HEPATITIS VIRUS

SJAMSUL ARIEF
Bagian Ilmu Kesehatan Anak
FK UNAIR-RSU Dr. Sutomo
Surabaya
HEPATITIS

Keradangan Jaringan Liver

 Inflamasi dan Nekrosis
 Kuman, Virus, Parasit
 Bahan kimia: Obat, racun
 Proses Imunologis: Auto-immune
 Viral Hepatitis Nomenclature

VIRUSES ANTIGENS ANTIBODIES

Hepatitis A Virus HAV Anti-HAV
IgM anti-HAV
Hepatitis B Virus HBsAg Anti-HBsAg
IgM anti-HBsAg
HBcAg Anti-HBcAg
HBeAg Anti-HBeAg
Hepatitis C Virus Anti-HCV
Hepatitis D Virus HDAg Anti-HDV
Hepatitis E Virus Anti-HEV
IgM anti-HEV
Hepatitis G Virus Anti-HGV
 Features of the six Hepatotropic Viruses

HAV HBV HCV

Nucleic acid RNA DNA RNA
Incubaton (mean) 30 days 100-120 days 7-9 wk
Transmission
Percutaneous Rare Common Common
Fecal-oral Common No No
Sexual Rare Common Rare
Transplacental No Common Rare
Chronic infection No Yes Yes
Fulminant disease Rare Yes Rare
 Features of the six Hepatotropic Viruses

HDV HEV HGV

Nucleic acid RNA RNA RNA
Incubaton (mean) 2-4 mo 40 days Unknown
Transmission
Percutaneous Common No Common
Fecal-oral No Common No
Sexual Rare Rare Rare
Transplacental No Probably no Rare
Chronic infection Yes No Yes
Fulminant disease Yes Rare Probably no
Afrika
Paparan virus HAV
Amerika Selatan
hampir mencapai
Asia Tengah 100%  usia 10 tahun
Asia Tenggara

Indonesia :
 Jakarta
 Bandung 35-45%  usia 5 tahun
 Surabaya 90%  usia 30 tahun
 Makasar

 Irian Jaya Hampir 100%  usia 5

tahun
 Kontaminasi air –
makanan 2.2% Kunjungan
Internasional
6.8%

Tidak diketahui TPA

43.6%
14.8%

Kontak erat
22.5%

Pengguna obat 5.0% Homosexual 5.1%

Cara penularan Hepatitis A

 Symptomatic Anti-HAV (IgG)

Infectious
Anti-HAV (IgM)

Fecal HAV

0 4 8 12 16 20
400 million people HBV carriers
78 % in Asia
HBsAg prevalence :
2% : Low
2% - 7% : Moderate
8% : High
Indonesia : moderate - high
Sulaiman (1990) : 19.1% (HBsAg)
Puslabkes Depkes RI (1990-91) : 14% (HBsAg)
Sulaiman & Julitasari (1995) : 6.7% (Blood donor)
 Clinical
Lab. Test Interpretation
syndrome
Acute, CAH,
HBsAg Current infection
Carrier
Active replication highly
HBeAg Acute, CAH
infectious
Anti HBs Resolution Immunity
Current or previous Acute, Chronic,
Anti HBc
infection Carrier, Immunity
IgM anti Acute or reactivation of
Acute, CAH
HBc chronic
Resolution of active
Anti HBe Carrier, Immunity
replication
ROUTE OF TRANSMISSION

Blood – borne

Contaminated body fluid

No environmental reservoir of HBV

Contaminated razors, tooth brushes, nedles, sharp

implements for tatoing, accupuncture, ear
piercingdental treatment have been incriminated
 Route of transmission

 Mainly percutaneous intimate

 Sexual contact, Homosexual
 Population high HBV carrier rates
 Health care personel : dentist, hemodialysis  high
risk for infection
 Converselly chronic HBV carrier health worker 
implicated transmission HBV to patients
Vertical Transmission
- 5 – 10 % infection in utero
- Exposure to maternal blood
- Perinatal period commonest route
- HBeAg (+) 90%
- HBsAg (+) 10%
- Infected infants 90 % develop chronic
infection
- Very young age  persistent infection
Clinical States
1. Acute Hepatitis
2. Fulminant Hepatic Failure
3. Healthy Carrier
4. Chronic Hepatitis
1. Acute Hepatitis
Symptoms Appear 45 – 180 days
Neonatal occurs rarely
10 % less than 4 years
30 % in adult

2. Fulminant Hepatic Failure

1 % of Symptomatic acute HBU
Encephalopathy, coagulopathy
3. Healthy Carrier
Normal LFT

No symptoms

4. Chronic Hepatitis

At least 6 month

ALT / AST minimal 20 times

Treatment
Goal : prevent cirrhosis and complications

HBeAG, HBV DNA positif, elevated

transaminases

Interferon Alfa

Nucleoside Analoques : Lamivudin,

Famciclovir
VACCINATION
Passive : HBIG
Active : HBsAg Recombinant
10 – 20 µg
At time 0,1 and 6 month
 HBeAg Anti-HBe
Infective
Anti-HBs
Symptomatic

Anti-HBc

HBsAg

0 8 16 24 32 40 52
 HBV

‘Healthy Acute
carrier’
Fulminant Icteric Anicteric

Chronic

Cirrhosis Cancer

Recovery Death
 The History of Parenterally Acquired NANB
(non-A, non-B : type C) HEPATITIS
Year
1947-1975 Recognition that post-transfusion hepatitis is
not due to hepatitis A and B
1975 First description of NANB hepatitis unrelated
to overt parenteral exposure
1977-1978 NANB hepatitis due to transmissible agents
1980 More that one aetological agents as a cause
of NANB hepatitis
1979-1982 Definition of clinical features and chronic
sequelae
1980-1983 Succesful chemical inactivatation of NANB
agents
1978-1988 A decade of unsuccessful efforts to identify
viruses or antigen/antibody systems
1989 Identification of hepatitis C virus, the major
agent of parenterally acquired NANB
hepatitis
References
Prince,Lancet,1975;ii:241; Alter,Lancet,
1975;ii:838; Feinstone,NEJM,1975;292:767
Villarejos,NEJM,1975;293:1350
Hoofnagle,AnnIntMed,1977;87:14; Tabor,
Lancet, 1978;I:459
Tsiquaye, JMedVirol, 1980;5:63; Hollinger,
JlnfDis, 1980;142:400
Berman, AnnIntMed, 1979;91:1; Realdi,Gut,
1982;23:270
Tabor,JInfDis, 1980;142:767; Yoshizawa,
Gastro, 1982;82:502
Dienstag,Gastro, 1983;85:743; Alter,
TransfusMedRev, 1982;2:288
Choo,Science,1989;244:359;
Kuo,Science,1989;244:362
Proposed Classification of Hepatitis C Virus Isolates
Based on Their Phylogenetic Analysis (Forns, 1999)

Clade Genotype Subtypes Isolates

1 1 Many Many
2 2 Many Many
3 3, 10 Many Many
4 4 Many Many
5 5 5a Many
6 6, 7, 8, 9, 11 Many Many
Genotype distribution of HCV worldwide (Forns, 1999)
 HAV secara elektron mikroskop
(250.000 X) 7.5 kb, single stranded RNA