This document provides an introduction and overview of hepatitis classification and viruses. It discusses the following key points: 1. Hepatitis is defined as inflammation of the liver caused by viruses. There are 5 main hepatitis viruses - Hepatitis A, B, C, D, and E viruses. Hepatitis B is the only DNA virus, while the others are RNA viruses. 2. The viruses are classified based on their nucleic acid and transmitted through different routes. Hepatitis A and E are transmitted via the fecal-oral route, while Hepatitis B, C, D are blood-borne. 3. Each virus is then discussed in more detail covering features like morphology, epidemiology, pathogenesis, diagnosis, and

1. Presentation Topic
Introduction to Hepatitis
&
Classification of Hepatitis
Subject: Microbiology
Muhammad Abbas
BS MLS(Medical Laboratory Sciences)
MS MLS (Medical Laboratory Sciences)
Baqai Institute Of Medical Technology (BIMT), Baqai Medical University
Karachi

2. Objectives of the Presentation
1. Define hepatitis
2. Classification of Hepatitis
3. Route of Transmission
4. HAV
5. HBV
6. HCV
7. HDV
8. HEV
9. HGV
10. Summary
11. Thank you

3. HEPATITIS
The hepatitis is the inflammation of the liver, hepatocytes by viruses reffered
as hepatitis.

4. Classification of Hepatitis
There are 5 known viruses that infect the liver.
The 5 RNA viruses are:
1) Hepatitis A virus (HAV).
2) Hepatitis C virus (HCV), which was previously called NON-A NON-B
until it was isolated.
3) Hepatitis D virus (HDV).
4) Hepatitis E virus (HEV).
5) Hepatitis G virus.
There is 1 DNA virus called:
1) Hepatitis B virus (HBV)

5. Route of transmission
 Hepatitis A and E are both transmitted via the fecaloral route, while the
rest are transmitted via blood-to blood (parenteral) contact.
 Just as A and E are at both ends of ABCDE, so they are transmitted by
elements of both ends of the GI tract. A = Anal, E = Enteric,
 BCD = BlooD.

6. VIRAL HEPATITIS Acute viral hepatitis:
Viral hepatitis can be a sudden illness with a mild to severe course followed by
complete resolution, this is Called acute viral hepatitis .
The incubation periods is different depend on virus type .
The growth of the virus first results in systemic symptoms much like
flu, with fatigue, low-grade fever, muscle/joint aches, cough, runny nose, and
pharyngitis

7. continue
After two weeks of infection the liver function enzymes elevated i.e
1. Aspartate aminotransferase (AST)
2. Alanine aminotransferase (ALT)
3. Gamma-Glutamyl Transpeptidase (GGT)
4. Alkaline phosphatase. (ALK)
 Chronic viral hepatitis: when virus have a prolonged course of active
disease or silent asymptomatic infection termed chronic viral hepatitis.
 It is more difficult to diagnose because the patient is often asymptomatic
with only an enlarged tender liver and mildly elevated liver function
enzyme levels.

8. The Pattern of Liver Enzyme Elevation
Different diseases result in different patterns of liver function enzyme
elevation.
In viral hepatitis ALT and AST elevate to very high levels, while
GGT,alkaline phosphatase, and bilirubin are only mildly elevated.
A gallstone in the bile duct causes the opposite to occur:
 bilirubin,alkaline phosphatase, and GGT rise higher than ALT and AST
Topic: ABC | By: EFG | Date:

9. Image

10. Hepatitis A Virus (HAV)
 HAV has a naked icosahedral capsid with a positive(+) single-stranded
RNA nucleic acid.
 Epidemiology:
 About 25,000 cases of hepatitis A infection are reported each year in the
U.S.
 Out- breaks often occur secondary to fecal-to-hand-to-mouth contact.
 Young children are the most frequently infected.
 At the other end of the spectrum, a small percentage (1-4%), usually
adults, will develop severe hepatitis.

