Viral

hepatitis
II
HEPATITIS B

▰ HBV is the only DNA virus among hepatitis viruses.

2
Morphology

Electron microscopic appearance of hepatitis B virus,

showing 1-spherical form, 2-tubular form and 3-Dane 3

particle
Viral Antigens
Hepatitis B surface antigen (HBsAg):
▰ Previously called as 'Australia antigen‘

4
Viral Antigens (Cont..)

Hepatitis B core antigen (HBcAg):

▰ Forms the intracellular core protein

▰ Not secreted

▰ Does not circulate in blood

▰ Can be demonstrated in hepatocytes by

immunofluorescence.
5
Viral Antigens (Cont..)

Hepatitis B precore antigen (HBeAg):

▰ Non-particulate soluble antigen possessing a signal protein

which enables it to be secreted.

▰ Present in circulation.

▰ Indicates active replication

6
Viral Genome

▰ Hepatitis B virus genome is compact and consists of four

overlapping genes:

 1. S gene

 2. C gene

 3. X gene

 4. P gene 7
Viral Genome (Cont..)

▰ S gene: code for surface antigen (HBsAg)

8
Viral Genome (Cont..)

▰ C gene: Consists of pre-C and C-regions, which code

for two nucleocapsid proteins

 i. Pre-C region—codes for HBeAg

 ii. C-region—codes for HBcAg.

9
Viral Genome (Cont..)

X gene:

▰ Codes for HBxAg, which can activate the transcription of

cellular and viral genes.

▰ It may contribute to the pathogenesis of carcinogenesis by

binding to p53

10
Viral Genome (Cont..)

▰ P gene: It is the largest gene and codes for polymerase (P)

protein

11
Transmission

▰ Parenteral route-

HBV (30%) is more infectious than HIV (0.3%) and HCV (3% ).
As little as 0.00001 ml of blood can be infectious.

12
Transmission (Cont..)

▰ Sexual transmission

▰ Vertical (perinatal) transmission-

 Transmission occurs at any stage; in utero, during

delivery (maximum risk) and during breast feeding

13
Epidemiology

▰ Reservoir of infection-Humans are the only reservoir

 Cases may range from inapparent to symptomatic

cases.

 Carries may be temporary (harbour the virus for weeks

to months) or persistent/ chronic (harbour the virus for >
6months).
14
Epidemiology (Cont..)
Situation in the world:

▰ 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 15
Epidemiology (Cont..)
▰ HBV followed by HCV are the most common cause of:

 Chronic hepatitis

 Cirrhosis: HBV accounts for 30% of cirrhosis

 Hepatocellular carcinoma (HCC): HBV accounts for 45%

of HCC

 Post-transfusion hepatitis: HBV (1:220,000)>HCV

16
Epidemiology (Cont..)

▰ Period of infectivity:
 People infected with HBV are - infectious as long as
the HBsAg is present in blood
 Become non-infectious once HBsAg disappears -
replaced by anti-HBs antibody.
 Maximum infectivity is observed when HBeAg is
elevated in serum.
17
Various outcomes of HBV
infection.

18
19
Clinical Manifestations
▰ Incubation period - 30–180 days.
▰ Patients may present with subclinical infection or acute or
chronic hepatitis
▰ Clinically, characterized by-
 Pre-icteric phase (predominant gastrointestinal
symptoms such as nausea and vomiting) followed by
 Icteric phase or jaundice
20
Clinical Manifestations
(Cont..)
▰ Clinical outcome may be either development of carrier state
or complete recovery.

▰ Hepatic complications: Fulminant hepatitis, Cirrhosis,

Hepatocellular carcinoma.
▰ Extrahepatic complications:
 Prodromal phase - Serum sickness-like syndrome (5–10%
of patients)
21

 This is due to immune complex deposition.

