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Hepatitis B Virus and others
viruses causing Hepatitis
Dr.Hamisi Mkindi
Dr.Lusato Bwire
Outline
• Introduction
• Epidemiology
• Molecular Virology
• Life cycle
• Diagnsosis-Biomarkers
• How HBV evade immune system
• Natural hx of HBV
• Treatment and Prevention
Introduction
• Viral hepatitis is a systemic disease with
primary inflammation of the liver by any one
of a heterogenous group of hepatotropic
viruses.
• Most common-HepA,HepB,HepC,HepD and
E.
• Others-herpses
simplex,cytomegalovirus,Epstein Barr virus
and yellow fever
Epidemiology
• 2.4B of the world infected with one/more hep
Virus1
• Viral hepatitis is responsible for approximately
1·34 million deaths annually1
• HepB and C responsible for 90% of these
fatalities,10% others1
• WHO estimates that 296 million people were
living with chronic hepatitis B infection in 2019,
with 1.5 million new infections each year2
• Hepatitis B is estimated to account for 87 890
deaths annually in sub-Saharan Africa3
1. Update on global epidemiology of viral hepatitis and preventive strategies. Jefferies, Meryem. s.l. : World J Clin Cases, 2018.
Epi-Cont….
• A seroprevalence of HBV infection in the country
was reported to be 6% in the general population
of Dar es Salaam4
• Chronic HBV infection is common among
Tanzanian HCWs-7%5
• High endemic areas-perinatal/horizontal
transmission-WHO
• Acquired in adulthood -chronic hepatitis < 5%
of cases,in infancy and early childhood-chronic
hepatitis in about 95%
4. Kilonzo, Semvua. Journal Of Tropical Medicine. Hindawi. [Online] 2018.
https://www.hindawi.com/journals/jtm/2018/4239646/#introduction. 4239646.
Molecular-Virology
VIRUS Hep A Hep B Hep C Hep D Hep E
Family Picornavirid
ae
Hepadnavir
idae
Flaviviridae Deltavirus Hepevirus
Envelope No Yes Yes Yes No
Stability Acid stable Acid
sensitive
Acid sensitive Acid
sensitive
Acid/Heat
stable
Transmissio
n
Fecal-oral parenteral parenteral Parenteral Fecal-oral
Prevalence High High moderate Low,regional regional
Chronic D’se Never Often,5-
10%
adult,90%
infacts-HPC
Often,80%,H
PC
Often,Co
Inf.HBV
Never,low
immune,pre
gnant
severe form
Genome ssRNA pdsDNA ssRNA ssRNA ssRNA
1/7/2023
https://wdrfree.com/stock-vector/viral-dna
7
1/7/2023 8
LIFE CYCLE
Clinical Presentation
• Illness ranges from asymptomatic to fulminant
• Jaundice,Fatigue ,Abdominal pain ,Loss of
appetite ,Nausea, vomiting and Joint pain and
fever
• Biomarkers
Biomarkers Terms
• HBsAg /Anti-HBs
• HBeAg /Anti-HBe
• IgM anti-HBc/IgG anti-HBc
Serologic Patterns
Serological pattern cont…
Patterns cont…
• 6 genotypes reported HBV-S gene
mutation
• Tanzania,phylogenetic analysis of S-gene
sequence revealed HBV genotype A1
(HBV/A1) to be the most common in
86.1%-Chronicity,HCC.
• Not responding to nucleotide analogs but
rather interferons
Immune system evasion
• Sequestration in sites that are inaccessible to the immune
system.
• Mutations within the pre-core/core genes of HBV can result
in loss of expression of the hepatitis e antigen (HBeAg)
• Mutations in the envelope gene that lead to a loss of
detectable HBsAg expression and viral persistence in the
face of anti-HBsAg antibodies
• Disrupting function of activated T cells
Natural History of HBV
• Two major determinants of the outcome of
acute HBV are age and immunocompetence at
time of infection.
• Children-Initial infection subclinical-chronicity
• Four stages of natural history
Natural History of HBV
Natural History of HBV
Treatment HBV
Prevention
• Universal vaccination of infants beginning at birth (≥3
intramuscular doses)-WHO reccomendation
• Prenatal maternal HBsAg screening and if HBsAg
positive, hepatitis B immune globulin 0.5 mL at birth
along with vaccination.
• Tenofovir 300 mg starting in the third trimester in
women with HBV DNA >108 IU/mL (some authorities
recommend antiviral therapy for mothers with HBV
DNA >106 IU/mL)
Vaccination
References
1. Update on global epidemiology of viral hepatitis and preventive strategies.
Jefferies, Meryem. s.l. : World J Clin Cases, 2018.
