Hepatitis Viruses

HEPATITIS VIRUSES
Fort Salvador
HEPATITIS A VIRUS
• Naked, icosahedral ssRNA virus – Picornaviridae

• Replicated like polio
• Transmitted oro-fecally – appear in the stool 2 weeks before symptoms appear
• Children most frequently affected
• Rarely transmitted via the blood
• Replicates in the GIT, goes to the liver
• Damage to hepatocytes dealt by T lymphocytes
• IgM detectable when jaundice appears; IgG appears 1-3 weeks later
HEPATITIS A VIRUS
• Fever, anorexia, nausea, vomiting, jaundice, pain at RUQ

• Dark urine, pale “acholic” feces, elevated ALT/AST
• Resolve spontaneously in 2-4 weeks
• Mostly asymptomatic; no chronicity
• Diagnosed via IgM antibody or fourfold rise in IgG
• Prevent by inactivated HAV vaccine or Igs
• Travelers, children (2-18 years), MSM
• PEPr (within 2 weeks)
HEPATITIS B
• Enveloped, icosahedral, partially dsDNA

• Contains a DNA polymerase
• Four genes: S gene, C gene, P gene, X gene
• S gene – surface antigen
• C gene – core and e antigen
• P gene – polymerase
• X gene – inactivates p53
• Begets spheres, filaments (both made of
surface antigen), and virions (1000:1)
HEPATITIS B
• Important antigens:
• HBsAg
• HBcAg – nucleocapsid protein
• HBeAg – released by infected cells into the blood; indicates transmissibility
• Four serotypes
HEPATITIS B
• DNA is completed in the nucleus by viral DNA polymerase

• mRNA synthesized by cellular RNA polymerase
• mRNA becomes template for DNA (reverse transcriptase)
• Takes place in the nucleocapsid
• Only virus that encodes genome DNA via reverse transcriptase
• DNA polymerase has reverse transcriptase activity
• Chronicity maintained by episome and some genome integration
• Transmitted via blood, sexual intercourse, intrapartum transmission
• Prevalent in Asia: HCC
HEPATITIS B
• Infects hepatocytes – CMI attacks

• Is not directly cytopathic
• 5% of adults and 90% of newborns become chronic carriers
• HBsAg in the blood for more than 6 months
• Predispose to cancer (HBV DNA in malignant cells)
• Some produce e antigen
• Immunity when Ab is produced against HBsAg
HEPATITIS B
• Incubates for 10-12 weeks

• More severe manifestations than hepatitis A
• Chronic carriers may be asymptomatic but cirrhotic
• Extrahepatic manifestations – mostly autoimmune
• Fever, rashes, arthralgias
• Neuropathies, glomerulonephritis, polyarteritis nodosa
• In HIV and HBV-infected people, treat HBV first
HEPATITIS B
• HBsAg, anti-HBc IgM

• HBsAg rises during incubation and prodrome;
falls during convalescence
• Anti-HBs only appears during convalescence;
not there during active disease
• Window period between fall of HBsAg and
formation of anti-HBs
• Use Anti-HBc
• Cannot be used to distinguish between acute and
chronic
HEPATITIS B
• HBeAg – rises during incubation

• Anti-HBe can be a gauge of transmissibility
• e antigen is encoded by the same gene for core
antigen
• Viral load can be used to monitor treatment
in chronic carriers
HEPATITIS B
• No antiviral therapy, pegylated interferon used

• Chronic therapy consists of reverse transcriptase inhibitors
• Lessen inflammation
• Prevented by vaccine (HBsAg) and Ig (HBsAb)
• Healthcare personnel; transfusion/dialysis patients
• Passive-active immunization
HEPATITIS C
• Enveloped, positive-sense ssRNA virus – Flaviviridae

• Many genotypes due to a hypervariable region in the envelope protein
• Multiple species occur in the blood of an infected person
• Genotype 1 most common
• 50% chronically-infected: predisposes to HCC
• Not much known about replication
• NS5A protein and miR-122 helps RNA polymerase replicate
• Protease helps budding
HEPATITIS C
• Transmission via IV drug use most common

• Incubates for 8 weeks
• Death of hepatocytes via CMI
• More oncogenic when paired with alcoholism
• Less infective than HBV in needlestick injuries
• Many infections are asymptomatic
• Antibodies against HCV are made, but may be incomplete
• Continue to shed virus for a year after
HEPATITIS C
• Mostly asymptomatic; symptoms are milder than other viruses

• Cirrhosis due to HCV – most common indication for liver transplantation
• Diagnosed via ELISA of antibodies against HCV
• Does not distinguish between acute and chronic infection
• PCR must be done to confirm active infection
• Detectable viral RNA for 6 months defines chronicity
• Treatment for acute hepC infection – pegylated interferon
• Treatment for chronic hepC infection – cocktail of NS5A, RNA polymerase, and
protease inhibitors
HEPATITIS D
• Enveloped, negative-sense, ssRNA virus

• Defective virus – cannot replicate by itself
• HBV is the helper virus
• Has HBsAg in its envelope
• Genome only encodes one protein – delta antigen
• No polymerase
• Transmitted in the same way and cause disease like HBV
• Coinfection or superinfection may occur
HEPATITIS D
• Superinfection increases the chances of fulminant hepatitis

• Coinfection does not carry this same risk but has more severe symptoms
• Diagnosed by detection of delta antigen or IgM to delta antigen
• Prevented by HBV vaccine
HEPATITIS E
• Naked, ssRNA virus – Hepeviridae

• Disease resembles HAV but results in a high mortality rate in pregnant women
• Chronic infection occurs mostly due to low CMI (transplant patients, HIV)
• Detected by IgM antibody

Hepatitis Viruses

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HEPATITIS VIRUSES

• Naked, icosahedral ssRNA virus – Picornaviridae

• Fever, anorexia, nausea, vomiting, jaundice, pain at RUQ

• Enveloped, icosahedral, partially dsDNA

• DNA is completed in the nucleus by viral DNA polymerase

• Infects hepatocytes – CMI attacks

• Incubates for 10-12 weeks

• HBsAg, anti-HBc IgM

• HBeAg – rises during incubation

• No antiviral therapy, pegylated interferon used

• Enveloped, positive-sense ssRNA virus – Flaviviridae

• Transmission via IV drug use most common

• Mostly asymptomatic; symptoms are milder than other viruses

• Enveloped, negative-sense, ssRNA virus

• Superinfection increases the chances of fulminant hepatitis

• Naked, ssRNA virus – Hepeviridae

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