Laboratory diagnosis of
Hepatitis B
▰ Antigen markers: HBsAg, HBeAg and HBcAg

 HBsAg: First marker to appear; elevated in acute,

chronic or in carriers

 HBeAg: Indicates active viral replication and high

infectivity

 HBcAg: Not detectable in serum; can be detected in

22

hepatocytes by immunofluorescence test

Laboratory diagnosis of
Hepatitis B (Cont..)
▰ Antibody markers: Anti-HBs, Anti-HBe and Anti-HBc

 Anti-HBc Ab: IgM indicates acute hepatitis and IgG

appears in chronic hepatitis or carriers or after recovery

 Anti-HBs Ab: Marker of recovery or vaccination

 Anti-HBe Ab: Indicates low viral replication and low

infectivity
23
Laboratory diagnosis of
Hepatitis B (Cont..)
▰ Molecular markers: HBV DNA detection

 Indicates active viral replication and high infectivity

 Viral DNA load helps in monitoring treatment response

▰ Non-specific markers: Elevated liver enzymes and serum

bilirubin; indicates clinically active infection

24
Serological markers of hepatitis B
virus in various stages of
hepatitis B virus infection

25
Interpretation of markers in
various stages of hepatitis B
infection
HBsag Anti- Anti- HBea anti- Sympto Liver DNa Interpretation
HBs HBc g HBe ms enzymes
+ – – – – Absent Normal + Early acute hepatitis
(incubating)
+ – IgM ++ – Present Elevated ++ Acute hepatitis B, high
infectivity
+ – IgG ++ – Present Elevated ++ Chronic hepatitis B, high
infectivity (Immunoreactive
chronic hepatitis)
+ – IgG – + Present Elevated + Chronic hepatitis B, low
infectivity (Chronic inactive
hepatitis)
+ – IgG + – Absent Normal ++ Immunotolerant chronic HBV
infection (previously called as
super carriers)
+ – IgG – +/– Absent Normal + Chronic inactive HBV infection26
(previously called as simple
Interpretation of markers in
various stages of hepatitis B
infection
HBsag Anti- Anti- HBea anti- Sympto Liver DNa Interpretation
HBs HBc g HBe ms enzymes
+ – IgG – – +/– Normal/ + Precore–mutant hepatitis B
elevated infection
– – IgG –/+ –/+ +/– Normal/ + Escape mutant hepatitis B
elevated infection
– + IgG – +/– Absent Normal – Recovery

– + – – – Absent Normal – Post-vaccination

– – IgG – – Absent Normal + Occult hepatitis B infection

(+/–)

27
Treatment of Hepatitis B
Indications - To initiate the treatment for patients with
hepatitis B infection are:
▰ Acute hepatitis with acute liver failure
▰ Chronic active hepatitis (immunoreactive hepatitis, HBeAg
positive)
▰ Chronic inactive hepatitis (HBeAg negative):
 HBV DNA >2,000 IU/mL plus ALT ↑ (> normal) plus
moderate degree of liver fibrosis 28
Treatment of Hepatitis B
(Cont..)
▰ Associated cirrhosis (regardless of ALT level, viral load)

▰ Carriers (super or simple) with family history of HCC or

cirrhosis

▰ Super carriers or immunotolerant hepatitis (here, treatment

is indicated if the person’s age is >30 years)

29
Treatment of Hepatitis B
(Cont..)
▰ Antiviral agents (nucleoside analogues): Tenofovir and
telbivudine are the agent of choice currently.
 Tenofovir and emtricitabine - HIV-HBV coinfection.
 Lamivudine, adefovir and entecavir can also be used,
but they are less preferred because of high risk of
development of resistance.

▰ Pegylated interferon alfa (used previously; now not in 30

Treatment options available for
chronic hepatitis B infection
Interferon alfa Antiviral agents*
Route and dosage Subcutaneous, weekly Oral, daily
Mode Monotherapy Monotherapy

Duration 48 weeks Long-term until HBsAg loss

Side effects High Minimal

In decompensated disease, Cannot be given Can be given

immuno- compromised
patients
HBV DNA <2000 IU/mL Undetectable, i.e.
<10 IU/mL**
HBsAg loss or HBeAg Occurs relatively earlier Occurs very slowly
seroconversion (1 year)
Preference Was preferred in the past First choice of treatment
currently 31
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

32

deltoid region (in infant- anterolateral thigh)