11. Pathogenesis
 The virus probably replicates in the gastrointestinal tract and spreads to the liver via
the blood. Hepatocytes are infected, but the mechanism by which cell damage occurs is
unclear. HAV infection of cultured cells produces no cytopathic effect. It is likely that
attack by cytotoxic T cells causes the damage to the hepatocytes.
 The infection is cleared, the damage is repaired, and no chronic infection ensues.
Hepatitis caused by the different viruses cannot be distinguished pathologically. The
immune response consists initially of IgM antibody, which is detectable at the time
jaundice appears.
 It is therefore important in the laboratory diagnosis of hepatitis A. The appearance of IgM
is followed 1 to 3 weeks later by the production of IgG antibody, which provides lifelong
protection.

12. Laboratory Diagnosis
The detection of IgM antibody is the most important test.
A fourfold rise in IgG antibody titer can also be used. Isolation
of the virus in cell culture is possible but not available
in the clinical laboratory.

13. Serology
 The HAV capsid is antigenic resulting in the host production of anti-HAV
IgM and later, the anti-HAV IgG.
 anti-HAV IgM in the serum indicates ----> active infection
 Anti-HAV IgG indicates old infection and no active disease.
 Treatment:
 A new vaccine is available and may be given to people at high risk of HAV
infection, such as travelers.

14. Hepatitis B Virus (HBV)
 Hepatitis B is an infectious illness caused by hepatitis B virus (HBV) which infects the liver of humans
 More than 2 billion people have been infected with the hepatitis B virus, and this includes 350
million chronic carriers of the virus.
Transmission:
Transmission of hepatitis B virus results from exposure to infectious blood or body fluids such as
semen and vaginal fluids, while viral DNA has been detected in the saliva, tears, and urine of chronic
carriers with high titer DNA in serum.
 Perinatal infection is a major route of infection in endemic (mainly developing) countries.
 Other risk factors for developing HBV infection include working in a health care setting, transfusions,
and dialysis, acupuncture, tattooing.
 However, Hepatitis B viruses cannot be spread by holding hands, sharing eating utensils or drinking
glasses, kissing, hugging, coughing, sneezing, or breastfeeding…..!
 The acute illness causes liver inflammation, vomiting, jaundice, and (rarely) death.
 Chronic hepatitis B may eventually cause cirrhosis and liver cancer
 The infection is preventable by vaccination

15. Hepatitis B Virus (HBV)
Description
 Hepatitis B virus is an hepadnavirus.
 has a circular genome composed of Double-stranded DNA.
 The viruses replicate through an RNA intermediate form by reverse
transcription.
 replication takes place in the liver,
 Blood tests Liver enzyme and antibodies are used to diagnose the
infection.

16. Hepatitis B Virus (HBV)
Classification
 Hepatitis B virus, ( HBV)
 Group: Group VII (dsDNA-RT)
 Family Hepadnaviridae
Genus : Orthohepadnavirus Avihepadnavirus
species: Hepatitis B virus Duck hepatitis B virus

17. Hepatitis B Virus (HBV)
Morphological characteristcs
1. Envelope
2. icosahedral nucleocapsid
3. The nucleocapsid encloses the viral DNA
4. DNA polymerase that has reverse transcriptase activity.
5. The outer envelope contains embedded proteins entry into,
susceptible cells.
6. The virus is one of the smallest enveloped ,microorganism, 42 nm

18. Hepatitis B Virus (HBV)
 Hepatitis B may exist in 3 different forms:
 Spherical 22nm
 Tubular 22 nm varying length
 Double walled spherical 42 nm(Dein’s particle)

19. Hepatitis B Virus (HBV)
Resistance
 HBV is a relatively heat stable virus (viable room temperature for long
periods
 60 C for 10 hours
 Susceptible to chemical agents(hypochlorine,Gluteraldehyde)
Pathogenesis
 The incubation period is very long from 2-6 months after artificial
inoculation of infected blood and blood products
 Transmission is done by parenteral way, sexual way, microtraumas and
transplacental way

20.  Hepatitis B virus primarily interferes with the functions of the liver by
replicating in liver cells, known as hepatocytes
 HBV virions (DANE particle) bind to the host cell via the preS domain
of the viral surface antigen and are subsequently internalized by
endocytosis.
 PreS and IgA receptors are accused of this interaction.
 HBV-preS specific receptors are primarily expressed on hepatocytes
 During HBV infection, the host immune response causes both
hepatocellular damage and viral clearance.
 adaptive immune response, particularly virus-specific cytotoxic T
lymphocytes (CTLs), contributes to most of the liver injury associated
with HBV infection. By antiviral cytokines

