Hepatitis B Virus

HEPATITIS B VIRUS
DR.HAMSADWANI.K.P
ASSISTANT PROFESSOR
DEPART,MENT OF MICROBIOLOGY
BMCH.
HEPATITIS B
 Discovered by Blumberg in 1963.

 Morphology: Electron microscopy of serum of the
patients infected with HBV reveals three morphologic
forms:
o Spherical forms (made up of HBsAg) -most numerous, small
forms measuring 22 nm in diameter.
o Tubular or filamentous forms (made up of HBsAg) - also
have the same diameter but 200 nm long.
Essentials of Medical Microbiology by Apurba S Sastry ©

2018, Jaypee Brothers Medical Publishers
Complete form or Dane particles (less frequent). They
are larger, 42-nm size spherical virions; made up of-
 Outer surface envelope - HBsAg (Hepatitis B surface antigen)
 Inner 27 nm size nucleocapsid- consists of core antigen (HBcAg)
and pre-core antigen(HBeAg) and partially double stranded DNA
EPIDEMIOLOGY
 Prevalence- Based on HBsAg carrier rates,
o Type 1 pattern (low endemicity)- Carrier rate is
<2%. It is observed in SriLanka and Nepal.
o Type 2 pattern (intermediate endemicity) – Carrier
rate is between 2-8%. It is observed in India,
Bhutan, Indonesia and Maldives.
o Type 3 pattern(high endemicity)-Carrier rate is >8%.
It is observed in Bangladesh and DPR Korea.
SITUATION IN THE WORLD
 World Hepatitis Day is celebrated on 28th July every year.
 WHO estimates that in 2015, about 257 million
population were living with chronic HBV infection with a
global prevalence of 3.5%.
 2.7 million persons were co-infected with HBV and HIV
 The widespread use of HBV vaccine in infants has led to
a considerable reduction in the incidence of new
chronic HBV infections.

SITUATION IN INDIA
 Intermediate level of HBV endemicity (3.7%
prevalence).
 40 million HBV carriers, which constitutes 11% of the
estimated global burden, which is second highest to
China (30%)
 Highest prevalence recorded from Andamans and
Arunachal Pradesh
 Tribal areas, the prevalence is extremely high (19%)
than non-tribal populations
 HBV accounts for 40–50% of hepatocellular carcinoma
(HCC) and 10–20% of cirrhosis in India.
EPIDEMIOLOGY (CONT..)
 HBV followed by HCV are the most common cause of:
o Chronic hepatitis
o Cirrhosis: HBV accounts for 30% of cirrhosis
o Hepatocellular carcinoma (HCC): HBV accounts for
45% of HCC
o Post-transfusion hepatitis: HBV (1:220,000)>HCV
(1:1800,000).

 Resistance- HBV can be destroyed by hypochlorite and heat
(autoclave).
 Period of infectivity:
o People infected with HBV are said to be infectious as long
as the HBsAg is present in blood i.e. during incubation
period (a month before jaundice) up to several months
thereafter (occasionally years for chronic carriers).
o Become non-infectious once HBsAg disappears and is
replaced by anti-HBs antibody.
o Maximum infectivity is observed when HBeAg is elevated
in serum.

VIRAL ANTIGENS
HEPATITIS B SURFACE ANTIGEN (HBSAG)
 Previously called as 'Australia antigen‘

 Antigenically complex and contains two components:
 Four subtypes of HBsAg - adw, ayw, adr, and ayr.

VIRAL ANTIGENS
HEPATITIS B CORE ANTIGEN (HBCAG)
 Forms the intracellular core protein

 Not secreted
 Does not circulate in blood
 Can be demonstrated in hepatocytes by
immunofluorescence.

VIRAL ANTIGENS
HEPATITIS B PRE CORE ANTIGEN (HBEAG)
 Non-particulate soluble antigen possessing a signal

protein which enables it to be secreted.
 Present in circulation.