Prophylaxis - Active
Immunization (Hepatitis B
Vaccine) (Cont..)
▰ Dosage: 10–20 µg/dose (half of the dose is given to
children below 10 years)

Schedule:

▰ Recommended schedule for adults: Three doses are

given at 0, 1 and 6 months

33
Prophylaxis - Active
Immunization (Hepatitis B
Vaccine) (Cont..)
▰ 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 34
Prophylaxis - Active
Immunization (Hepatitis B
Vaccine) (Cont..)
▰ 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)
35
Prophylaxis - Active
Immunization (Hepatitis B
Vaccine) (Cont..)
▰ Non/low responders: About 5–10% of individuals mount
an impaired immune response following vaccination. They
may be either:

 Non-responders (do not show seroconversion after two

series of vaccination; i.e six doses of vaccination.).

36
Prophylaxis - Active
Immunization (Hepatitis B
Vaccine) (Cont..)
▰ 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
37
Prophylaxis - Passive
Immunization (Hepatitis B
Immunoglobulin or HBIG)
▰ Indications: HBIG is used in the following situations where
an immediate protection is warranted.
 Acutely exposed to HBsAg positive blood- e.g. surgeons,
nurses, laboratory workers
 Sexual contact of acute hepatitis B patients
 Neonates borne to hepatitis B carrier mothers
 Post liver transplant patients who need protection
against HBV infection
38
Prophylaxis - Passive
Immunization (Hepatitis B
Immunoglobulin or HBIG) (Cont..)
▰ Timing: Following accidental exposure, HBIG - started
immediately (ideally within hours, but not later than 7 days)

▰ Recommended dose is 0.06 mL/kg (or 10–12 IU/kg) single

dose, given IM

▰ HBIG provides a temporary protection for 3–6 months.

39
Prophylaxis - 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). 40
Prophylaxis - 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
41
HEPATITIS C
42
HEPATITIS C

▰ Hepatitis C virus (HCV) - common cause of post-transfusion

hepatitis in developing countries.

▰ It was discovered in 1989 and first labeled as “non-A, non-B

hepatitis virus while performing the experiments in
chimpanzees.

43
Morphology

▰ Hepatitis C virus - classified under family Flaviviridae, genus

Hepacivirus.

▰ It is spherical, 60 nm size and enveloped

▰ Nucleic acid: It contains a positive sense ssRNA

44
Morphology (Cont..)

▰ Proteins: HCV possesses:

 Three structural proteins: The nucleocapsid core protein
C; two envelope glycoproteins (E1 and E2)
 Six nonstructural (NS) proteins: NS2, NS3, NS4A, NS4B,
NS5A, and NS5B
 One p7 membrane protein: It functions as an ion
channel; was earlier considered as NS1.
45
Genetic Diversity of HCV

▰ Similar to HIV, Hepatitis C virus displays diversity in the

RNA genome that occurs because of high rates of mutations
seen in the virus which in-turn is due to (i) the high
replicative activity and (ii) the lack of proofreading activity
of the RNA polymerase.

▰ Genotypes: HCV is divided into six major genotypes

46
Genetic Diversity of HCV
(Cont..)

▰ Subtypes: Genotypes are further divided into more than

100 subtypes.

▰ Within any given patient, the subtypes of HCV circulate as

complex closely related viral population known as
quasispecies.

▰ The E2 envelope protein is the most variable region of

47

the entire HCV genome followed by the non-structural

Genetic Diversity of HCV
(Cont..)

▰ Unfortunately, E2 protein happens to be the target against

which most of the neutralizing (protective) antibodies are
produced

▰ Diversity in the gene coding E2 protein enables the

emergent mutant virus strains to escape from host’s
humoral immunity, which in turn can result in:
 Establishment of chronic infection 48
Genetic Diversity of HCV
(Cont..)

▰ The genotypes also vary from each other in their—

▰ Epidemiological distribution:

 Genotype 1 and 2 - most common variants in Western

countries

 In India, genotypes 1 and 3 are more prevalent.

49
Transmission

▰ Parenteral: Most commonly transmitted through exposure

to infectious blood.

▰ Vertical transmission from infected mother to fetus may

occur but at much lower rate (6%) than that of HBV (20%)

▰ Sexual transmission (rare).

