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Hepatitis A-E Viruses. Enock Anassi MD, PharmD. Viral Hepatitis - Historical Perspectives. Enterically transmitted. “ Infectious”. A. E. Viral hepatitis. NANB. Parenterally transmitted. B. D. C. “ Serum”. F, G, TTV ? other. Type of Hepatitis. A. B. C. D. E. Source of.

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hepatitis a e viruses

Hepatitis A-E Viruses

Enock Anassi MD, PharmD

slide2

Viral Hepatitis - Historical Perspectives

Enterically

transmitted

“Infectious”

A

E

Viral hepatitis

NANB

Parenterally

transmitted

B

D

C

“Serum”

F, G, TTV

? other

slide3

Type of Hepatitis

A

B

C

D

E

Source of

feces

blood/

blood/

blood/

feces

virus

blood-derived

blood-derived

blood-derived

body fluids

body fluids

body fluids

Route of

fecal-oral

percutaneous

percutaneous

percutaneous

fecal-oral

transmission

permucosal

permucosal

permucosal

Chronic

no

yes

yes

yes

no

infection

Prevention

pre/post-

pre/post-

blood donor

pre/post-

ensure safe

exposure

exposure

screening;

exposure

drinking

immunization

immunization

risk behavior

immunization;

water

modification

risk behavior

modification

hepatitis a signs and symptoms
HEPATITIS A: signs and symptoms
  • Nausea and vomiting, anorexia, jaundice
  • Self limited
  • No chronic disease
  • Stool excretion 2 weeks before and 1 week after appearance
slide6

Hepatitis A - Clinical Features

  • Incubation period: Average 30 days

Range 15-50 days

  • Jaundice by <6 yrs, <10%age group: 6-14 yrs, 40%-50% >14 yrs, 70%-80%
  • Complications: Fulminant hepatitis Cholestatic hepatitis Relapsing hepatitis
  • Chronic sequelae: None
slide7

Hepatitis A Infection

Typical Serological Course

Total anti-HAV

Symptoms

Titre

ALT

Fecal

HAV

IgM anti-HAV

4

5

6

12

24

0

1

2

3

Months after exposure

slide8

Hepatitis A Virus Transmission

  • Close personal contact(e.g., household contact, sex contact, child day care centers)
  • Contaminated food, water(e.g., infected food handlers, raw shellfish)
  • Blood exposure (rare)(e.g., injecting drug use, transfusion)
slide9

Global Patterns of Hepatitis A Virus Transmission

Disease

Peak Age

Endemicity

Rate

of Infection

Transmission Patterns

High

Low to

Early

Person to person;

High

childhood

outbreaks uncommon

Moderate

High

Late

Person to person;

childhood/

food and waterborne

young adults

outbreaks

Low

Low

Young adults

Person to person;

food and waterborne

outbreaks

Very low

Very low

Adults

Travelers; outbreaks

uncommon

laboratory diagnosis
Laboratory Diagnosis
  • Acute infection is diagnosed by the detection of HAV-IgM in serum by EIA.
  • Past Infection i.e. immunity is determined by the detection of HAV-IgG by EIA.
slide12

Hepatitis A Vaccination Strategies

Epidemiologic Considerations

  • Many cases occur in community-wide outbreaks
    • no risk factor identified for most cases
    • highest attack rates in 5-14 year olds
    • children serve as reservoir of infection
  • Persons at increased risk of infection
    • travelers
    • homosexual men
    • injecting drug users
slide13

Hepatitis A Prevention - Immune Globulin

  • Pre-exposure
    • travelers to intermediate and high HAV-endemic regions
  • Post-exposure (within 14 days)

Routine

    • household and other intimate contacts

Selected situations

    • institutions (e.g., day care centers)
    • common source exposure (e.g., food prepared by infected food handler)
viral hepatitis

VIRAL HEPATITIS

HEPATITIS B

slide16

Hepatitis B - Clinical Features

  • Incubation period: Average 60-90 days

Range 45-180 days

  • Clinical illness (jaundice): <5 yrs, <10%5 yrs, 30%-50%
  • Acute case-fatality rate: 0.5%-1%
  • Chronic infection: <5 yrs, 30%-90%immunocompetent 5 yrs, 1%-5%
  • Premature mortality fromchronic liver disease: 15%-25%
spectrum of chronic hepatitis b diseases
Spectrum of Chronic Hepatitis B Diseases

1Chronic Persistent Hepatitis - asymptomatic

2. Chronic Active Hepatitis - symptomatic exacerbations of hepatitis

3. Cirrhosis of Liver

4. Hepatocellular Carcinoma

hepatitis b
Hepatitis B

ACUTE CHRONIC- 5-10%

<6 months (infection >6months)

