- picornavirus, ssRNA - enteric, fecal-oral - endemic in developing countries - incubation: 4 weeks (SHORT) - self-limited infection (no chronic) - vaccine >90% efficacious

- ssRNA - enteric, feca-oral - asia, Middle East, N. Africa - genotypes 1 and 2 - incubation- 4 weeks (SHORT) - self-limited

HEV - acute hepatitis in young adults - zoonotic w/ reservoirs in swine (genotypes 3 and 4 - no vaccine commercially available - cases of chronic infection reported in immunosuppressed hosts

- pre-exposure-HBV Ig +HBV vaccine for intimate contacts only - acute exposure - infants: HBIg + HBV vaccine started <12 hr after birth, + antivirals for mom - chronic exposure- HBV vaccine

- defective RNA virus - envelope: HBV surface antigen - need HBV for infection/replication - where HBV is present, (mediterranean, Russia, Africa, Amazon)

Viral Hepatitis I/II Flashcards by Alegra Mendez

hepatitis leads to failure to excrete _____

bilirubin –> jaundice

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prodrome

2-10 days

flu-like, fever, N/V

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HAV in children presentation

mild, non-specific sx

infection often not diagnosed

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HBV extra-hepatic manifestations

skin rash
arthritis
glomerulonephritis
cyroglobulinemia

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jaundice is minimal in H__

HCV

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transaminase elevations may be <500-1000 in H__

HCV

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most common acute hepatitis

HBV

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most common chronic hepatitis

HCV

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HAV

picornavirus, ssRNA
enteric, fecal-oral
endemic in developing countries
incubation: 4 weeks (SHORT)
self-limited infection (no chronic)
vaccine >90% efficacious

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self-limiting (no chronic disease) hepatitides

HAV

HEV

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HAV pre-exposure prophylaxis

HAV vaccine at 0 and 6 mo

immunity in ~3wk after first vax

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HAV post-exposure prophylaxis

within 2 weeks of exposure

single dose of HAV vaccine or IgM dependent on age

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HEV

ssRNA
enteric, feca-oral
asia, Middle East, N. Africa
genotypes 1 and 2
incubation- 4 weeks (SHORT)
self-limited

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enteric viruses

HAV
HEV

(vowel=bowel)

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HEV vs. HAV

HEV

acute hepatitis in young adults
zoonotic w/ reservoirs in swine (genotypes 3 and 4
no vaccine commercially available
cases of chronic infection reported in immunosuppressed hosts

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HBV transmission

-blood borne (IDU, sex, HIV coinfection, med equipment, VERTICAL TRANSMISSION 90% if mother has HBV in 3rd trimester, hemodialysis, correctional facilities

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HBV inculation

2-3 mo. (LONG)

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Out comes of HBV w/ %

90% –> RECOVERY (anti-HBs+)

10% –> chronic (HBsAg+)

1% fulminant hepatitis

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risk of hepatocellular CA

chronic HBV or HCV

viral replication (HBV-DNA + or HCV-RNA +)

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HBV pre-exposure prophylacis

vaccine at 0,1,6 mo.

recombinant HBsAg so vaccinated pt has protective Ab, anti-HBs

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acute HBV exposure

pre-exposure-HBV Ig +HBV vaccine for intimate contacts only
acute exposure - infants: HBIg + HBV vaccine started <12 hr after birth, + antivirals for mom
chronic exposure- HBV vaccine

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chronic HBV infection

immune active phase

HBsAg +
HBV-DNA +
high ALT

fibrosis and inflammation on liver biopsy

–> TREAT

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HBV tx

lamivudine (RESISTANCE)
endeavor
tenofovir
combos

not curative

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HDV

defective RNA virus
envelope: HBV surface antigen
need HBV for infection/replication
where HBV is present, (mediterranean, Russia, Africa, Amazon)

HDV transmission

blood borne -IDU, sexual COINFECTION (acute infec w/ HBV and HDV) SUPERINFECTION (chronic HBV carrier gets acute HDV --> chronic HDV ... small amount get fulminant hepatitis

HDV tx

none but prevented via HBV vaccination no specific tx/complex

HCV

- flavivirus - ssRNA - genotypes 16-6 - incubation: 2 mo. (LONG) - clinically mild infections

HCV transmission

-blood borne (IVDU, medical/dental practices, sexual, transfusions, vertical mother--> child

Which has vertical transmission more commonly HCV or HBV

HBV

acute hepatitis C outcomes w/ %

acute hepatitis --> 70% chronic HCV 30% recovery

Everyone born between this time period should be screened for hep C

between 1945 and 1965

when should HBV carriers w/ chronic hep C

treatment if in immune active phase

HCV tx/vaccine

tx: yes vaccine: NO

past infection immunoglobulin

IgG

IgM --> IgG shift around _ months

4 months

Anti-HBs protective or non-protective?

protective | via vaccination with HBsAg

Anti-HCV protective or non-protective?

non-protective no vaccine against HCV

viral antigens in blood means

virus is present in body

anti-HAV is a combined capture assay of both

IgM | IgG

HEV assays

poorly standardized

HBV

- dsDNA virus - blood borne - chronic infection: 5-10% of adults)

Dane particle

HBV - outer lipoprotein envelope made of HBsAg - inside: genome, HBcAg, HBeAg

window period

Both HBsAg and anti-HBs are in the blood but in immeasurably low amounts check anti-HBc IgM

What is the best way to dx early HBV infection?

test for anti-HBc IgM Abs | earliest host response to HBV infection, present during window period

Anti-HBc IgM

first antibody to be positive AND positive during the “window period” when HBsAg has disappeared and Anti-HBs has not yet appeared

Acute HBV outcomes w/ %

90% --> recovery (Anti-HBs+) 10% --> chronic HBV (HBsAg) ***age-dep 1% --> fulminant

Anti-HBc IgG protective or non-protective?

non-protective

The presence of ____ in the blood is the main marker of HBV infection. It appears during the _______ period and remains positive as long as there is _______.

HBsAg appears during the latter part of the incubation + as long as there is active infection

HDV dx

- HDV-RNA in blood - rare to find HDAg - anti-HDV IgM and IgG

exception when dx HDV

Ant-HDV IgM is present in acute and chronic HDV

dx of HCV | 2 tests

anti-HCV by EIA HCV-RNA

HCV tx

interferon-free therapy

acute viral hepatitis histo

- portal and lobular mononuclear inflammation - ballooning degeneration - apoptosis - macrophage/kupffer cells - cholestasis - no fribrosis

chronic viral hepatitis histo

- portal and periportal predominant inflammation (lobular component variable) - development of FIBROSIS

interface hepatitis

hallmark of active and progressive diseae

stage of chronic viral hepatitis is based on

degree of fibrosis

cirrhosis histo

- diffuse fibrosis/scarring w/ regenerative nodules - altered vascular architecture --> portal HTN - regression/revversible? - histo --> non-specific once cirrhosis establishments - HCC risk

activated stellate cells

``` myofibroblast proliferation contraction chemotaxis fibrogenesis ```