21. Hepatitis B Virus (HBV)
SYMPTOMS & ILLNESS
 Acute infection with hepatitis B virus is associated with acute
viral hepatitis, loss of appetite, nausea, vomiting, body aches, mild fever,
dark urine, and then progresses to development of jaundice. itchy skin has
been an indication as a possible symptom of all hepatitis virus types.
 The infection may be entirely asymptomatic and may go unrecognized.
Chronic infection with hepatitis B virus may be either asymptomatic or
may be associated with a chronic inflammation of the liver (chronic
hepatitis),

22. LABORATORY DIAGNOSIS
Detection of hepatitis B virus infection involve serum or blood tests that detect
either viral antigens or antibodies.
The hepatitis B surface antigen (HBsAg) is most frequently.
Hepatitis B core antigen, or HBcAg. IgM antibodies to the hepatitis B core
antigen anti-HBc IgM
A person negative for HBsAg but positive for anti-HBs has either cleared an
infection or has been vaccinated previously.
Individuals who remain HBsAg positive for at least six months are considered to
be hepatitis B carriers.
Carriers of the virus may have chronic hepatitis B, which would be reflected by
elevated serum alanine aminotransferase (ALT)
PCR tests have been developed to detect and measure the amount of HBV DNA

23. Hepatitis B Virus (HBV)
PREVENTION
 Infants born to mothers known to carry hepatitis B can be treated with antibodies to the
hepatitis B virus (HBIg).
 When given with the vaccine within twelve hours of birth, the risk of acquiring hepatitis
B is reduced 90%.
 The risk of vertical transmission to the newborn can be drastically reduced from 20–90%
to 5–10% by administering to the newborn hepatitis B vaccine (HBV 1) and hepatitis B
immune globulin (HBIG) within 12 hours of birth,
 followed by a second dose of hepatitis B vaccine (HBV 2) at 1–2 months and
 a third dose at and no earlier than 6 months (24 weeks).
WHO recommended joint immunoprophylaxis starting from the newborn, multiple
injections of small doses of hepatitis B immune globulin (HBIg, 200–400 IU per month)
or oral lamivudine (100 mg per day) in HBV carrier mothers with a high degree of
infectiousness (>106 copies/ml) in late pregnancy (the last three months of pregnancy

24. NON-A, NON-B HEPATITIS VIRUSES
 The term “non-A, non-B hepatitis” was coined to describe the cases of
hepatitis for which existing serologic tests had ruled out all known viral
causes. The term is not often used because the main cause of non-A, non-
B hepatitis, namely, HCV, has been identified. In addition, HDV and HEV
have been described.

25. HEPATITIS C VIRUS (HCV)
 Disease
HCV causes hepatitis C.
Important Properties
 HCV is a member of the flavivirus family. It is an enveloped virion
containing a genome of single-stranded, positive polarity RNA.

26. Transmission & Epidemiology
Humans are the reservoir for HCV. It is transmitted primaril via blood. At
present, injection drug use accounts for almost all new HCV infections.
Transmission from
mother to child during birth is another very common mode of transmission.
Transmission via blood transfusion rarely occurs because donated blood
containing antibody to HCV is discarded.
 Transmission via needlestick injury occurs, but the risk is lower than for
HBV. Sexual transmission is uncommon, and there is no evidence for
transmission across the placenta or during breast feeding.
 HCV is the most prevalent blood-borne pathogen in the United States.

27.  Approximately 4 million people in the United States (1%– 2% of the
population) are chronically infected with HCV. Worldwide, it is estimated
that 180 million people are infected with HCV. In the United States, about
1% of blood donors have antibody to HCV. People who share needles when
taking intravenous drugs are very commonly infected.

28. Pathogenesis & Immunity
HCV infects hepatocytes primarily, but there is no evidence for a virus-induced
cytopathic effect on the liver cells. Rather, death of the hepatocytes is probably
caused by immune attack by cytotoxic T cells.
Alcoholism greatly enhances the rate of hepatocellular carcinoma in HCV-
infected individuals. This supports the idea that the cancer is caused by
prolonged liver damage and the consequent rapid growth rate of hepatocytes as
the cells attempt to regenerate rather than by a direct oncogenic effect of HCV.
 Added support for this idea is the observation that patients with cirrhosis of any
origin, not just alcoholic cirrhosis, have an increased risk of hepatocellular
carcinoma.