▰ Hepatitis C virus does not spread through breast milk,

food or casual contacts including hugging or kissing.
50
Clinical Manifestations

▰ Incubation period - 15–160 days (average 50 days).

▰ Following an infection with HCV:

 Asymptomatic infection: >75% of cases.
 Acute hepatitis: About 20% of people develop acute
hepatitis.
 Spontaneous clearance: In about 5–15% of infections,
the virus gets cleared spontaneously within 12 weeks 51
Clinical Manifestations
(Cont..)
 Chronic disease: About 75–85% directly develop chronic
disease
 Extrahepatic manifestations:

 Mixed cryoglobulinemia

 Glomerulonephritis

 Arthritis and joint pain.

52
Epidemiology
▰ Hepatitis C virus infection occurs worldwide.
▰ Every year, 3–4 million people are infected with HCV with
more than 3.5 lakhs deaths.
▰ Population prevalence rate:
 3% of the world population - infected with HCV
worldwide with more than 170 million chronic carriers
 Higher prevalence rates - Africa (up to 10%) , South
America and Asia 53
Laboratory Diagnosis - HCV
Antibody Detection Assay
(ELISA)
▰ ELISA is the most common platform used; followed by rapid
test and chemiluminescence formats.

 First and second generation ELISA – used

previously; now obsolete.

 Third generation ELISA – Standard method for HCV

serology - employs antigens from NS5 region in addition
54

to core, NS3 and NS4 regions

Laboratory Diagnosis - HCV
Antibody Detection Assay
(ELISA) (Cont..)
▰ Advantages include:

 (i) increased sensitivity and specificity (>99%),

 (ii) not influenced by HCV genotype,

 (iii) becomes positive in 5 weeks of infection.

55
Laboratory Diagnosis - HCV
Antibody Detection Assay
(ELISA) (Cont..)
▰ Disadvantages: These assays detect IgG antibodies to HCV,
hence,

 Do not discriminate between active or past infection -

HCV RNA test is required

 Cannot differentiate acute and chronic HCV infection (as

IgG appears early and stays long) - IgG avidity test is
56

performed.
Laboratory Diagnosis -
Recombinant Immunoblot
Antibody Assay (RIBA)
▰ RIBA - used in the past as a supplementary test to confirm
the ELISA result, - works on the principle of western blot ;
not in use currently.

57
Laboratory Diagnosis - HCV Core
Antigen Assay
▰ Automated quantitative HCV antigen test detecting core
antigen has been available recently (e.g. Abbott ARCHITECT
HCV antigen assay).

▰ This test is less expensive and less time consuming than

HCV RNA PCR.

▰ Advantages: Antigen detection assays can be used as an

alternative to HCV RNA testing for: (i) diagnosis of 58
Laboratory Diagnosis - HCV Core
Antigen Assay (Cont..)
▰ Disadvantage: They are less sensitive than RT-PCR; hence
not recommended for blood screening purpose.

▰ An ELISA format has recently been available that detects

simultaneously antigen (core Ag) and antibody (to NS3 and
S4 Ag).

59
Laboratory Diagnosis -
Molecular Methods
▰ Real time reverse transcriptase PCR detecting HCV RNA has
been the gold standard method for:

 Confirmation of active HCV infection.

 Quantification of HCV RNA for monitoring the response

to treatment.

 For determining HCV genotype and subtype (also done

60
Laboratory Diagnosis - Hepatitis
C Testing Sequence
▰ CDC recommends a two-step testing: First, anti‑HCV
antibody test is performed

 If positive, then test for HCV RNA to identify active

infection

 If negative, then no further action is required, except for

immunocompromised patients where HCV RNA should
61

be tested.
Laboratory Diagnosis - Hepatitis
C Screening
▰ CDC recommends one-time hepatitis C screening

 For all aged >18 years and all pregnant women (during
each pregnancy) in areas with HCV prevalence (HCV
RNA‑positivity) is >0.1%

 For high-risk group, regardless of HCV prevalence—

people with HIV, IV drug users, etc.
62
Laboratory Diagnosis - Biopsy for
Staging HCV Infection
▰ It is a ‘gold standard’ test for staging HCV infection.

