Hepatitis Viruses Flashcards

Question 1

Q

Viral Hepatitis

Overview

Answer

A

Hepatitis A-E, which are all antigenically and genetically unrelated
- 3 most common: Hep A, Hep B, and Hep C
HAV and Hep E Virus (HEV) ⇒ acute infections only
- Acquired from the environment by oral ingestion
- Both reside in the liver, where replication takes place
- Infected hosts mount an effective immune response that clears virus from liver and blood
  - Generates long-lasting immunity
- Infections can be severe but fatalities are infrequent
  - Resolution occurs in most cases
Hep B and Hep C ⇒ acute & chronic infections
- Extensive viral replication in the liver
- Acute infection w/ ± disease sx
- Immune response is not always effective at clearing infection ⇒ persistent infection
- Persistent infection: continued virus replication in the liver and release of infectious virus into the blood
  - 5-10% of HBV infections
  - 80% of HCV infections
Hep D Virus (HDV) intrinsically linked to HBV

Question 2

Q

Hep A

Properties

Answer

A

Picornavirus in genus Heparnavirus
- 27nm naked, icosahedral capsid
- Linear ⊕-sense, ssRNA genome
Only one serotype
Interacts specifically w/ HAV cell receptor 1 glycoprotein (HAVCR-1) aka “T-cell immunoglobulin and mucin domain protein (TIM-1)”
- HAVCR-1 expressed on liver cells and T-cells
  - Specific forms correlated w/ severity of disease
Unlike other picornaviruses, HAV is not cytolytic ⇒ released by exocytosis
Spread via fecal-oral route
- Consumption of contaminated water, shellfish, or other foods
- Resistant to detergents, acid (pH of 1) and temperatures as high as 60°C
- Survives for several months in fresh and salt water

Question 3

Q

Hep A

Pathogenesis

Answer

A

Incubation period 15-40 days
Ingested → bloodstream through epithelial lining of OP or intestines
Replicates in hepatocytes and Kupffer cells
- Replicates slowly ⇒ no apparent cytopathic effects
Virions → bile → stool
- Present in feces for up to 2 wks prior to sx onset or Ab detection
Immune response:
- Interferon shown to limit viral replication
- NK cells and cytotoxic T cells required to eliminate infection
- Ab, complement, and ADCC also facilitate clearance of the virus
Liver damage likely caused by immunopathology
- HAV damage indistinguishable from HBV
Cannot initiate chronic infection
Not ass. w/ hepatic cancer

Question 4

Q

Hep A

Epidemiology

Answer

A

Leading cause of acute viral hepatitis worldwide (> 40%)
- In some developing areas, HAV seropositivity close to 100%
Virus is spread readily
- Pts contagious for up to 2 wks prior to sx
- 90% of infected children and 25-50% of infected adults have inapparent but productive infections
HAV outbreaks usually originate from a common source

Question 5

Q

Hep A

Transmission and Risk Factors

Answer

A

1° transmitted via fecal-oral route
- Most commonly acquired via ingestion of contaminated food or during sexual activity
In the US, 3 leading risk factors for Hep A infection are:
- Sexual or household contact
- International travel
- Male-male sexual activity

Question 6

Q

Hep A

Clinical Syndromes

Answer

A

Incubation phase 2-7 wks (mean 28-30 days)
Prodromal sx are non-specific:
- Anorexia, fever, nausea, and malaise
Jaundice typically appears within 1 wk after sx onset & resolves within 2 wks
- Occurs in 70-80% of adults
- < 10% of children < 6 y/o
- ± Bilirubinuria several days before jaundice ⇒ dark urine
- Jaundice and hepatomegaly are the most commonly observed PE abnl
± Extra-hepatic manifestations
- Less frequent than w/ HBV or HCV
After onset of jaundice, most constitutional sx abate quickly
- Some pts c/o residual fatigue for several wks
Most cases of hep A are self-limited
- 85% show complete resolution of sx by 3 months
Hep A carries no risk for chronic hepatitis
< 100 HAV-related deaths/yr reported

Question 7

Q

Hep A

Serology

Answer

A

Serum IgM anti-HAV almost always detectable @ onset of sx
- Peak before 3 months, gradually decline until they become undetectable
IgG anti-HAV levels rise soon after
- IgG levels remain elevated and confer lifelong immunity
Acute HAV Infection
- [Serum IgM anti-HAV] ⇒ diagnostic test of choice
  - Sensitivity ~100%, specificity 99%, positive predictive value 88%
  - Completed by standard ELISA or radioimmunoassay

