg
+
AntiHBs
-
AntiHBc
-
Interpretation
+
+/-
+
-
=
+
-
-
+
Possibilities include: HBV infection in remote past; “lowlevel” HBV carrier; “window” between disappearance of
HBsAg and appearance of Anti-HBs; or false+ or nonspecific
reaction. Investigate with IgM anti-HBc. When present, AntiHBe helps validate the Anti-HBc reactivity
-
-
-
Never infected with HBV. Possibilities include another
infectious agent, toxic injury to liver etc.
-
+
-
Vaccine-type response
Early acute HBV infection.
HBV infection either acute or chronic. Differentiate with IgM
Anti-HBc. Determine level of replicative activity (infectivity)
with HBeAg or HBV DNA
Indicates previous HBV infection and immunity to Hepatitis B

18. • Diagnosis: Serology, viral antigen detection
and PCR
• Treatment: Antivirals and liver transplant for
fulminant disease
• Prevention:
– HBV vaccine; hepatitis B immune globulin