TYPING OF HBV -
SEROTYPES
 HBV is divided into four major serotypes (adr, adw, ayr, ayw) -
Based on antigenic epitopes present on its envelope protein
HBsAg.
 Serotypes - not important in immunity as the dominant ‘a’
antigen is shared by all, but they are useful for epidemiologic
investigations, as all the cases during an epidemic would likely
to have the same subtype.
 Serotypes exhibit distinct geographical distribution:
o adw - predominant sub type in Europe, Australia and America.
o adr - South and East India
o ayw - Western and Northern India
TYPING OF HBV-
GENOTYPES
 HBV can also be divided into eight genotypes

(A–H)
 According to overall nucleotide sequence
variation of the genome.
 Genotypes A and D are prevalent in India.

VIRAL GENOME
 Partially circular dsDNA, of 3200 bp in

length.
 minus strand of DNA (L or long strand)is
complete and full-length and is identical in
all HBV isolates
 The positive strand (S or short strand) is
incomplete and of variable length (50-80%).
 HBV genome is compact and consists of four
overlapping genes:
o S gene
o C gene
o X gene
o P gene
VIRAL GENOME-
S GENE
 Three regions- S, pre-S1 and pre-S2

 Code for surface antigen (HBsAg)
 S region codes for the major protein
(S).
 Product of S region plus the adjacent
Pre-S2region is the middle (M) protein
 Pre-S1, Pre-S2combines with S to code
for Large (L) protein.
 The L protein is present only in the
virion, while the M and S proteins are
found in the circulating HBsAg
particles also.
VIRAL GENOME-
C GENE
 Consists of pre-C and C-regions, which

code for two nucleocapsid proteins
o Pre-C region codes for HBeAg
o C-region codes for HBcAg

VIRAL GENOME-
X GENE
 Codes for HBxAg, which can activate

the transcription of cellular and viral
genes.
 Contribute to carcinogenesis by
binding to p53.
 HBxAg and its antibody are elevated in
patients with severe chronic hepatitis
and hepatocellular carcinoma.

VIRAL GENOME-
X GENE
 Codes for HBxAg, which can activate

the transcription of cellular and viral
genes.
 Contribute to carcinogenesis by
binding to p53.
 HBxAg and its antibody are elevated in
patients with severe chronic hepatitis
and hepatocellular carcinoma.

VIRAL GENOME-
P GENE
 Largest and codes for polymerase (P)

protein which has three enzymatic
activities
o DNA polymerase activity
o Reverse transcriptase activity
o RNase H activity

HEPATITIS B VIRUS MUTANTS
 Pre-core mutants: have defect in pre-core region of C
gene which leads to their inability to synthesize HBeAg.
o Mutation- Nonsense mutation in the pre-C gene leading to
formation of premature stop codon.
o Geographical distribution- Mediterranean countries and in
Europe.
o Patients infected with precore mutants may be diagnosed
late and they tend to have severe chronic hepatitis that
progresses more rapidly to cirrhosis.
o Markers-They lack HBeAg. Other viral markers are present as
such.
 Escape mutants: Mutations in the S gene leads to
alteration of HBsAg.
o Mutation occurs in the immunodominant aantigen of HBsAg
o Escape mutants are observed in three situations-
 Infants born to HBeAg positive mothers
 Liver transplant recipients who underwent the procedure for
hepatitis B and who were treated with a high-potency human
monoclonal anti-HBs preparation.
 A small proportion of recipients of active and passive
immunization, in whom antibody pressure may favor evolutionary
change in gene coding a antigen
o Pose problems in hepatitis B vaccination strategies as well
as in the diagnosis of the disease.
 YMDD mutation:
o HBV infected patients on lamivudine therapy
o May develop resistance to the drug due to mutation
in the YMDD locus of the HBV reverse transcriptase
region of polymerase gene.

HEPATITIS B REPLICATION

TRANSMISSION
 Parenteral route- Via blood & blood products transfusion

and needle prick injuries or by inoculation during surgical
or dental procedures or percutaneous inoculation via shared
razors and tooth brushes.
o HBV (30%) is more infectious than HIV (0.3%) and HCV (3% ). As
little as 0.00001 ml of blood can be infectious.
 Sexual transmission
 Vertical (perinatal) transmission- Risk is maximum if the
mother is HBeAg positive
o Transmission occurs at any stage; in utero, during delivery
(maximum risk) and during breast feeding
 Direct skin contact
TRANSMISSION
 High risk groups which are more prone for

acquiring infection are:
o Surgeons(maximum risk)
o Paramedical workers
o Sex workers especially homosexual males
o Recipients of blood transfusion and organ
transplantation
o Drug addicts