Question 8

Q

Hep A

Treatment and Prevention

Answer

A

No specific antiviral therapy for acute hep A infection
Most pts tx symptomatically as an outpatient w/ lab and clinical f/u
Pts w/ acute HAV infection who do not develop acute liver failure will have complete recovery w/o any permanent sequelae
Interrupt fecal-oral spread by avoiding contaminated food and water, proper hand-washing, and chlorine treatment of drinking water
Killed HAV vaccines available for all children and adults at high risk

Question 9

Q

Hep B

Properties

Answer

A

Member of hepadnavirus family
- Enveloped, icosahedral nucleocapsid
- Nicked, circular, partially dsDNA genome
Pt’s serum may contain:
- Complete infectious virus (42 nm)
- Non-infectious spheres and filaments (composed of HBsAg)
Viral antigens and antibodies:
- HBsAg = hepatitis B envelope surface antigen
- HBcAg = hepatitis B core antigen
- HBeAg = hepatitis B e antigen
- anti-HBs = Ab against hepatitis B surface antigen
- anti-HBc = Ab against hepatitis B core antigen
- anti-HBe = Ab against hepatitis B e antigen
Carry DNA-dependent DNA polymerase
One major serotype (based on HBsAg)
Humans are the only natural reservoir
Highly hepatotropic
Very complicated lifecycle
One of a few known pararetroviruses ⇒ non-retroviruses that still use reverse transcriptase

Question 10

Q

Hep B

Entry and Replication

Answer

A

Viral entry via endocytosis by binding to NTCP (sodium/bile acid cotransporter)
Virus multiplies via RNA made by a host enzyme:
- Viral genomic DNA → cell nucleus
- Viral partially dsDNA → fully dsDNA → covalently closed circular DNA (cccDNA) ⇒ template for transcription of 4 viral mRNAs
  - Largest mRNA ⇒ new copies of genome, capsid core protein, viral DNA polymerase
- 4 viral transcripts undergo additional processing
  - Form progeny virions ⇒ released from the cell or returned to the nucleus and re-cycled to produce even more copies
Long pre-genomic mRNA → cytoplasm ⇒ virion P protein (DNA polymerase) synthesizes DNA by its RT activity
- 3 basic functions of HBV polymerase:
  1. Priming ⇒ initiates ⊖ strand synthesis
  2. Reverse transcriptase ⇒ generates ⊖ strand of DNA
  3. DNA synthesis ⇒ generates ⊕ strand of DNA
Virus released by exocytosis w/o killing cell

Question 11

Q

Hep B

Pathogenesis

Answer

A

Incubation period 10-12 wks
Viremia
Entry via HBsAg ↔︎ NTCP on hepatocyte cell surface
Penetration and uncoating
Virus replication
Effective immune response ⇒ inflammation → elimination of infected hepatocytes → resolution
- ↑ NK cell activity & INF-α production
- Early sx such as arthralgia caused by Ag-Ab reactions ⇒ Type III hypersensitivity
- Cytotoxic T cells attack and destroy infected hepatocytes
  - Inflammation and necrosis
- Lifelong immunity after resolution of infection
  - Mediated by anti-HBs Ab
~9-10% become chronic carriers
- More common in newborn and immunocompromised adults
- Jaundice and other sx occur less often than in older children and adults

Question 12

Q

Hep B

Epidemiology

Answer

A

HBV is found throughout the world
- Endemic areas: majority of infections acquired at birth
- Non-endemic areas: infection is usually acquired venereally or through IV drug abuse
  - In the US: 50% of infections are sexually transmitted
Chronic carriers are the major reservoir of HBV
- Many are asymptomatic
- Usually identified only when they become ill or routine serologic screen done
- In the US: about 1/250k individuals are chronically infected

Question 13

Q

Hep B

Transmission and Risk Factors

Answer

A

4 recognized modes of transmission:
- Mother to child at birth (perinatal)
- Contact w/ an infected person (horizontal)
- Sexual contact (venereal)
- Parenteral (blood-to-blood) exposure to blood or other infected fluids
Can be carriers w/ or w/o hepatitis
Transmission occurs by percutaneous and permucosal exposure to infective body fluids
- Percutaneous exposures:
  - Transfusion of unscreened blood/blood products
  - Sharing unsterilized needles for IV drug use
  - Hemodialysis
  - Acupuncture
  - Tattoos
  - Injuries from contaminated sharp instruments sustained by hospital personnel
- Sexual and perinatal HBV transmission usually result from mucous membrane exposures to infectious blood and body fluids
- Perinatal transmission is common in hyperendemic areas of south-east Asia and the far East
  - Esp. when HBsAg carrier mothers are also HBeAg ⊕
Infectious HBV can be present in blood w/o detectable HBsAg
- Failure to detect Ag does not exclude the presence of infectious virus
Natural reservoir for HBV is man