29. Clinical Findings
 The acute infection is often asymptomatic. If symptoms, such as malaise,
nausea, and right upper quadrant pain do occur, they are milder than
occur with infection by the other hepatitis viruses. Fever, anorexia,
nausea, vomiting, and jaundice are common. Dark urine, pale feces, and
elevated transaminase levels are seen.

30. Laboratory Diagnosis
 HCV infection is diagnosed by detecting antibodies to HCV in an enzyme-
linked immunosorbent assay (ELISA)
 The test does not distinguish between IgM and IgG and does not
distinguish between an acute, chronic, or resolved infection.
 Assays for HCV RNA are the most sensitive tests for HCV infection and
represent the “gold standard” in establishing a diagnosis of hepatitis C.

31. HEPATITIS D VIRUS (HDV, DELTA VIRUS)
Disease
HDV causes hepatitis D (hepatitis delta).
Important Properties
 HDV can replicate only in cells also infected with HBV because HDV uses
the surface antigen of HBV (HBsAg) as its envelope protein. HBV is
therefore the helper virus for HDV. HDV is an enveloped virus with an
RNA genome that is a single-stranded, negative-polarity, covalently closed
circle.

32. The RNA genome of HDV is very small and encodes only one protein, the
internal core protein called delta Antigen.
HDV has no virion polymerase; the genome RNA is replicated and
transcribed by the host cell RNA polymerase.

33. Transmission & Epidemiology
HDV is transmitted by the same means as is HBV (i.e., sexually, by blood,
and perinatally). In the United States, most HDV infections occur in
intravenous drug users who share needles. HDV infections occur
worldwide, with a similar distribution to that of HBV infections.

34. Pathogenesis & Immunity
 It seems likely that the pathogenesis of hepatitis caused by HDV and HBV is
the same (i.e., the virus-infected hepatocytes are damaged by cytotoxic T
cells). There is some evidence that delta antigen is cytopathic for hepatocytes.
IgG antibody against delta antigen is not detected for long periods after
infection; it is therefore uncertain whether long-term immunity to HDV
exists.

35. Laboratory Diagnosis
 The diagnosis of HDV infection in the laboratory is made by detecting
either delta antigen or IgM antibody to delta antigen in the patient’s
serum.

36. HEPATITIS E VIRUS (HEV)
 HEV is a major cause of hepatitis transmitted by the fecal–oral route. It is thought
to be more common than HAV in many developing countries. It is a common cause
of waterborne epidemics of hepatitis in Asia, Africa, India, and Mexico but is
uncommon in the United States. HEV is a nonenveloped, single-stranded RNA
virus classified as a member of the hepevirus family.
 Clinically the disease resembles hepatitis A, with the exception of a high mortality
rate in pregnant women. Chronic infection resulting in chronic hepatitis and
cirrhosis but not hepatocellular carcinoma, occurs in immunocompromised
individuals such as HIV-infected patients, those who are receiving cancer
chemotherapy, and patients who are receiving immunosuppressive drugs to
prevent rejection of solid-organ transplants.

37. Lab Diagnosis
 The diagnosis is typically made by detecting IgM antibody
 to HEV. A PCR assay that detects HEV RNA in
 patient specimens is available. There is no antiviral drug
 available for acute infection in immunocompetent patients.

38. HEPATITIS G VIRUS (HGV)
In 1996, hepatitis G virus (HGV) was isolated from patients with post
transfusion hepatitis. HGV is a member of the flavivirus family.
However, unlike HCV, which is clearly the cause of both acute hepatitis
and chronic active hepatitis and predisposes to hepatocellular carcinoma,
HGV has not been documented to cause any of these clinical findings.

39. Epidemiology and transmission
HGV is transmitted via sexual intercourse and blood. It is carried in the
blood of millions of people worldwide. In the United States, it is found in
the blood of approximately 2% of random blood donors, 15% of those
infected with HCV, and 35% of those infected with HIV.
 Patients co-infected with HIV and HGV have a lower mortality rate
and have less HIV in their blood than those infected with HIV alone. It is
hypothesized that HGV may interfere with the replication of HIV. (HGV is
also known as GB virus C.)