EPIDEMIOLOGY
 Reservoir of infection-Humans are the only reservoir
o Cases may range from inapparent to symptomatic cases.
o Carries may be temporary (harbour the virus for weeks to
months) or persistent/ chronic (harbour the virus for >
6months).
 Carriers can also be grouped into-
o Simple carriers- Low infectivity, transmit the virus at a
lower rate. They possess low level of HBsAg and no HBeAg.
o Super carriers- Highly infectious and transmit the virus
efficiently. They possess higher levels of HBsAg and also
have HBeAg, DNA polymerase, and HBV DNA.

VARIOUS OUTCOMES OF HBV
INFECTION

 Age- The outcome of HBV infection depends on the age.
Following HBV infection-
 Chance of developing acute hepatitis is directly related to
the age-
o 1% (perinatal)
o 10% (early childhood; 1-5 years age)
o 30% (late child hood; after 5 years age)
 Chance of developing chronic hepatitis or carrier state is
inversely related to age-
o 80-90% (perinatal)
o 30% (early child hood; 1-5 years age)
o 5% (late child hood; after 5 years age)
 Age- The outcome of HBV infection depends on the age.
 Explanation-
o Pathogenesis HBV infection is immune mediated
o Hepatocytes carrying viral antigen are subjected to NK
cell mediated antibody dependent cell cytotoxicity(ADCC)
or CD8 T cell mediated cytotoxicity
o Absence of an effective immune system (infants) - leads
to carrier state

 The global HBV prevalence in HIV-infected persons is 7.4%.
Conversely, about 1% of HBV-infected persons are also
infected with HIV.
 The highest burden (71%) for HIV–HBV coinfection is found
in sub-Saharan Africa
 Although HBV does not alter the progression of HIV, the
presence of HIV greatly enhances the risk of developing
HBV-associated cirrhosis and liver cancer
 Tenofovir, a drug recently included in the treatment
regimen of HIV is also active against HBV. This may have a
role in controlling HIV-HBV coinfection.

CLINICAL MANIFESTATIONS
 Incubation period - 30–180 days.

 Onset is slow and insidious
 Patients may present with subclinical infection or
acute or chronic hepatitis
 Clinically, HBV infection is indistinguishable from other
hepatitis viruses; characterized by-
o Pre-icteric phase (predominant gastrointestinal symptoms
such as nausea and vomiting) followed by
o Icteric phase or jaundice
 Clinical outcome may be either development of carrier
state or complete recovery.
COMPLICATIONS
 Hepatic complications:
o Fulminant hepatitis
o Cirrhosis
o Hepatocellular carcinoma.
 Extrahepatic complications:
o Prodromal phase - Serum sickness-like syndrome (5–10% of
patients)
o This is due to immune complex deposition.

LABORATORY DIAGNOSIS
 Viral markers of HBV infection:
 Definitive diagnosis of hepatitis B depends on the
serological demonstration of the viral markers which can
be classified as-
o Antigen markers- HBsAg and HBeAg
o Antibody markers- Anti-HBs, Anti-HBe and Anti-HBc
o Molecular markers- HBV DNA
o Non-specific markers- elevated liver enzymes and serum bilirubin
 Detection method – ELISA, ICT
 Viral DNA can be detected by PCR; but quantified by real
time PCR.
 HBV does not grow in any conventional culture system.

SEROLOGICAL MARKERS OF HEPATITIS B VIRUS IN
VARIOUS STAGES OF HEPATITIS B VIRUS INFECTION

HEPATITIS B SURFACE ANTIGEN (HBSAG)
 First marker to be elevated following infection; appears within

1–12 week (usually between 8–12 weeks of infection)
 Appears during incubation period;2–6 weeks before the
biochemical and clinical evidence of hepatitis.
 Presence of HBsAg indicates onset of infectivity (i.e. patient is
capable of transmission of HBV)
 Remains elevated in the entire duration of acute hepatitis;
o Becomes undetectable 1-2 months after the onset of jaundice or
o Rarely persists beyond 6 months during chronic hepatitis and carrier
state
 HBsAg is used as an epidemiological marker of hepatitis B
infection.