Question 14

Q

Hep B

Clinical Syndromes

Answer

A

Many 1° infections are asymptomatic
Effective immune response ⇒ inflammation → elimination of infected hepatocytes → resolution
Ineffective immune response ⇒ ↑ likelihood of chronic HBV infection
- Definition: persistence of HBsAg for ≥ 6 mos
  - Hepatocytes remain infected instead of being destroyed by cytotoxic T cells
  - Most chronic carriers are asymptomatic
    - Detected by routine screening
- Characterized by replicating virus (HBV-DNA), persistence of HBeAg and HBsAg
  - When replication ends: HBV-DNA levels ↓ and anti-HBe levels ↑
  - Detection of HBeAg is a measure of virus replication, infectivity and transmissibility
- Chronic Hep B presentations:
  - Asymptomatic: pt appears healthy, no liver damage, hepatocytes contain HBsAg
  - Chronic persistent hepatitis: mild hepatitis w/ minimal or mild histologic changes
  - Chronic active hepatitis: marked hepatic inflammation
    - Can lead to cirrhosis and death
- Outcomes:
  - Acute Hep B Infection
    - 5-10% ⇒ chronic carriers
    - ~ 25% ⇒ chronic hepatitis
  - Chronic carriers
    - 80-85% ⇒ complete resolution
    - 15-20% ⇒ complications
Remission
- Can occur after yrs/decades of persistent illness
- ~ 10% of pts who go into remission have subsequent reactivation
- Some go thru cycles of remission then reactivation
- Each reactivation results in more severe disease
Hepatocellular Carcinoma occurs at a relatively high rate in chronic carriers
- HBV has no oncogenes
- ? D/t persistent cell regeneration to replace dead hepatocytes
- ? D/t insertion of viral DNA into hepatocyte DNA ⇒ activation of cellular oncogene

Question 15

Q

Hep B

Serology

Answer

A

HBsAg
- Detectable several wks before sx onset to months after onset
- ⊕ during acute infections and persists in chronic infections
- ⊕ HBsAg ⇒ person is potentially infectious
HBeAg
- Detectable shortly after HBsAg
- ⊕ HBeAg ⇒ high infectivity and severity of disease
Anti-HBc Ab
- 1^st Ab to appear
- ⊕ anti-HBc Ab ⇒ current or past HBV infection
- IgM anti-HBc
  - High titers during acute infection
  - Usually disappears within 6 months
  - Can persist in some cases of chronic hepatitis
- IgG anti-HBc
  - Remains detectable for a lifetime
Anti-HBe Ab
- Appears after anti-HBc Ab
- ⊕ anti-HBe Ab ⇒ ↓ infectivity
  - Anti-HBe Ab replaces HBeAg w/ resolution
Anti-HBs Ab
- Anti-HBs replaces HBsAg as acute infection resolves
- Persists for a lifetime in > 80% of pts
- ⊕ anti-HBs Ab ⇒ immunity
Constant [HBsAg] or persistent [HBeAg] 8-10 wks after sx have resolved
- ↑ likelihood of being carriers
- ↑ risk of chronic liver disease

Question 16

Q

Hep B

Treatment and Prevention

Answer

A

Chronic HBV infection
- INF-alpha
- Lamivudine, telbividune, entecavir, adfovir, and tenofovir
  - Nucleoside analogs
  - Inhibits reverse transcriptase
- Appears to be no advantage to combined therapy of nucleoside/nucleotide analogue and interferon
HBsAg vaccine
- Produced in yeast
- Required in most states before children can attend school
Passive-active immunization
- Used when immediate and long-term protection is needed
  - E.g. newborn whose mother is HBsAg ⊕

Question 17

Q

Nucleoside/Nucleotide Analogues

Drugs & MOA

Answer

A

⊗ HBV polymerase at one or all of steps
- Priming, reverse transcriptase, DNA synthesis
Drugs:
- Entecavir, Tenofovir ⇒ currently used in primary tx
- Lamivudine, telbivudine, and adefovir ⇒ now considered 2^nd and 3^rd line therapy
  - Lamivudine: competes w/ CTP
  - Telbivudine: competes w/ TTP
  - Adefovir: competes w/ ATP

