Hepatitis A, D, E & G

HEPATITIS A ,D, E & G
INTRODUCTION
• VIRAL HEPATITIS- is a primary infection of the liver caused by heterogeneous
group of ‘hepatitis viruses’.
• hepatitis viruses cause inflammation of liver producing identical histopathologic

lesions similar to illness such as fever, nausea, vomiting and jaundice.
CLASSIFICATION
1. INFECTIVE OR INFECTIOUS HEPATITIS
- occurs sporadically or as epidemics.
- affects mainly children and young adults.
- transmitted through faecal-oral route.
2. HOMOLOGOUS SERUM JAUNDICE/SERUM HEPATITIS/TRANSFUSION

HEPATITIS
-transmitted mainly by inoculation or blood transmission.
-associated with human or homologous antisera used for prophylaxis or therapy
TYPES OF HEPATITIS VIRUSES
• Hepatitis A and B
• Non-A non-B hepatitis (NANB): C, D, E and G.
• All are RNA viruses except type B a DNA type.
• HAV: causes infectious hepatitis.

• HBV: causes serum hepatitis.
• HCV: causes post-transfusion hepatitis.
• HDV: is defective virus, need HBV for replication.
• HEV: agent of enterically transmitted Non-A, Non-B hepatitis.
• HGV.
HEPATITIS A VIRUS -HAV
• belongs to the family PICORNAVIRIDAE.
• GENUS: Hepatovirus.
MORPHOLOGY
• Size: 27-32nm
• Shape: spherical particles with icosahedral symmetry-with
linear ssRNA.
• Has one serotype
• Does not cross-react with other hepatitis viruses.
• Genotypes: about seven are known.
Electron micrograph of 27-nm
hepatitis A virus aggregated
with antibody
RESISTANCE
• HAV is resistant to disinfectants.
-It is stable to acid, heat (60°C for 1 hour) and 20% ether
-preservation: in dried state for 1 month and stored for years at -20°C.
-It is destroyed by autoclaving, boiling in water for 5 minutes, by hot air oven, by
UV rays and by treatment with formalin or chlorine (10-15 ppm for 30 minutes).
MODE OF TRANSMISSION
• Is by faecal-oral route.
• Rarely transmitted by sexual (homosexuals through oro-genital contact)
• And parental routes (infected blood products or needle pricks).
Epidemiology
• Hosts: humans.
• Age: children and adolescents (5-14 years), majority is subclinical (80-95%) who
excrete viruses in faeces for longer time.
• Adults: more icteric (75-90%) than children-higher mortality rate
EPIDEM. CONTI…
Risk factors
• Poor personal hygiene and overcrowding.
-Mostly in children of age 10 years (90%) in developing countries.
-Adults have protective antibodies and are immune to HAV.
-Outbreaks: common in summer camps, day-care centers, families and institutions,
neonatal ICUs and among military troops.
• Recurrent epidemics: common due to faecal contamination of a single source, e.g.
Drinking water, milk or food such as raw vegetables, salad, frozen strawberries, green
onions and shell fish.
• Seasonal incidence: usually in rainfall and early winter.
• Virus excretion: in faeces may be 2 weeks before 2 weeks after appearance of jaundice.
CLINICAL MANIFESTATION
• Incubation period: 15 to 45 days (mean 30)
• Onset is subacute.
Characteristics of infection
-Pre-icteric phase: mainly GIT symptoms such as nausea and vomiting
-Icteric phase or jaundice: dark urine, yellowish sclera and mucus membrane.
• Complete recovery: occurs in 98% cases.
• No chronic or carrier cases.
COMPLICATIONS OF HAV
• Fulminant hepatitis -with severe necrosis of hepatocytes.

• Relapsing hepatitis- develops weeks to months after apparent recovery from
acute hepatitis.
• Cholestatic hepatitis: with protracted cholestatic jaundice and pruritus.
LABORATORY DIAGNOSIS OF HAV
• Specimen: Stool and serum.
• Direct demonstration: virus can be visualized by immunoelectron microscopy (IEM) in fecal

extracts during late incubation period and in the preicteric phase.
• Serology: diagnosis is usually by antibody demonstration.

• Anti HAV antibody detection by ELISA.
-Appearance of IgM during acute phase
- Liver enzymes elevated after 2 weeks- rise in IgM abs
-IgM disappears within 3-6 months
-IgG antibodies appear after a week after IgM appears, it persists for years.
Interpretation
• Anti-HAV IgM positive: indicates acute infection with HAV.
• Anti-HAV IgG antibody detection-in absence of IgM: indicates past infection or recovery.
• Detection of HAV particles
-HAV appears in stool from -2 to +2 weeks of jaundice.
-HAV is also detected in liver, bile and blood by immunoelectron microscopy.
• HAV antigen detection