HEPATITIS B PRECOREANTIGEN (HBEAG) AND HBV DNA
 Appear concurrently with or shortly after appearance of HBsAg

in serum
 They are the markers of
o Active viral replication
o High viral infectivity (i.e. they are highly infectious to others)
 Present in either acute, chronic and carrier state and it cannot
differentiate between these stages.
 Indicates that the virus is actively multiplying, which could be
either-
o Acute active hepatitis
o Chronic active hepatitis
o Or a carrier in whom HBV is actively multiplying and highly infectious

HEPATITIS B COREANTIGEN (HBCAG)
 Hidden antigen due to surrounding HBsAg coat.

 Also non-secretory in nature - hence, it cannot be
detected in blood.
 HBcAg may be detected in hepatocytes by
immunofluorescence microscopy.

ANTI-HBC
 Anti-HBc IgM(Hepatitis B core antibody)

o Anti-HBc IgM is the first antibody to elevate following infection.
o Appears within the first 1–2 weeks after the appearance of HBsAg and
lasts for 3-6months.
o Indicates acute hepatitis B infection,
o Only marker (sometimes anti-HBc IgG)present during the period
between appearance of anti-HBs antibody and disappearance of HBsAg.
 Anti-HBc IgG (Hepatitis B core antibody)
o Appears in late acute stage and remains positive indefinitely whether
the patient proceeds to
 Chronic stage (with persistence of HBsAg, symptomatic and elevated liver
enzymes)
 Carrier state (with persistence of HBsAg but asymptomatic) or
 Recovery (appearance of Anti-HBs antibody)

ANTI-HBE (HEPATITIS B PRE-CORE ANTIBODY)
 Appear after the clearance of HBeAg and remain

elevated for variable period
 Signifies diminished viral replication and decreased
infectivity.

ANTI-HBS (HEPATITIS B SURFACE ANTIBODY)
 Appears after the clearance of HBsAg and remains

elevated indefinitely
 Indicates recovery , immunity and non-infectivity (i.e.
stoppage of transmission)
 Only marker of vaccination.

INTERPRETATION OF MARKERS IN VARIOUS
STAGES OF HEPATITIS B INFECTION
HBsA Ant Ant HBe Ant Sympt Liver DN Interpretation
g i- i- Ag i- oms enzy A
HBs HBc HB mes
e
+ - - - - Absent Norm + Early acute hepatitis
al (Incubating)
+ – IgM + – Presen Eleva + Acute hepatitis B, high
t ted infectivity
+ – IgG ++ – Presen Eleva ++ Chronic hepatitis B, high
t ted infectivity
(Immunoreactive chronic
hepatitis)
+ – IgG – + Presen Eleva + Chronic hepatitis B, low
t ted infectivity
(Chronic inactive hepatitis)
+ - IgG + - Absent Norm ++
Essentials of Medical Microbiology by Apurba S Sastry © Immuno tolerant chronic HBV
INTERPRETATION OF MARKERS IN VARIOUS
STAGES OF HEPATITIS B INFECTION
HBsA Ant Ant HBe Ant Sympt Liver DN Interpretation
g i- i- Ag i- oms enzy A
HBs HBc HB mes
e
+ - IgG - +/- Absent Norm + Chronic inactive HBV
al infection
(previously called as simple
carriers)
+ – IgG – - Presen Eleva + Precore–mutant hepatitis B
t ted infection
- - IgG -/+ -/+ Presen Eleva + Escape mutant hepatitis B
t ted infection
- + IgG - +/– Absent Norm - Recovery
al
- + - - - Absent Norm - Post vaccination
Essentials of Medical Microbiology by Apurba S Sastry © al
TREATMENT OF HEPATITIS B
 Most acute hepatitis B infection is self-limiting; do not
require any specific treatment.
 In contrast, treatment of chronic hepatitis B has
perceived many recent advances.
 With the advent of newer antiviral drugs, now it’s
possible to contain the disease.
Adapted from EACL guideline 2017 (European Association for the Study of the Liv