Question 18

Q

Entecavir

Answer

A

Nucleoside analogue used in primary treatment
⊗ All three functions of the HBV polymerase
Low rate of drug resistance
Excellent choice for pts not exposed to lamivudine
- Resistance may develop in pts resistant to lamivudine

Question 19

Q

Tenofovir

Answer

A

Nucleotide analogue used in primary treatment
Low rate of drug resistance
Effective against lamivudine resistant HBV
Possible renal impairment

Question 20

Q

Nucleoside/Nucleotide Analogues

General Adverse Effects

Answer

A

Headache, fatigue, nausea

Lactic acidosis, hepatotoxicity

Question 21

Q

Interferon α

“Pegylated Interferon”

Answer

A

Used in primary treatment
- Approved for adults and children
Maybe associate w/ a severe flare of the disease
- Often a prelude to HBeAg clearance
- Can lead to liver failure in pts w/ cirrhosis
AE: headache, fevers, chills, myalgias, and malaise in 30% of pts within 1^st wek of therapy
- Multiple potential adverse effects during chronic therapy
- Some advantages but AEs and need to be injected have limited its use

Question 22

Q

Hep D

Properties

Answer

A

Envelope containing HBsAg
Circular ⊖-sense ssRNA genome
Defective virus
- Lacks genetic info for envelope proteins
- Does code for an internal protein ⇒ delta antigen
No virion polymerase
HDV RNA has no sequence homology to HBV RNA
1 serotype
No animal reservoir

Question 23

Q

Hep D

Pathogenesis

Answer

A

HDV can only replicate in cells infected w/ HBV
- HBsAg in HBV envelope also in HDV envelope
Genomic RNA replicated and transcribed in the nucleus by host cell DNA-dependent RNA polymerase
HDV RNA’s are RNA catalysts or ribozymes
- Capacity to self-cleave and self-ligate
  - Involved in genome replication
- Causes production of mRNA for delta-Ag
delta-Ag ⇒ ⊕ association of HDV genome and HBsAg ⇒ forms HDV⇒ ⊕ association of HDV genome and HBsAg ⇒ forms HDV

Question 24

Q

Hep D

Epidemiology & Transmission

Answer

A

HDV infections are found worldwide
- > 10 million people infected
Prevalence varies in different geographical areas
- Anti-HDV Ab found in 20-40% of HBsAg carriers in Africa, the Middle East, and Southern Italy
Transmission of HDV is similar to HBV:
- Sexual
- Vertical
- Parenteral
HDV infection in the US is relatively uncommon
- High-risk groups:
  - IV drug users and hemophiliacs ⇒ prevalence rates of 1-10%
  - Hemodialysis pts
  - Sex contacts of infected individuals
  - Infants born to infected mothers (rare)
- HDV occurs most often in IV drug users who share needles and only in a person who is also infected w/ HBV

Question 25

Q

Hep D

Clinical Syndromes

Answer

A

Incubation period 6 wks
Pathologic changes in HDV are limited to the liver
- Only organ in which HDV has been shown to replicate
- Histologic changes consist of hepatocellular necrosis and inflammation
HBV is an essential cofactor in the evolution of hepatocellular damage
- Infection w/ HBV + HDV ass. w/ more severe liver injury than HBV alone
  - Direct cytopathic effect of delta agent
  - Immunopathology ass. w/ disease caused by HBV
- Disease in HBV carriers superinfected w/ HDV more severe than when HBV and HDV coinfect at same time

Question 26

Q

Hep D

Serology

Answer

A

Acute HDV infection:
- Total anti-HDV Ab detected by RIA/EIA kits
- Markers of HDV infection (IgM and IgG Ab)
  - Disappears within months after recovery
To monitor ongoing HDV infection, RT-PCR should be used
In chronic HDV infection: HDV RNA, HDAg, IgM anti-HD Ab, and IgG anti-HD Ab persist

Question 27

Q

Hep D

Treatment and Prevention

Answer

A

No effective antiviral therapy available for tx of acute or chronic type D hepatitis
Control of HDV infection is achieved by targeting HBV infections
- HDV dependent on HBV for replication
- ↓ HBV transmission ⇒ ↓ HDV transmission
- HBV vaccination recommended to avoid HBV-HDV coinfection
- Cannot prevent HDV infection of chronic HBV carriers
  - Education to reduce risk behaviors
  - HBV Ig and HBV vaccine do not protect HBV carriers from infection by HDV