2. WHO. World Helath Organization. [Online] 2021. who.int/news-room/fact-
sheets/detail/hepatitis-b.
3. The lancet. [Online] 2017.
www.thelancet.com/journals/langas/article/PIIS2468-1253(17)30295-
9/fulltext.
4. Kilonzo, Semvua. Journal Of Tropical Medicine. Hindawi. [Online] 2018.
https://www.hindawi.com/journals/jtm/2018/4239646/#introduction. 4239646.
5. A.Mueller. BMC Infectious Disease. Biomed Central. [Online] 2015.
https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-015-1129-z.

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Viral hepatitis 2022.pptx

  • 1. Hepatitis B Virus and others viruses causing Hepatitis Dr.Hamisi Mkindi Dr.Lusato Bwire
  • 2. Outline • Introduction • Epidemiology • Molecular Virology • Life cycle • Diagnsosis-Biomarkers • How HBV evade immune system • Natural hx of HBV • Treatment and Prevention
  • 3. Introduction • Viral hepatitis is a systemic disease with primary inflammation of the liver by any one of a heterogenous group of hepatotropic viruses. • Most common-HepA,HepB,HepC,HepD and E. • Others-herpses simplex,cytomegalovirus,Epstein Barr virus and yellow fever
  • 4. Epidemiology • 2.4B of the world infected with one/more hep Virus1 • Viral hepatitis is responsible for approximately 1·34 million deaths annually1 • HepB and C responsible for 90% of these fatalities,10% others1 • WHO estimates that 296 million people were living with chronic hepatitis B infection in 2019, with 1.5 million new infections each year2 • Hepatitis B is estimated to account for 87 890 deaths annually in sub-Saharan Africa3 1. Update on global epidemiology of viral hepatitis and preventive strategies. Jefferies, Meryem. s.l. : World J Clin Cases, 2018.
  • 5. Epi-Cont…. • A seroprevalence of HBV infection in the country was reported to be 6% in the general population of Dar es Salaam4 • Chronic HBV infection is common among Tanzanian HCWs-7%5 • High endemic areas-perinatal/horizontal transmission-WHO • Acquired in adulthood -chronic hepatitis < 5% of cases,in infancy and early childhood-chronic hepatitis in about 95% 4. Kilonzo, Semvua. Journal Of Tropical Medicine. Hindawi. [Online] 2018. https://www.hindawi.com/journals/jtm/2018/4239646/#introduction. 4239646.
  • 6. Molecular-Virology VIRUS Hep A Hep B Hep C Hep D Hep E Family Picornavirid ae Hepadnavir idae Flaviviridae Deltavirus Hepevirus Envelope No Yes Yes Yes No Stability Acid stable Acid sensitive Acid sensitive Acid sensitive Acid/Heat stable Transmissio n Fecal-oral parenteral parenteral Parenteral Fecal-oral Prevalence High High moderate Low,regional regional Chronic D’se Never Often,5- 10% adult,90% infacts-HPC Often,80%,H PC Often,Co Inf.HBV Never,low immune,pre gnant severe form Genome ssRNA pdsDNA ssRNA ssRNA ssRNA
  • 9.
  • 11. Clinical Presentation • Illness ranges from asymptomatic to fulminant • Jaundice,Fatigue ,Abdominal pain ,Loss of appetite ,Nausea, vomiting and Joint pain and fever • Biomarkers
  • 12. Biomarkers Terms • HBsAg /Anti-HBs • HBeAg /Anti-HBe • IgM anti-HBc/IgG anti-HBc
  • 15. Patterns cont… • 6 genotypes reported HBV-S gene mutation • Tanzania,phylogenetic analysis of S-gene sequence revealed HBV genotype A1 (HBV/A1) to be the most common in 86.1%-Chronicity,HCC. • Not responding to nucleotide analogs but rather interferons
  • 16. Immune system evasion • Sequestration in sites that are inaccessible to the immune system. • Mutations within the pre-core/core genes of HBV can result in loss of expression of the hepatitis e antigen (HBeAg) • Mutations in the envelope gene that lead to a loss of detectable HBsAg expression and viral persistence in the face of anti-HBsAg antibodies • Disrupting function of activated T cells
  • 17. Natural History of HBV • Two major determinants of the outcome of acute HBV are age and immunocompetence at time of infection. • Children-Initial infection subclinical-chronicity • Four stages of natural history
  • 21. Prevention • Universal vaccination of infants beginning at birth (≥3 intramuscular doses)-WHO reccomendation • Prenatal maternal HBsAg screening and if HBsAg positive, hepatitis B immune globulin 0.5 mL at birth along with vaccination. • Tenofovir 300 mg starting in the third trimester in women with HBV DNA >108 IU/mL (some authorities recommend antiviral therapy for mothers with HBV DNA >106 IU/mL)
  • 23. References 1. Update on global epidemiology of viral hepatitis and preventive strategies. Jefferies, Meryem. s.l. : World J Clin Cases, 2018. 2. WHO. World Helath Organization. [Online] 2021. who.int/news-room/fact- sheets/detail/hepatitis-b. 3. The lancet. [Online] 2017. www.thelancet.com/journals/langas/article/PIIS2468-1253(17)30295- 9/fulltext. 4. Kilonzo, Semvua. Journal Of Tropical Medicine. Hindawi. [Online] 2018. https://www.hindawi.com/journals/jtm/2018/4239646/#introduction. 4239646. 5. A.Mueller. BMC Infectious Disease. Biomed Central. [Online] 2015. https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-015-1129-z.