TREATMENT OF HEPATITIS B
 Indications
o The indications to initiate treatment for patients with hepatitis B
infection are:
o Acute hepatitis with acute liver failure (coagulopathy or encephalopathy)
o Chronic active hepatitis (immunoreactive hepatitis, HBeAg+ve)
o Chronic inactive hepatitis (HBeAg-ve)
o HBV DNA > 2,000 IU/ml plus ALT ↑ (> normal) plus moderate degree of
liver ﬁbrosis
o HBV DNA > 20,000 IU/ml and ALT ↑↑(>2 times normal); regardless of the
degree of liver ﬁbrosis
o Associated cirrhosis (regardless of ALT level, viral load)
o Super carriers or immunotolerant hepatitis (if >30 years age)
o Carriers (super or simple) with family history of HCC or cirrhosis
Adapted from EACL guideline 2017 (European Association for the Study of the Liv

ANTIVIRAL AGENTS
 Antiviral agents (nucleoside analogues)- such as
telbivudine and tenofovir.
 Lamivudine, adefovir, entecavir were used previously;
now not in use because of high risk of developing
resistance.
 Pegylated interferon alfa (used previously; now not in
use because of adverse effects)

MENT OPTIONS AVAILABLE FOR CHRONIC HEPATITIS B
TION
Interferon alfa Antiviral agents

(Telbivudine and
tenofovir)
Route and dosage Subcutaneous, Oral, daily
weekly
Mode Monotherapy Monotherapy
Duration 48 weeks Long-term until
HBsAg loss
Side effects High Minimal
Decompensated Cannot be given Can be given
disease, immuno-
compromised
patients
HBV DNA <2000 IU/mL Undetectable i.e.
<10 IU/mL
**HBV DNA clearance from blood may occur early; however cccDNA may be present in hepatocytes quiescently; which may get activated later. Hence, HBeAg
HBsAg
seroconversion lossHBeAg
(for previously or positive
HBeAg cases) and Occurs
loss of HBsAg withrelatively
seroconversion are moreOccurs very
reliable indicator slowly
of successful therapy.
seroconversion earlier (1 year)

Preference
2018, Jaypee Brothers Medical PublishersWas preferred in First choice of
PROPHYLAXIS
ACTIVE IMMUNIZATION (HEPATITIS B VACCINE)
 Hepatitis B vaccine is a recombinant subunit vaccine.

 The surface antigen (HBsAg) is used as vaccine candidate
which is prepared in Baker’s yeast by DNA recombinant
technology by cloning the S gene into the yeast
chromosome
 Route of administration: Intramuscular route over deltoid
region (in infant- anterolateral thigh)
 Dosage: 10–20 µg/dose (half of the dose is given to
children below 10 years)

PROPHYLAXIS
Schedule:
 Recommended schedule for adults: Three doses are
given at 0, 1 and 6 months
 Under national immunization schedule: It is given at 6,
10, 14 weeks (along with DPT vaccine). Additional dose
at birth may be given in areas with prevalence of HBV
more than 8%.
 Minimum interval between the doses—4 weeks
 If there is documentation of partial vaccination (1 or 2
doses): Then do not restart; just complete the vaccine
series regardless of when the last dose was taken.
PROPHYLAXIS
 Marker of protection: Recipients are said to be protected

if they develop seroconversion with an anti-HBsAg antibody
titer of more than 10 mIU/mL
 Re-vaccination: If titer remain <10 mIU/mL after first
series of vaccination; the HCW is subjected to second
series of vaccination (3 doses at 0, 1, 6 months)
 Non/low responders: About 5–10% of individuals mount an
impaired immune response following vaccination. They may
be either:
o Non-responders (do not show seroconversion after two series of
vaccination; i.e six doses of vaccination.) or;
o Low responders (seroconversion occurs slowly after the second
series of vaccination.).
PROPHYLAXIS
 Seroconversion:
o 95% of infants, children and young adults
o Older people (>60 years), the protection is about 65–75% only
 Protection may last for about 30 years or even longer
 Booster doses are not needed: The health care workers
once protected, should not check their titer again or should
not take booster vaccines. They remain protective even if
the titer falls <10 mIU/mL. This is because the memory
cells get stimulated much faster and the titer rises very
soon following an infection with HBV
 Newer vaccine containing whole HBsAg (i.e. product of Pre
S1 + Pre S2 + S genes) is under development which may
provide a better seroconversion.
PASSIVE IMMUNIZATION (HEPATITIS B
IMMUNOGLOBULIN OR HBIG)
 Indications: HBIG is used in the following situations