-ELISA is used to detect HAV antigen from stool sample from -2 to +2 weeks of
jaundice.
Isolation
• HAV is difficult to grow in cell line.
• Non-specific findings: elevated liver enzymes and serum bilirubin level.
TREATMENT
• No specific antiviral drug available.
Prevention
• Improving hygiene
-Hand hygiene before and after use of toilet.
- Sanitary disposal of infected faecal material b (disinfection with 0.5%
hypochlorite).
-Purification of drinking water by effective filtration and adequate chlorination with
1 mg/l chlorine.
-Use of boiled water during outbreaks.
VACCINES
• Formaldehyde inactivated vaccine:
-Prepared from human fetal lung fibroblast cell lines such as MRC5 and WI 38.
-Given to children after 12 months of age.
-Single dose given intramuscularly
-booster dose: given at 6-12 months gap.
• Live attenuated vaccine

-Is a single dose given subcutaneously
- Uses H2 and L-A-1 strains of HAV
- Prepaid in human diploid cell line
• Human immunoglobulin (HAV-Ig)
-Used for post-exposure prophylaxis of intimate contacts of persons with HAV or to
travellers.
Dosage: 0.02ml/kg- gives protection for 1-2 months.
HEPATITIS D VIRUS
• Is a defective virus
• Cannot replicate by itself- depends on HBV for survival.
Morphology
• Resembles viroids
• Small size: 35nm
• Consists of circular, negative-sense ssRNA.
• Protein coat made of single protein-hepatitis d antigen (HDAg).
• Surrounded by envelope protein derived from HBsAg from HBV-hence called
defective virus.
TRANSMISSION
Parenteral route, sexual and vertical routes.
Co-infection: occurs when person is exposed to serum containing both HDV and HBV.
Super-infection: occurs when a chronic carrier of HBV is exposed to serum with HDV.
-Results in disease 30-50 days later with 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, disease progresses to cirrhosis and hepatocellular carcinoma (HCC).
- Mortality rate higher (> 20%).
LABORATORY DIAGNOSIS
A. In co-infection: IgM against both HDAg and HBcAg are elevated
-IgM anti-HDV appears late and is short-lived.
B. In super-infection: HBV appears already as carrier, IgG anti-HBc is detected

-Anti-HDV would be IgM type initially
-In chronic state: mixture of IgM and igg persists for months or longer.
C. Anti HBc antibody differentiates 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.
• HDV RNA is detected in blood and liver before and early days of acute phase of both
infections.
Epidemiology
• Globally- 15 million people are infected with HDV- where 5% of 350 million are infected
with HBV.
• Infection occurs world wide.
Treatment
-IFN-a
Prevention
HBV vaccination and prophylaxis measures.
HEPATITIS E VIRUS (HEV)
• Causes an enterically transmitted hepatitis- in young adults.
Morphology
• Resembles caliciviruses.
• Size: small (30-32 nm), non-enveloped with icosahedral symmetry.
• Contains positive-sense, ssRNA and a specific antigen (HEV-Ag).
Genotypes
• HEV has a single serotype, five genotypes.
• Genotypes: -four are detected in humans.
- Type 1 and 2 appear to be more virulent.
- Type 3 and 4 are more attenuated and account for subclinical infections.
CLINICAL MANIFESTATION
• Incubation period: 14-60 days.
• Mostly present as self-limiting acute hepatitis lasting for several weeks.
• Fulminant hepatitis- occurs in 1-2% of cases; except for pregnant women at
higher risk (20%).
• No chronic infection or carrier state.
EPIDEMIOLOGY
• HEV is a zoonotic disease- affects monkeys, cats, pigs and dogs.
• Transmission: faecal-oral route via sewage contamination of drinking water or
food.
• Epidemics: most common in India, Asia, Africa and Central America.
• Age: young adults (20-40 years).
LABORATORY DIAGNOSIS
• Specimens: stool, serum.
• HEV RNA is detected by reverse transcriptase PCR.
• HEV virions- detected by electron microscopy.
• Serum antibody detection- by ELISA.

IgM anti-HEV: appears in serum same time with appearance of liver enzymes-
indicates acute infection.
 Igg anti-HEV: replace IgM in 2-4 weeks- indicates recovery or past infection.
TREATMENT
• No specific antiviral drugs available.
Prevention
• Same prevention measures like for HAV.
HEPATITIS G VIRUS (HGV)
• Also referred as GB virus C.
• Related to hepatitis c.
• Family: flaviviridae, genus: Pegivirus.
• Transmission: contaminated blood or blood products via sexual contact.
• Does not cause hepatitis- replicates in bone marrow and spleen.
• Classified into 6 genotypes.
• Commonly co-infects people with HIV.
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HEPATITIS A ,D, E & G

• hepatitis viruses cause inflammation of liver producing identical histopathologic

2. HOMOLOGOUS SERUM JAUNDICE/SERUM HEPATITIS/TRANSFUSION

• HAV: causes infectious hepatitis.

• Fulminant hepatitis -with severe necrosis of hepatocytes.

• Direct demonstration: virus can be visualized by immunoelectron microscopy (IEM) in fecal

• Serology: diagnosis is usually by antibody demonstration.

• HAV antigen detection

• Live attenuated vaccine

B. In super-infection: HBV appears already as carrier, IgG anti-HBc is detected

C. Anti HBc antibody differentiates between co-infection and super-infection.

• Serum antibody detection- by ELISA.

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