▰ It is helpful to determine the ideal timing of HCV treatment

(in some settings).

▰ When biopsy is not obtained, Fibroscan (elastography) is

used to assess liver fibrosis.

63
Treatment of Hepatitis C

▰ The goal of treatment in HCV infection is:

 To prevent development of complications – cirrhosis and

liver cancer

 To achieve sustainable viral response (SVR) –

defined as undetectable HCV RNA in blood (≤15 IU/mL)
at the end of treatment.
64
Treatment of Hepatitis C
(Cont..)
Interferon alfa plus ribavirin:

▰ Earlier, pegylated-interferon (PEG-IFN) alpha plus ribavirin

(RBV) was used for treatment of HCV infection.

▰ This was associated with high adverse effects with a

moderate degree of viral clearance.

65
Treatment of Hepatitis C
(Cont..)
Direct-acting antiviral agents (DAAs):

▰ After the discovery of direct-acting antiviral agents (DAAs),

the treatment of HCV infection has been revolutionized.

▰ DAAs are the now the treatment of choice for HCV infection
as they can produce SVR rate up to 90% with minimal side
effects.
66
Treatment of Hepatitis C
(Cont..)
▰ Three classes of DAAs are available:

 NS3/4A (proteases) inhibitors,

 NS5B (polymerases) inhibitors and

 NS5A inhibitors

67
Treatment of Hepatitis C
(Cont..)
▰ Combination therapy: Combinations of different DAAs
with or without PEG-IFN and ribavirin

 Genotype specific: Most DAAs are genotype specific;

except sofosbuvir/velpatasvir which are active against
all genotypes

 Duration: 12 or 24 weeks; depending upon the HCV

68

genotype and presence or absence of liver cirrhosis.

Drugs used for hepatitis C
virus infection
Class Agents
Directly acting antiviral agents (Daas)
NS3/4A (proteases) inhibitors Ends with suffix ‘previr’ - Grazoprevir,
Paritaprevir, Simeprevir
NS5B (polymerases) inhibitors Ends with suffix ‘buvir’ - Dasabuvir, Sofosbuvir

NS5A inhibitors Ends with suffix ‘asvir’ - Daclatasvir,

Ledipasvir, Velpatasvir
Other classes
Interferons Pegylated interferon alfa-2a and 2b

Nucleoside inhibitor Ribavirin 69

Predictors of Treatment
Response
▰ Genotypes: HCV genotype 1 and 4 are associated with
poor prognosis than other genotypes
▰ Stage of disease and associated co-infections such as
HIV and HBV: associated with poor prognosis
▰ Adherence: Poor compliance to treatment, is associated
with worse prognosis
▰ Viral RNA load: Higher the viral load (> 800,000 IU/mL),
worse is the prognosis 70
Predictors of Treatment
Response (Cont..)
▰ People possessing a subtype of IL 28B (called CC
genotype), produce a stronger immune response to HCV
infection - inducing IFN-α release - have a better outcome
▰ Race: Caucasians and African Americans lack CC genotype
- poor treatment response than Asians
▰ Others: Metabolic disorders such as insulin resistance,
obesity metabolic syndrome, steatosis, lack of vitamin D
supplement, older age, alcohol consumption—all reduce the
71

chance of responding to HCV therapy.

Prevention

▰ There is no effective vaccine available for HCV.

▰ General prophylactic measures are essentially same as that

for HBV.

72
HEPATITIS D
73
HEPATITIS D

▰ Hepatitis D virus (HDV) is a defective virus; cannot replicate

by itself; depends on Hepatitis B virus for its survival.

74
Morphology

▰ Hepatitis D is taxonomically unclassified though resembles

viroids. It is small in size(35nm), consisting of-
 Circular, negative-sense ssRNA
 Protein coat made up of single protein called as-
hepatitis D antigen (HDAg)
 Surrounded by envelope protein derived from HBsAg
from hepatitis B; hence it is called as defective virus.
75
Transmission

▰ Transmission is similar to that of HBV and HCV.