  • Every year 1 to 2 million people die due to an infection by this virus

complications of chronic hepatitis

slide20

Global Patterns of Chronic HBV Infection

  • High (>8%): 45% of global population
    • lifetime risk of infection >60%
    • early childhood infections common
  • Intermediate (2%-7%): 43% of global population
    • lifetime risk of infection 20%-60%
    • infections occur in all age groups
  • Low (<2%): 12% of global population
    • lifetime risk of infection <20%
    • most infections occur in adult risk groups
slide22

Acute Hepatitis B Virus Infection with Recovery

Typical Serologic Course

Symptoms

anti-HBe

HBeAg

Total anti-HBc

Titre

anti-HBs

IgM anti-HBc

HBsAg

0

4

8

12

16

24

28

32

52

100

20

36

Weeks after Exposure

slide23

Progression to Chronic Hepatitis B Virus Infection

Typical Serologic Course

Acute

(< 6 months)

Chronic

(>6 months)

HBeAg

anti-HBe

HBsAg

Total anti-HBc

Titre

IgM anti-HBc

Years

0

4

8

16

20

24

28

36

12

32

52

Weeks after Exposure

slide24

Outcome of Hepatitis B Virus Infection

by Age at Infection

100

100

80

80

Chronic Infection (%)

60

60

Chronic Infection

Symptomatic Infection (%)

40

40

Chronic Infection (%)

20

20

Symptomatic Infection

0

0

1-6 months

7-12 months

Older Children

and Adults

Birth

1-4 years

Age at Infection

serological marker hep b
Serological Marker Hep B
  • 1) HBsAg (Hepatitis B surface antigen):
      • if positive, person is infectious
      • Sensitivity = 0.15 ng/ml
      • Specificity = 99.5%
  • 2) Anti-HBs (Antibody to HBV surface antigen):
      • indicates immunity to HBV and protection from disease
      • Protective level is >10 IU/ml
serological markers hep b
Serological Markers Hep B
  • 3) Anti - HBc (Antibody to HBV core antigen):
      • Total - indicates past or active infection; present whether person is immune or chronic carrier
      • Specificity = 99.8% to 99.9%
      • IgM - early indicator of acute infection
      • No antigen test
serological marker hep b1
Serological Marker Hep B
  • 4) HBeAg (Hepatitis Be antigen):
      • indicates person is highly infectious
      • Selecting patients for therapy
  • 5) Anti-HBe (Antibody to HBVe antigen):
      • prognostic for resolution of infection; less infectious; spontaneous seroconversion in 10 to 20% of healthy adults per year
slide30

Serologic markers – caveats:

  • Precore or HBeAg negative mutants:
    • Due to mutation in precore (abolishes HBeAg production) or core promoter region (down-regulates HBeAg production)
    • No effect on viral replication (may be enhanced)
    • More difficult to treat; greater risk of cirrhosis
  • Co-infection with HCV may suppress both HBeAg and HBsAg
slide31

Serologic markers – caveats:

  • Persistent HBsAg for >6 mos = chronic infection
  • HBsAg and anti-HBs may co-exist in up to 24% of chronically infected individuals; likely due to mutations in the “a” determinant of the S gene
    • Surface antigen escape mutants described in infants infected with HBV after HBIG + vaccination and in Liver transplants after prolonged HBIG
  • Anti-HBc IgM may persist for up to 2 years in 20%; chronically infected individuals may have low titres which rise during acute flares
hepatitis b laboratory tests
Hepatitis B – Laboratory Tests

Serologic markers – caveats:

  • Isolated HBcAb may be due to:
    • Remote infection (immune or chronic carrier)
    • “Window” period between HBsAg and HBsAb
    • Co-infection with HCV
    • False positive test result – HBcAb is marker most prone to false positives
  • HBV DNA may help sort this out
slide33