Editor's Notes

  1. www.ncbi.nlm.nih.gov/pmc/articles/PMC6232563/#_ffn_sectitle
  2. Update on global epidemiology of viral hepatitis and preventive strategies. Jefferies, Meryem. s.l. : World J Clin Cases, 2018. WHO. World Helath Organization. [Online] 2021. who.int/news-room/fact-sheets/detail/hepatitis-b. The lancet. [Online] 2017. www.thelancet.com/journals/langas/article/PIIS2468-1253(17)30295-9/fulltext.
  3. 4. Kilonzo, Semvua. Journal Of Tropical Medicine. Hindawi. [Online] 2018. https://www.hindawi.com/journals/jtm/2018/4239646/#introduction. 4239646. 5. A.Mueller. BMC Infectious Disease. Biomed Central. [Online] 2015. https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-015-1129-z. https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-015-1129-z 4.https://www.hindawi.com/journals/jtm/2018/4239646/#introduction
  4. Protein capsid of naked viruses is less susceptible to environmental consitions(lipid solvents,pH,temperature) than enveloped viruses because the envelopeis made in part with phopspholipids.Once the envelope is lysed,the virus loses its functional receptorss and is not still able to infect susceptible host
  5. The hepatitis B virus can survive outside the body for at least 7 days. During this time, the virus can still cause infection if it enters the body of a person who is not protected by the vaccine. The incubation period of the hepatitis B virus ranges from 30 to 180 days. The virus may be detected within 30 to 60 days after infection and can persist and develop into chronic hepatitis B, especially when transmitted in infancy or childhood
  6. Viruses may escape immune recognition by sequestration in sites that are inaccessible to the immune system
  7. HBsAg,(HBeAg),high levels of serum HBV DNA characterize the first immunotolerant phase.   In adult acquired infection this phase marks the incubation period of acute HBV infection and lasts about 2–4 weeks. By contrast, in perinatal infection this phase often lasts for decades. During this phase patients have no symptoms, normal or slightly increased serum alanine aminotransferase (ALT) levels and minimal histological activity, which implies that there is a lack or very weak immune response against the infected hepatocytes.   During the course of HBV infection, for unknown reasons, patients may enter the second immunoactive phase which is associated with a decrease of HBV DNA and an increase of ALT and histologic activity, reflecting the host immune mediated lysis of infected hepatocytes. In acute HBV infection this phase is the period of clinical symptoms and jaundice and usually lasts for 3–4 weeks, whereas in patients with chronic HBV infection it lasts from months to years.     The third low or non-replicative phase involves seroconversion from HBeAg to anti-HBe usually preceded by a marked reduction of serum HBV DNA levels below 105 copies per ml, not detectable by hybridization techniques, and followed by ALT normalization and resolution of necroinflammation. Serum HBV DNA remains detectable only by ultrasensitive polymerase chain reaction (PCR) technique in many patients. In chronic HBV infection this phase is also referred to as inactive HBsAg carrier state [3, 4]. The inactive carrier state may last for lifetime, but a proportion of patients may undergo subsequent spontaneous or immunosuppression induced reactivation of HBV replication with reappearance of high levels of HBV DNA with or without HBeAg seroreversion and rise of ALT levels [[3]]. For reasons that are not yet known during HBeAg clearance or later on after HBeAg seroconversion replication-competent HBV variants with mutations in the precore or core promoter regions preventing HBeAg production may be selected [[5]]. Patients who become HBsAg negative and develop anti-HBs have resolved their hepatitis B [3, 4]. This is an uncommon phenomenon in chronic HBV infection. During this stage HBV-DNA may still be detectable by PCR assay both in serum and liver [[6]]. In rare cases of severe immune suppression, such as cancer chemotherapy or after organ transplantation resolved hepatitis B can be reactivated
  8. Children who are infected perinataly remain phase 1 to adoloscent or early adult hood