where an immediate protection is warranted.
o Acutely exposed to HBsAg positive blood- e.g. surgeons,
nurses, laboratory workers
o Sexual contact of acute hepatitis B patients
o Neonates borne to hepatitis B carrier mothers
o Post liver transplant patients who need protection against
HBV infection
o Following accidental exposure, HBIG should be started
immediately (ideally within 6hr, but not later than 48 hrs).

PASSIVE IMMUNIZATION (HEPATITIS B
IMMUNOGLOBULIN OR HBIG)
 Recommended dose - 0.05-0.07ml/kg body weight,

two doses of HBIG should be given 30 days apart
 HBIG gives short term passive protection which lasts
for about 100 days. Since the median incubation
period is less than 100 days, two doses given one
month apart should suffice.
Essentials of edical Microbiology by Apurba S Sastry © 2018,

Jaypee Brothers Medical Publishers
COMBINED IMMUNIZATION
 Combined immunization with HBIG + vaccine is more
efficacious than HBIG alone.
 Recommended for neonates born to HBV infected
mother, where a single injection of 0.5 ml of HBIG is
given to the neonate immediately after the birth,
followed by full course of vaccine given at a different
site (the first dose being given within 12 hours of
birth).

GENERAL PROPHYLACTIC
MEASURES
 Screening of blood bags, semen and organ donors
 Following safe sex practices (e.g. using condoms,
avoiding multiple sex partners)
 Following safe injection practices - use of the
disposable syringes and needles
 Following safe aseptic surgical practices
 Health education


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 Discovered by Blumberg in 1963.

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

 Previously called as 'Australia antigen‘

Essentials of Medical Microbiology by Apurba S Sastry ©

 Forms the intracellular core protein

Essentials of Medical Microbiology by Apurba S Sastry ©

 Non-particulate soluble antigen possessing a signal

Essentials of Medical Microbiology by Apurba S Sastry ©

 HBV can also be divided into eight genotypes

Essentials of Medical Microbiology by Apurba S Sastry ©

 Partially circular dsDNA, of 3200 bp in

 Three regions- S, pre-S1 and pre-S2

 Consists of pre-C and C-regions, which

Essentials of Medical Microbiology by Apurba S Sastry ©

 Codes for HBxAg, which can activate

Essentials of Medical Microbiology by Apurba S Sastry ©

 Codes for HBxAg, which can activate

Essentials of Medical Microbiology by Apurba S Sastry ©

 Largest and codes for polymerase (P)

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

 Parenteral route- Via blood & blood products transfusion

 High risk groups which are more prone for

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

 Incubation period - 30–180 days.

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

 First marker to be elevated following infection; appears within

Essentials of Medical Microbiology by Apurba S Sastry ©

 Appear concurrently with or shortly after appearance of HBsAg

Essentials of Medical Microbiology by Apurba S Sastry ©

 Hidden antigen due to surrounding HBsAg coat.

Essentials of Medical Microbiology by Apurba S Sastry ©

 Anti-HBc IgM(Hepatitis B core antibody)

Essentials of Medical Microbiology by Apurba S Sastry ©

 Appear after the clearance of HBeAg and remain

Essentials of Medical Microbiology by Apurba S Sastry ©

 Appears after the clearance of HBsAg and remains

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©

Interferon alfa Antiviral agents

seroconversion earlier (1 year)

 Hepatitis B vaccine is a recombinant subunit vaccine.

Essentials of Medical Microbiology by Apurba S Sastry ©

 Marker of protection: Recipients are said to be protected

 Indications: HBIG is used in the following situations

Essentials of Medical Microbiology by Apurba S Sastry ©

 Recommended dose - 0.05-0.07ml/kg body weight,

Essentials of edical Microbiology by Apurba S Sastry © 2018,

Essentials of Medical Microbiology by Apurba S Sastry ©

Essentials of Medical Microbiology by Apurba S Sastry ©