Concentration of Hepatitis B Virus in Various Body Fluids

Low/Not

High

Moderate

Detectable

blood

semen

urine

serum

vaginal fluid

feces

wound exudates

saliva

sweat

tears

breastmilk

slide34

Hepatitis B Virus

Modes of Transmission

  • Sexual - sex workers and homosexuals are particular at risk.
  • Parenteral - IVDA, Health Workers are at increased risk.
  • Perinatal - Mothers who are HBeAg positive are much more likely to transmit to their offspring than those who are not. Perinatal transmission is the main means of transmission in high prevalence populations.
diagnosis
Diagnosis
  • A battery of serological tests are used for the diagnosis of acute and chronic hepatitis B infection.
  • HBsAg - used as a general marker of infection.
  • HBsAb - used to document recovery and/or immunity to HBV infection.
  • anti-HBc IgM - marker of acute infection.
  • anti-HBcIgG - past or chronic infection.
  • HBeAg - indicates active replication of virus and therefore infectiveness.
  • Anti-Hbe - virus no longer replicating. However, the patient can still be positive for HBsAg which is made by integrated HBV.
  • HBV-DNA - indicates active replication of virus, more accurate than HBeAg especially in cases of escape mutants. Used mainly for monitoring response to therapy.
treatment
Treatment
  • Interferon (PEGinterferon-2α) , - for HBeAg +ve carriers with chronic active hepatitis. Response rate is 30 to 40%.
  • Lamivudine - a nucleoside analogue reverse transcriptase inhibitor. Well tolerated, most patients will respond favorably. However, tendency to relapse on cessation of treatment. Another problem is the rapid emergence of drug resistance.
  • Entecavir and Adefovir
  • Successful response to treatment will result in the disappearance of HBsAg, HBV-DNA, and seroconversion to HBeAg.
prevention
Prevention
  • Vaccination - highly effective recombinant vaccines are now available. Vaccine can be given to those who are at increased risk of HBV infection such as health care workers. It is also given routinely to neonates as universal vaccination in many countries.
  • Hepatitis B Immunoglobulin - HBIG may be used to protect persons who are exposed to hepatitis B. It is particular efficacious within 48 hours of the incident. It may also be given to neonates who are at increased risk of contracting hepatitis B i.e. whose mothers are HBsAg and HBeAg positive.
  • Other measures - screening of blood donors, blood and body fluid precautions.
complications
Complications
  • Arthritis
  • Glomerulonephritis
  • Polyarteritis nodosa
  • Hepatocellular carcinoma
hepatitis d
Hepatitis D
  • Subviral satellite because it can propagate only in the presence of hepatitis B

coinfection superinfection

  • Transmission: parenteral (intravenous drug use mostly)
  • > 60% develop cirrhosis
slide41

Hepatitis D (Delta) Virus

antigen

HBsAg

RNA

hepatitis d1
Hepatitis D
  • Anti-HDV Total (IgG & IgM) available
  • Incubation time – similar to Hepatitis B
  • High titires of HDV antibodies indicate ongoing chronic infection
  • Treatment same as HBV
  • If acquired as superainfection in chronic HBV there is in severity of infection i.e fulminant hepatitis, chronic hepatitis with rapid progression to cirhosis
slide43

HBV - HDV Superinfection

Typical Serologic Course

Jaundice

Symptoms

Total anti-HDV

ALT

Titre

HDV RNA

HBsAg

IgM anti-HDV

Time after Exposure

slide44

Hepatitis D - Prevention

  • HBV-HDV Coinfection

Pre or postexposure prophylaxis to prevent HBV infection.

  • HBV-HDV Superinfection

Education to reduce risk behaviors among persons with chronic HBV infection.

hepatitis c
Hepatitis C
  • Affects each person differently
  • No vaccine available
  • Many people have the virus and do not even know it
  • By blood transfusion and IV drug abuse
  • Intranasal cocaine use, piercing
  • Type 1 (most resistant) type II and III
slide46

Hepatitis C - Clinical Features

Incubation period: Average 6-7 wks

Range 2-26 wks

Clinical illness (jaundice): 30-40% (20-30%)

Chronic hepatitis: 70%

Persistent infection: 85-100%

Immunity: No protective antibody

response identified

chronic hepatitis c infection
Chronic Hepatitis C Infection
  • The spectrum of chronic hepatitis C infection is essentially the same as chronic hepatitis B infection.
  • All the manifestations of chronic hepatitis B infection may be seen, albeit with a lower frequency i.e. chronic persistent hepatitis, chronic active hepatitis, cirrhosis, and hepatocellular carcinoma.
  • Waxing and waning aminotransferases (ALT/AST)
slide48