▰ Parenteral route is the most common mode; followed by

sexual and vertical routes.

76
HDV and HBV Association
▰ Co-infection occurs when a person is exposed
simultaneously to serum containing both HDV and HBV.
 Hepatitis B infection sets in first so that HBsAg becomes
available for HDV
 Transient and self-limited condition (indistinguishable
from acute hepatitis B)
 Rarely progresses to chronic stage; at a rate similar to
that of HBV. 77
HDV and HBV Association
(Cont..)
▰ Super-infection occurs when a chronic carrier of HBV is
exposed to serum containing HDV. This results in disease
30–50 days later which may have two phases:
 Acute phase - HDV replicates actively with high
transaminase levels with suppression of HBV.
 Chronic phase - HDV replication decreases, HBV
replication increases, transaminase levels fluctuate, and
the disease progresses to cirrhosis and hepatocellular 78

carcinoma (HCC). Mortality rate is much higher (>20%).

HDV and HBV Association
(Cont..)
▰ Super-infection occurs when a chronic carrier of HBV is
exposed to serum containing HDV. This results in disease
30–50 days later which may have two phases:
 Acute phase - HDV replicates actively with high
transaminase levels with suppression of HBV.
 Chronic phase - HDV replication decreases, HBV
replication increases, transaminase levels fluctuate, and
the disease progresses to cirrhosis and hepatocellular 79

carcinoma (HCC). Mortality rate is much higher (>20%).

Differences between Hepatitis D and
Hepatitis B virus (HDV-HBV) co-
infection and super-infection
Features Co-infection Super-infection

Definition HBV and HDV HDV infection occurs

infection occurs to a carrier of HBV
simultaneously
Patient status Healthy HBV carrier

Risk of development of:

Fulminant disease More than that of More than that of

HBV alone co-infection
Chronic hepatitis Rare Much greater

Cirrhosis Rare More

80
Differences between Hepatitis D and
Hepatitis B virus (HDV-HBV) co-
infection and super-infection (Cont..)
Features Co-infection Super-infection

HCC Rare More

Mortality Rare >20%

Diagnosis  HBsAg  HBsAg

 Anti-HBc (IgM)  HBeAg
 Anti-HDV (IgM)  Anti-HBc (IgG)
 HDV RNA  Anti-HDV:
 In acute phase-
IgM
 In chronic
phase- IgG and
IgM
 HDV RNA
81
Laboratory Diagnosis

▰ In co-infection: IgM against both HDAg and HBcAg are

elevated, although IgM anti-HDV appears late and is
frequently short-lived

▰ In super-infection: As HBV infection is already established

as carrier, IgG anti-HBc will be detected.

▰ Anti-HDV would be IgM type initially; but as the patient

progresses to chronic state, mixture of IgM and IgG would 82
Laboratory Diagnosis (Cont..)

▰ Anti-HBc antibody - key to differentiate between co-

infection and super-infection

 IgM anti-HBc + IgM anti-HDV: Indicates co-infection

 IgG anti-HBc + mixture of IgM and IgG anti-HDV:

Indicates super-infection.

83
Laboratory Diagnosis (Cont..)

▰ HDV RNA is detectable in the blood and liver just before and
in the early days of acute phase of both co-infection and
super-infection

▰ HBeAg, the marker of active HBV replication may be

present in super-infection.

84
Epidemiology

▰ Globally, about 15 million people, i.e., 5% of HBV infected

persons are co-infected with HDV.

▰ Hepatitis D virus infection occurs worldwide, but prevalence

varies greatly.

▰ HDV - not prevalent in Southeast Asia including India; where

HBV carriers are maximum.
85
Epidemiology (Cont..)

Two epidemiologic patterns have been identified:

▰ 1. In endemic areas: Transmitted predominantly by non-

percutaneous means - close personal contact

▰ 2. In non-endemic areas: HDV infection is confined to

persons frequently exposed to blood and blood products,
primarily injection drug users and hemophiliacs who are
infected with HBV 86
Treatment of Hepatitis D

▰ Patients with HDV infection can be treated with IFN-α.

▰ Treatment for HBV should be continued as described earlier.

87