HEPATITIS INDUCING

VIRUSES
BWANIKA RICHARD
Hepatitis
Hepatitis Viruses xtics
Virus family and Presence Disease course Mode of
type genome type of vaccine transmission
Hepatitis A (Picornaviridae) Yes Acute Enteric

ssRNA
Hepatitis B Hepadnavirdae Yes Acute, chronic, Parenteral,
ds DNA oncogenic Sexually
Hepatitis C Flaviviridae No Chronic, Parenteral
ssRNA oncogenic
Hepatitis D Deltavirus No Fulminant only Parenteral
ss RNA satellite virus with HBV
Hepatitis E Calciviridae No Fulminant disease Enteric
ssRNA) in pregnant
women
Hepatitis G Flaviviridae No Asymptomatic Parenteral
ssRNA
 Hepatitis Viruses

Other viruses ie EBV, CMV, and yellow

fever virus cause the inflammation of the
liver but are not called hepatitis viruses.
 Hepatitis Viruses
• Enterical transmitted hepatitis viruses,
(HAV, HEV)
• Parenteral transmitted hepatitis viruses,
(HBV, HDV, HCV and HGV)
Hepatitis A Virus(HAV)
Transmission
• Mainly oral-fecal
• Contaminated food or
water (consumption
of shellfish)
• Rarely blood products
• Disease common in
children
Symptoms
• Initially fatigue, abdominal
pain, nausea
• Later Jaudice, dark urine,
pale stool
• Children show lesser
symptoms than adults
• 99% show complete
recovery within 2-4 wks
• No risk for Cancer
 Treatment

• None available
• Supportive
• Hepatitis A immune globulin early (two
weeks-5 mths) for symptomatic relief
 Control

• Improve hygiene
• Chlorination of water
• Vaccination (HAVRIX) and VAQTA both
are killed vaccine. Are given in the 1st yr of
life or to none immune travellers
Hepatits E
Epidemiology
• HEV is endemic in
many tropical
countries where
sanitation is poor
• Causes sporadic
hepatitis
• In US > 2% have anti-
HEV
• Infection is fueled by
poverty
 Symptoms
• Incubation period (16-60 days)
• Sudden onset of Hepatitis symptoms;
malaise, abdominal pain, nausea and
Jaundice.
• No evidence of chronic HEV hepatitis
• Mortality highest in pregnant women
 Diagnosis, treatment and control
• No available tests for routine diagnosis
• Treatment is supportive,
• Immunoglobulin only useful if collected
from donors from endemic areas
• Avoid contaminated drinking water, and
uncooked food in endemic areas
• No vaccine
 Hepatitis viruses transmitted
parentally
• Include hepatitis B, C, D and G
Hepatitis B
• Is the Prototype of
Hepadnavirus family
• Cause serum
hepatitis
• DNA genome which is
partly double
stranded
• Envelope but stable
to organic solvents,
heat and PH resistant
• Genome is associated with the
Polymerase (P) protein and is sorrounded
by the inner antigens (HBcAg and HBeAg)
• HBeAg is secreted while HBcAg is
assembled into progeny viruses
• Surface lipid layer contains surface
antigen (HBsAg) which is secreted in
serum.
 Immunology
• HBV infection induces a cell mediated response
(CTR) against HBsAg, HBeAg and HBcAg
• Infected cells shed HbsAg which combines with
anti-HBS Abs limiting the humoral response
• Ab-HBsAg complexes causes a type
hypersensitivity reaction presenting as a rash,
arthlagia and kidney damage.
• Anti-HBsAg confer life long immunity
Epidemeology
• World wide presence
• Spread parentally,
sexually, or neonatally
• Virus occurs in semen,
saliva, blood, vaginal
secretions in high
concentrations
• Is a risk factor to
Hepatocellular carcinoma
Serologic and clinical patterns observed during acute HBV
infection
 Symptoms of HBV infection
• Similar to other forms of Hepatitis
• Jaundice, malaise, abdominal pain,
nausea
• Most individuals are asymptomatic
• Elevated liver enzymes ALT and AST
 Diagnosis of HBV

• From clinical symptoms

• In acute infection there are Abs (IgM) against
the HBcAg, thus in acute hepatitis is best
diagnosed by demostrating anti-HBc IgM
• Detection of HBsAg, HBcAg, and antibodies to
HBcAg, HBsAg, and HBeAg
• The presence of HBeAg is the best marker
for infectious virus
 Diagnosis of HBV
• Presence of anti-HBc alone is evidence
for an active HBV infection
• Chronic hepatitis B patients may be
tested for HBeAg, anti-HBe, or HBV DNA
• HBeAg-positive patients are more likely
to transmit hepatitis B sexually, and
perinatally
 Treatment of HBV

• Mainly supportive
• Immunoglobulin within 24 hrs of birth, or
exposure
• Interferon-alpha 2b, mimics natural host defence
mechanisms
• Hepsera (Adefovir Dipivoxil) inhibits HBV DNA
polymerase, for chronic hepatitis B in adults with
evidence of active viral replication.
• Lamivudine inhibits reverse transcriptase
 Control

• Vaccination using a sub-unit vaccine

• In infants born to infected mothers, the
vaccine should be supplemented with an
Immunoglobulin
• Safe sexual practices
 Hepatitis C
• HCV is a Flavivirus
• Humans and chimpanzees are the only
reservoirs
• Major cause of transfusion assed Hepatitis
• Causes 40-60% of Chronic Liver Disease
leading to 10000-12000 deaths/year.
Higher in males 30-39yrs
Sources of infection
• IV drug abuse
• Blood transfusion
• Occupational
exposure to blood
and other fluids
• MTC at time of
delivery
• Sexual intercourse
 Pathogenesis

• HCV enters the blood stream and infects

hepatocytes
• Host cells are not killed but become
persistently infected leading to chronic
disease
• Symptoms of HCV are similar to the viral
infection, and are due to immune response
esp from the Cytotoxic T cells
• 5% of infected patients develop Liver
Cancer
 Disease course

• Viremia detected 1-3/52 after infection

• Prodromal phase 6-7/52, followed by
symptoms like jaundice, abdominal pain,
nausea, loss of appetite and dark urine
• Milder disease compared to HBV
• 15-25%, HCV is cleared but in majority
sets up a chronic active hepatitis which
leads to liver cirrhosis, and failure
 Predisposing factors
• Alcohol consumption and HIV infection or
Chronic HBV promotes chronic HCV
 Treatment and control

• Assess for Chronic Liver Disease and

counsel to avoid factors that worsen the
disease
• Ribavirin and Pegylated interferon-2a and 2b
for 24-28 weeks
• Post exposure Immunoglobulin are NOT
recommended
• Avoid contact with blood or other body fluids
that are infected
 Hepatitis D Virus (Delta Agent)

• HDV causes hepatitis D (hepatitis

delta)
Important Properties and Replicative
Cycle
HDV is a defective virus i.e. it cannot
replicate by itself.
 Hepatitis D Virus (Delta Agent)

 replicate only in cells infected with HBV

because HDV uses the surface antigen of
HBV (HbsAg) as its envelope protein
HBV is the helper virus for HDV
HDV is enveloped virus
HDV replicates in the nucleus
 Treatment

Alpha interferon can mitigate some of

the effects of the chronic hepatitis
caused by HDV but does not
eradicate the chronic carrier state
 no vaccine
 Hepatitis G Virus

HGV has not been documented to

cause any of clinical findings.