The document summarizes different types of hepatitis viruses (A-E and G). It provides details on the structure, transmission, clinical presentation, diagnosis, and treatment of Hepatitis A, B, C, D, and E. Hepatitis A and E cause acute liver infection spread through contaminated food or water. Hepatitis B, C, and D can result in chronic infection and lead to cirrhosis or liver cancer. While symptoms vary, jaundice is common. Diagnosis involves antibody, antigen, or nucleic acid detection. Prevention relies on vaccination, safe blood supply, and hygiene.

1. Hepatitis Viruses
Microbiology students seminars:
Bshr Nammouz

2. Hepatitis viruses:
- From A to E (HAV, HBV, HCV, HDV, HEV) and G (HGV).
- HAV and HBV are the classic.
- All infect and damage liver.

3. Hepatitis A

4. Hepatitis A
- Known as infectious hepatitis, Spread
by fecal-oral route, results from the
consumption of contaminated water,
shellfish, or other food.
- It is a picornavirus, 27-nm, naked,
icosahedral capsid, A positive-sense
single-stranded RNA, One serotype.

5. Hepatitis A: Replication:
- Like other picornaviruses, but HAV is not cytolytic and is released by exocytosis.
- Clinical isolates are difficult to grow in cell culture.

6. Hepatitis A: Pathogenesis:
- HAV is shed in large quantity into the
stool approximately 10 days before
symptoms of jaundice appear or
antibody can be detected.
- Although interferon limits viral replication, natural
killer and cytotoxic T cells are required to eliminate
infected cells.
- Antibody, complement, and antibody-dependent
cellular cytotoxicity also facilitate clearance of the
virus and induction of immunopathology.

7. - Icterus resulting from the damage of
the liver occurs when cell-mediated
immune response and antibody to the
virus can be detected.
- Antibody protection against reinfection
is lifelong.
- Unlike HBV, HAV is not associated with
hepatic cancer.

8. Hepatitis A: Epidemiology:
- Spread rapidly because most infected people
are contagious 10 to 14 days before
symptoms occur.
- HAV is released in stool in high
concentrations and is spread via fecal-oral
route.
- Spread in contaminated water, in food, and
in dirty hands.
- Raw or improperly treated sewage can taint
the water supply and contaminate shellfish.

9. Hepatitis A: Clinical Syndrome:
- Similar to HBV.
- Immune-mediated damage to the liver.
- Intensify for 4-6 days before the icteric (jaundice) phase.
- Can last up to 2 months.
- Initial symptoms: fever, fatigue, nausea, loss of appetite,
vomiting, and abdominal pain.
- May be accompanied: dark urine (bilirubinuria), pale stool,
and then jaundice, abdominal pain and itch.
- Rare fulminant (high fulminant mortality).

10. Hepatitis A: Laboratory Diagnosis:
- The course of clinical symptoms, identification for known infected source.
- Most important: anti-HAV IgM.
- Virus isolation is not performed.
Treatment, Prevention, Control:
- Interrupt the fecal-oral spread.
- Prophylaxis: immune serum globulin: before or early in incubation period
- Vaccine: killed HAV, recommended for all children < 1 yo.

11. Hepatitis B

12. Hepatitis B:
- Previously known as serum hepatitis.
- Spread parenterally by blood or needles, by sexual
contact, and perinatally.
- Incubation period of 3 months.
- After which icteric symptoms start insidiously. Might be followed by chronic
hepatitis.
- Causally associated with primary hepatocellular carcinoma (PHC).

13. - Specifically, the genome is small, circular,
partly double-stranded DNA of 3200 bases.
- Encodes a reverse transcriptase and replicates
through an RNA intermediate.
- Major member of hepadnaviruses.
- Difficult to culture.
- Small enveloped DNA virus with several unusual properties.

15. - The virion includes a protein kinase and a
polymerase with reverse transcriptase and
ribonuclease H activity, as well as a P protein
attached to the genome.
- The virion is surrounded by an icosahedral
capsid formed by the hepatitis B core antigen
(HBcAg) and an envelope containing three
forms of glycoprotein hepatitis B surface
antigen (HBsAg).

16. - HBsAg-containing particles are released into the
serum, outnumber the actual virions. Has two
forms: spherical, filamentous.
- These particles serve as antigen decoy particles.

17. Hepatitis B: Replication:
- Attachment by HBsAg.
- Nucleocapsid delivers the genome to the
nucleus.
- The partial DNA strand becomes complete to
form completed double-stranded DNA circle.
- Many points to start transcription on DNA
resulting in three classes of mRNA causing
sometimes shedding of the HBe and
incorporation of HBc into the virion.