Hepatitis C Virus Infection

Waxing and Waning ALT/AST

anti-HCV

Symptoms

Titre

ALT

Normal

6

1

2

3

4

0

1

2

3

4

5

Months

Years

Time after Exposure

slide49

Risk Factors Associated with Transmission of HCV

  • Transfusion or transplant from infected donor
  • Injecting drug use
  • Hemodialysis (yrs on treatment)
  • Accidental injuries with needles/sharps
  • Sexual/household exposure to anti-HCV-positive contact
  • Multiple sex partners
  • Birth to HCV-infected mother
hepatitis c dispelling myths
Hepatitis C Dispelling Myths
  • Hepatitis C is not spread by:
    • Casual contact
        • Hugging/kissing
        • Sharing eating utensils and drinking glasses
        • Sneezing/coughing
        • Shaking hands
        • Sitting on a toilet seat
prevention1
Prevention
  • Never share drug equipment
    • Straws, bills, needles, syringes, water, filter, cooker, pipes etc…
  • Never share tooth brushes/razors or any personal hygiene articles that have blood on them (even tiny amounts).
  • Practice safer sex
prevention2
Prevention
  • Always make sure new & sterilized equipment is being used for tattooing & piercing
    • Make sure ink for tattooing is not being shared
  • Do not touch dirty needles without proper equipment or following proper procedures
laboratory diagnosis1
Laboratory Diagnosis
  • HCV antibody - generally used to diagnose hepatitis C infection. Not useful in the acute phase as it takes at least 4 weeks after infection before antibody appears.
  • HCV-RNA- various techniques are available e.g. PCR and branched DNA. May be used to diagnose HCV infection in the acute phase. However, its main use is in monitoring the response to antiviral therapy.
  • HCV-antigen - an EIA for HCV antigen is available. It is used in the same capacity as HCV-RNA tests but is much easier to carry out.
treatment1
Treatment
  • Types 1 II and III
  • Type I is resistant than II and III
  • Acute HCV –alfa- interferon for 6 months also type II and III
  • Chronic HCV –alfa interferon+ ribavirin or peginterferon +ribavirin
  • Type I use alfa interferon +Ribavirin for 1 year, Telaprevir, Betapravir
  • HAV and HBV vaccination.
slide56

Prevention of Hepatitis C

  • Screening of blood, organ, tissue donors
  • High-risk behavior modification
  • Blood and body fluid precautions
complications1
Complications
  • Cryoglobulinemia
  • Membranoproliferative glomerulonephritis
  • Hepatocellular Carcinoma
  • Cirrhosis
  • Alfa interferon is contraindicated with major depression and organ transplant
  • Ribavirin contraindicated in pregnancy, avoid for 6 months after therapy
treatment2
Treatment
  • Alcoholics should stop for 1 month before starting treatment
  • Screen for hepatocellular carcinoma every 6 months
  • Inteferon S/E: flu like syndrome (malasia, HA, fever, myalgia) depression, myelosuppression (neutropenia, anemia)
  • Ribavirin S/E HA, fatigue, hemolysis
slide60

Hepatitis E - Clinical Features

  • Incubation period: Average 40 days
  • Range 15-60 days
  • Case-fatality rate: Overall, 1%-3%Pregnant women, 15%-25%
  • Illness severity: Increased with age
  • Chronic sequelae: None identified
slide61

Hepatitis E Virus Infection

Typical Serologic Course

Symptoms

IgG anti-HEV

ALT

Titer

IgM anti-HEV

Virus in stool

0

1

2

3

4

5

6

7

8

9

10

11

12

13

Weeks after Exposure

slide62

Hepatitis E -

Epidemiologic Features

  • Most outbreaks associated with faecally contaminated drinking water.
  • Several other large epidemics have occurred since in the Indian subcontinent and the USSR, China, Africa and Mexico.
  • In the United States and other nonendemic areas, where outbreaks of hepatitis E have not been documented to occur, a low prevalence of anti-HEV (<2%) has been found in healthy populations. The source of infection for these persons is unknown.
  • Minimal person-to-person transmission.
slide64

Prevention and Control Measures for Travelers to HEV-Endemic Regions

  • Avoid drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruit/vegetables not peeled or prepared by traveler.
  • IG prepared from donors in Western countries does not prevent infection.
  • Unknown efficacy of IG prepared from donors in endemic areas.
  • Vaccine?
hepatitis virus molecular tests
Hepatitis Virus – Molecular Tests
  • Molecular assays available as follows:
    • Commercial assays for HBV DNA and HCV RNA
    • In-house assays for HAV RNA & HDV RNA
    • No molecular assay for HEV RNA
  • HCV RNA & HBV DNA, plasma or serum must be separated from cells within 6 hrs and plasma can be stored at 4oC for several days or -70oC for long-term
  • No licensed tests for diagnostic purposes; all tests are for monitoring or donor screening
    • HCV RNA will be done in HIV or other immunocompromised patients if requested
nucleic acid amplification tests naat for detection of rna dna
Nucleic Acid Amplification Tests (NAAT) for Detection of RNA/DNA
  • Quantitation of RNA or DNA may be reported as copies/ml or IU/ml
  • Conversion factor for copies/ml to IU/ml is not the same for different assays measuring the same target or different targets
    • HBV DNA: 5.82 copies/IU
    • HCV RNA: PCR - 2.4 copies/IU; bDNA: 5.2 copies/IU
  • Coefficient of variation (COV) may range from 15 to 50%
hbv dna in clinical practice
HBV DNA in Clinical Practice
  • Routine monitoring on therapy to assess response to treatment
    • Every 3 months X years on oral agents
    • Every 1 month X 6-12 on PEG/IFN
  • Routine monitoring off therapy to estimate prognosis and to evaluate need for treatment
    • Every 6 –12 months normally
    • Diagnosis of occult HBV infection