Question 28

Q

Hep C

Properties

Answer

A

Enveloped, linear ⊕-sense, ss RNA-containing flavivirus
Humans are the reservoir
Multiple serotypes exist
More likely to cause persistent chronic infection than HBV
No vaccine
Transmission:
- Blood-containing virus (1° method)
- Venereal
- Mother to child during delivery

Question 29

Q

Hep C

Replication & Diversity

Answer

A

Single open reading frame
Encodes a large polyprotein
Posttranslational processing by host and viral enzymes ⇒ structural and non-structural proteins and enzymes of HCV
Highly conserved 5’ and 3’ UTRs
5’ UTR essential for replication
Contains elements that coordinate viral protein synthesis
Region is highly conserved
HCV lacks proofreading ability ⇒ tremendous viral diversity
- Heterogeneity important in:
  - Dx of infection
  - Pathogenesis of disease
  - Allows virus to escape eradication by host’s immune system
  - Response to treatment / completeness of response to antiviral therapies such as interferon
  - Prevents development of conventional vaccines

Question 30

Q

Hep C

Pathogenesis

Answer

A

Acute infection:
- Transmission → viremia → hepatocytes, lymphocytes, others
- Replication ⇒ virus becomes cell-associated
- 1° infection commonly asymptomatic
- Infections frequently become chronic and persistent
  - HCV inhibits apoptosis and INF-alpha ⇒ prevents death of host cell
- Cell injury d/t cell-mediated immunologic mechanisms, not to virus- induced lysis
- Multiple serotypes of HCV ⇒ reinfection possible
Chronic infection:
- May occur despite the presence of Ab
- Relatively common (~70-80%)
- Of those chronically infected, ~10% become diseased
Factors:
- Viral load or genotypes do not influence disease severity or progression
- Size of viral inoculum may determine course of disease
  - Posttransfusion cases may proceed more aggressively than infections ass. w/ IV drug use
- Disease expression is related to viral expression
  - Low levels of circulating HCV RNA usu. found in asymptomatic pts w/ normal ALT levels
HCC may occur as a result of frequent cell repair and new cell growth

Question 31

Q

Hep C

Epidemiology

Answer

A

Worldwide distribution
Major cause of transfusion-associated hepatitis b4 screening started
transmission by blood products ↓ to almost zero
New HCV infections ↓ by over 80% since 1990 in the US
Most new infections d/t high-risk drug behavior (60%) or unsafe injection practices
Acute infection is generally asymptomatic ⇒ incidence unclear
- > 70% HCV seropositivity in IV drug users and hemophiliacs
- 20-30% HCV seropositivity in pts receiving hemodialysis
New cases annually: ~150k in US and Western Europe, ~350k in Japan
- 25% are symptomatic
- 60-80% progress to chronic liver disease
- 20% of these develop cirrhosis
- 5-7% of pts ultimately die of the consequences of infection
Chronic infections: > 170 million chronic carriers
- Risk of developing liver cirrhosis and/or liver cancer

Question 32

Q

Hep C

Transmission and Risk Factors

Answer

A

↑ Risk for HCV infection:
- Current or former injection drug users, including those who injected only once many yrs ago
- Recipients of clotting factor concentrates before 1987
- Recipients of blood transfusions or solid organ transplants before July 1992
- Chronic hemodialysis pts
- Persons w/ known exposures to HCV
  - Ex. health care workers after needlesticks involving HCV ⊕
- Blood recipients of blood or organs from a donor who tested HCV ⊕
- Persons w/ HIV infection
- Children from HCV ⊕ mothers
Most common modes of transmission: IV drug use, hemophilia, and tattoos

Question 33

Q

Hep C

Clinical Syndromes

Answer

A

Most common signs and sx: fever, fatigue, dark urine, clay-colored stool, abd pain, loss of appetite, nausea, vomiting, joint pain, and jaundice
- > 70% of pts asymptomatic
- ~25% w/ jaundice
- 10-20% develop GI sx (N/V or abd pain)
Sx typically manifest 6-8 wks after exposure and last for 2-12 wks
Acute fulminant Hep C is rare

