Viral Hepatitis & HIV

BLOOD-BORNE VIRAL HEPATITIS

A severe and sometimes chronic form of viral

hepatitis, known as blood-borne viral hepatitis,
is transmitted via blood transfusions, blood
products, shared drug users, breast-feeding, and
sexual contact.
ETIOLOGY
There are three different viruses that infect the
liver and result in blood-borne viral hepatitis:
hepatitis B virus (HBV), hepatitis C virus
(HCV), and hepatitis D virus (HDV).
HBV is an enveloped partially double-strand
DNA virus in the hepadnavirus family.

HCV is an enveloped single-strand RNA virus

in the flavivirus family.

HDV is a single-strand RNA viroid called the

delta agent. The HDV agent is a defective virus
that cannot infect a hepatocyte without the
hepatocyte also being infected with HBV.
 MANIFESTATIONS
The incubation period for HBV infection is longer
than that for HAV infection and is anywhere from 7
to 160 days in duration.
Most children do not have any symptoms of HBV
infection; however, when symptoms occur in children,
they are usually less severe than symptoms in adults.
 Early symptoms of acute infection include fatigue,
nausea, pain and fullness in the upper right
quadrant, and fever.
Manifestations that develop later may include
arthritis, rash, and jaundice),and tend to be more
severe than in patients infected with HAV.
PATHOGENESIS
HBV enters the bloodstream and infects the cells of
the liver by replicating within the cells.
Symptoms may not be observed form45 days or more,
depending on the dose of HBV, the route of infection,
and the individual.
 HBV genomes integrate into host chromosomes
during replication and are the basis of chronic
infections. Large amounts of HBV surface antigen
(HBsAg) and virions are released in the blood.
Immune complexes formed by HBsAg and
antibody are responsible for hypersensitivity
reactions that occur in some patients (e.g.,
arthritis, rash, liver damage & vasculitis).
Liver parenchymal cell degeneration results
from cellular swelling and necrosis; resolution
of the infection allows the liver parenchyma
to regenerate
DIAGNOSIS
Initial diagnosis of HBV, HCV, and HDV infection is usually
determined clinically if signs and symptoms are present.
Laboratory evaluation of the blood for elevations in ALT,
AST, alkaline phosphatase, and bilirubin aids in making an
initial diagnosis.
A confirmatory diagnosis can be determined following
reactivity in various serologic tests for HBV, HCV, and
HDV.
Blood tests for HBV infections are somewhat more
complicated than most serologic tests.
Tests for HBV infection detect both viral antigens and
antibodies to viral antigens. To confirm a patient has HBV
infection, three blood tests are usually ordered: HBV
surface antigen (HBsAg), antibody to HBV core antigen
(anti-HBcAg), and antibody to HBsAg (anti- HBsAg).
 THERAPY AND PREVENTION
Treatment of acute infections with HBV, HCV, and
HDV involves supportive care. Treatment of chronic
HBV infections can include human interferon alpha
(IFN), lamivudine (3TC), or adefovir (given for 4–12
months). Adefovir and lamivudine are that suppress
HBV replication through inhibition of HBV-DNA
polymerase.
Patients with chronic hepatitis who are HBeAg positive
usually are more responsive to therapy than patients
with chronic hepatitis who are HBeAg negative.
Treatment with conventional IFN not only results in
loss of viremia and normalization of liver enzymes, but
it also improves long-term outcomes and survival and
alters the natural history of the disease.
Two different treatment strategies exist for treating
chronic HCV patients:
(1) immediate treatment with Peginterferon alfa-2a
and ribavirin for up to 48 weeks;
(2) watchful waiting with liver biopsy performed every
3 years and drug therapy To prevent infection of both
HBV and HDV,
immunization with the HBV vaccine is recommended
for all children. This vaccine was called the first
“cancer vaccine” because of its ability to prevent
chronic HBV infection and the resultant HCC that
occurs in some chronically infected HBV patients.
The vaccine contains purified recombinant HBsAg
THE VIRUS:
HIV is a complex RNA virus of the genus Lentivirus
within the Retroviridae family.
The virus is an approximately 100 nm icosahedral
structure with 72 external spikes that are formed by
the two major envelope glycoproteins gp120 and gp41
Transmission is by sexual intercourse (especially
homosexual) and by inoculation of infectious blood or
blood products.
The virus can be transmitted from mother to child,
transplacentally, during birth or via breast feeding.
Time from exposure to HIV until onset of acute
clinical illness is 1–4 weeks.
After primary infection there is a period ranging from
a few months to more than 10 years with no or mild
symptoms before the appearance of severe
immunodeficiency.
THERAPY AND PROPHYLAXIS
Various antiretroviral combination therapies are
beneficial. There is no specific immunoglobulin or
vaccine.
Both clinical trials and clinical practice have
demonstrated a significant reduction in mother-to-
child HIV transmission if zidovudine is given as
prophylaxis during pregnancy or nevirapine is given as
a single-dose during delivery.
Prophylaxis
There is no effective HIV vaccine.
Antiretroviral drugs are used as post-exposure
prophylaxis (PEP) for healthcare workers sustaining
accidental exposure or needle-stick injuries from HIV
infected patients. Triple therapy is given for 4 weeks.
Antiretroviral therapy of pregnant mothers from 14
weeks onward and at labour, followed by
prophylactic treatment of the newborn for 6 weeks,
has reduced the incidence of vertical infection from
about 25% to <3% provided that breast feeding is
also avoided.
LABORATORY DIAGNOSIS
Tests to identify HIV infection can be divided into
different categories: virus cultivation, antigen
detection and viral genome amplification (PCR).
Specific antibodies appear 2–4 weeks to 3 months
after infection and remain for life.
Viraemia is detected at high levels before
seroconversion.
It is present at moderate levels during the clinically
asymptomatic period.
Low numbers of CD4+ T-cells in the blood are
characteristic