18. Hepatitis B: Pathogenesis and Immunity:
- HBV can cause acute or chronic, symptomatic or
asymptomatic disease determined by person’s
immune response.
- HBV found majorly in blood (most effective
infection), but also in semen, saliva, milk, vaginal
and menstrual secretions, and amniotic fluid.
- The virus starts replication after three days of
acquisition, symptoms may not be observed for
45 days or longer because they are primarily
caused by immunopathology.

19. Hepatitis B: Epidemiology:
- In the world one out of three people have been infected with HBV.
- Chronic HBV infection > 350 million people.
- Transmission through contaminated blood and through very close personal contact involving
the exchange of semen, saliva, and vaginal secretions.
- Importance of blood screening.
- 1-2 million deaths per year.
- It’s decreasing due to vaccines.

20. Hepatitis B: Clinical Syndrome:
Acute infection:
- Less symptomatic or asymptomatic in children.
- Long incubation, insidious onset.
- Prodromal period: fever, malaise, anorexia.
- Followed by: nausea, vomiting, abdominal discomfort, and chills.
- Soon thereafter: the classic icteric symptoms: (e.g., jaundice, dark
urine, pale stool).
- May promote hypersensitivity reactions caused by immune
complexes of HBsAg and antibody.

21. Chronic infection:
- 5-10% of cases.
- Usually after mild or inapparent initial disease.
- One third of those people have chronic active
hepatitis (continues destruction and causes
scarring of the liver, cirrhosis, liver failure, or
PHC).
- The other two third have chronic passive
hepatitis.

22. PHC (primary Hepatocellular Carcinoma):
Hepatic carcinoma, primary. Large multifocal hepatocellular carcinoma (HCC) in an 80-
year-old man without cirrhosis.

23. Hepatitis B: Laboratory Diagnosis:
- The initial diagnosis can be made on basis of the clinical symptoms and the presence of liver
enzymes in blood.
- Serology describes the course and the nature of the disease.

24. - IgM anti-HBc is the best way to diagnose a recent acute infection.
- The amount of virus in blood: determined by quantitative genome assays using PCR.

25. Hepatitis B: Treatment, prevention, and control:
- Hepatitis B immune globulin may be administered
within a week of exposure.
- Chronic infection treatment: drugs targeted at the
polymerase or the nucleosides analogs for a year.
- Prevention: screening blood, safe sex, avoiding some
lifestyles, wearing gloves in hospitals....
- Vaccination: recommended for infants, children, and
high risk groups of people, a series of three
injections.

26. Hepatitis C

27. Hepatitis C: Structure, replication, and pathogenesis:
- The only member of the Hepacivirus genus of the Flaviviridae family.
- 6 genotypes. Positive-sense RNA genome, enveloped.
- Viral RNA-dependent RNA polymerase (gives antigen variability).
- The ability of HCV to remain cell associated and prevent host cell death promotes persistent
infection but results in liver disease later in life.
- Virus particles can be produced in chronically infected, potentially asymptomatic individuals.
- As for HBV, once established, the chronic infection can exhaust CD8 cytotoxic T cells so they
cannot resolve the infection.
- It’s suggested that HCV may predispose the development of PHC.

28. Hepatitis C: Epidemiology:
- HCV is transmitted primarily in infected blood and sexually.
- Almost every HIV-infected people are HCV-infected too.
- The high incidence of chronic asymptomatic infections
promotes the spread.
Clinical Syndrome:
- Acute Hepatitis ends with recovery.
- Severe rapid progression to cirrhosis.
- Chronic persistence often progresses to chronic
active hepatitis.

29. Hepatitis C:
- Laboratory diagnosis: based on ELISA recognition of anti-HCV antibody or detection
of the RNA genome. Antibody is not always detectable: the gold standard for
confirming diagnosis and following antiviral therapy:
Genome detection and quantitation by RT-PCR, branched-chain DNA, and related
techniques.
- Drugs: recombinant interferon-⍺ or pegylated interferon, alone or with ribavirin -
boceprevir - telaprevir - ledipasvir - sofosbuvir.
- Precautions for preventing HCV are similar for HBV.

30. Hepatitis G

31. Hepatitis G:
- Resembles HCV in many ways.
- Flavivirus. Transmitted in blood, and has a predilection for chronic hepatitis
infection.
- It is identified by detection of the genome by RT-PCR or other RNA detection
methods.

32. Hepatitis D

33. Hepatitis D:
- Single-stranded RNA, circular, forms a rod shape as a result of its extensive base
pairing.
- Uses HBV and targeted cell to replicate and produce its protein.
- HBsAg is essential for packaging the virus.
- 40% of fulminant hepatitis infections.

34. Hepatitis E

35. Hepatitis E:
- Spreads by fecal-oral route. Especially in contaminated water.
- Calicivirus, RNA genome, naked capsid.
- More problematic in developing countries.
- Symptoms are similar to HAV, causes only acute disease.
- Infection is serious in pregnant women (mortality of 20%).

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