Question 34

Q

Hep C

Serology

Answer

A

Dx of acute HCV infection difficult due to:
- # of asymptomatic cases
- No reliable and specific IgM-based serologic test
- Potential overlap of labs for acute and chronic hep C infection
Criteria for definitive acute HCV diagnosis:
1. Pt reports recent risk factors for acquiring HCV
2. Current ⊕ HCV RNA, ⊕ HCV Ab, ↑ ALT
3. Labs within the past 12 months: ⊖ HCV RNA, ⊖ HCV Ab, nl AST/ALT
  - Most pts will not have recent retrospective labs for comparison

Question 35

Q

Hep C

Serology

Answer

A

Possible HCV exposure within past 6 mos ⇒ test for HCV RNA or f/u testing for HCV Ab
Immunocompromised pts ⇒ testing for HCV RNA can be considered
Differentiate past/resolved HCV infection vs false ⊕ for HCV Ab ⇒ testing w/ another HCV Ab assay can be considered
Repeat HCV RNA testing in 16-24 wks if:
- Pt had previous ⊖ qualitative results
- Pt had a ⊖ anti-HAV test result at 4-6 wks after suspected exposure
- HCV exposure within 6 mos suspected
- Clinical evidence of HCV disease
- Concern regarding handling or storage of test specimen
Consider treatment if pt tests ⊕ for HCV RNA 8-12 wks after infection

Question 36

Q

Hep C

Testing Algorithm

Question 37

Q

Hep C

Treatment and Prevention

Answer

A

Goal: undetectable HCV RNA at least 6 months after cessation of therapy.

Historical tx:
- Interferon monotherapy ⇒ combined interferon & ribavirin ⇒ combined pegylated interferon & ribavirin
  - Response rates 40–80%
    - ≤ 50% for genotype 1 (most common genotype in the US)
    - ≤ 80% for genotypes 2 or 3
  - Approved for use in adults & children ages 3-17 yrs
  - Ribavirin: severe ADRs, major drug interactions, resistance issues
  - Peg-interferon: numerous ADR, no resistance issues
Direct Acting Antiviral Agents
- Target enzymes and proteins involved in hep C replication
- ↑ Tx success rates
- Expensive ⇒ priority to pts w/ most urgent need
- 3 classes of drugs:
  - NS3/4A Protease Inhibitors
  - NS5B RNA Polymerase Inhibitors
  - NS5A Inhibitors
- Many new agents on the market
  - Tx will vary depending on the genotype
  - Different classes used in combo to ⊗ HCV replication @ multiple steps
Length of treatment for acute hep C ranges 4 wks to 1 yr

Question 38

Q

NS3/4A Protease Inhibitors

Answer

A

NS3/4A serine protease
- Responsible for cleavage at 4 sites of HCV polyprotein
  - NS3 protein ⇒ catalytic subunit
  - NS4A protein ⇒ activating cofactor
- Essential for viral replication
Drugs:
- Simeprevir [Olysio]
  - Resistance a significant issue
  - No longer a recommended tx for HCV
- Voxilaprevir
  - Now preferred tx
  - Usu. given in combo w/ sofosbuvir and velpatasvir ⇒ combo pill “Vosevi”

Question 39

Q

NS5B RNA Polymerase Inhibitors

Answer

A

NS5B RNA-dependent RNA polymerase
- Essential for HCV viral replication
Sofosbuvir
- Nucleotide analogue
- ⊗ NS5B

Question 40

Q

NS5A Inhibitors

Answer

A

NS5A protein ⇒ important role in RNA replication

Drugs in this class include Ledipasvir and Velpatasvir

Question 41

Q

Question 42

Q

Question 43

Q

Hep E Virus

Properties

Answer

A

Non-enveloped
Linear ⊕-sense ssRNA genome
Caliciviridae family
Genus within Norovirus group

Question 44

Q

Hep E Virus

Epidemiology & Transmission

Answer

A

Cause of water-borne epidemics throughout world
- Mostly in developing countries
- Transmitted mainly via fecal-oral route
  - Fecal contamination of drinking water
  - Sporadically ingestion of raw shellfish
Humans are natural host
Risk factors for HEV related to poor sanitation

Question 45

Q

Hep E

Clinical Syndromes

Answer

A

HEV causes acute sporadic and epidemic viral hepatitis
Symptomatic infection most common in young adults aged 15-40 yrs
Frequent infection in children, disease mostly asymptomatic or very mild w/o jaundice
- Usu. undiagnosed
No chronic or carrier state
HEV mortality rate higher vs HAV, esp. in pregnant women

Question 46

Q

Hep E

Serology