1
Q
HAV class
A
Picornaviridae
2
Q
HBV class
A
Hepadnaviridae
3
Q
HCV class
A
Flaviviridae
4
Q
Hep D class
A
Satellite, coinfect with B
5
Q
Hep F class
A
???
6
Q
Hep G class
A
Flaviviridae
7
Q
HAV genome and structure
A
ss+RNA
Icosahedral capsid of 4 polypeptides (VP1-4)
Non-enveloped
8
Q
HAV genome distinguishing feature:
A
VPg (protein) on 5’ end
9
Q
HAV inactivated by (5 things)
A
Chlorine
Formalin
Peracetic acid
Beta-propiolactone
UV
10
Q
Replication of HAV (6 steps)
A
Receptor binding
Uncoating (+RNA)
Translation/Proteolytic processing
Replication
Assembly
Maturation and release
11
Q
HAV produces _____ infection
A
acute
12
Q
HAV incubation period length
A
2-6 weeks
13
Q
2 phases of HAV infection
A
1. Prodrome (flu-like, immune mediated hepatic damage)
2. Icteric (billirubinemia, jaundice, abdominal pain)
- symptoms wax/wane
- complete recovery in 99% cases
14
Q
Immunogically, acute HAV infection results in
A
lifelong immunity
15
Q
icterus is an increase in
A
unconjugated bilirubin
16
Q
What happens to conjugated bilirubin?
A
Water soluble, renal excretion
17
Q
HAV replication occurs in __________ (in body)
A
Oropharynx or GI tract
18
Q
HAV is shed in the _______
A
bile and feces
19
Q
Does HAV cause viremia?
A
Yes
Brief
20
Q
HAV can be detected…
A
in the stool before symptoms occur
21
Q
Three serological peaks during HAV infection
A
ALT at 2 months
IgM anti-HAV at 3 months (recent infection)
Total anti-HAV (immunity
22
Q
HAV transmission routes (3 categories)
A
Close personal contact
Contaminated food
Blood exposure (rare)
23
Q
Seroprevalence of HAV antibodies
A
40-70% of adults
24
Q
Serological distinction between acute and past HAV infection
A
IgM = Acute
IgG = Past
25
IgM and IgG are detected by
ELISA
26
Is RT PCR useful in detection of HAV?
It may detect earlier than serology, but it is rarely performed
27
HAV vaccines
HAVRIX
VAQTA
TWINRX
28
Who is TwinRx not recommended for? What's the dosing schedule?
All patients **under 18** years of age.
3 doses @ **0, 1, 6** months
29
HBV genome and structure
Genome: Circular dsDNA
Capsid: Icosahedral
Enveloped
30
HBV capsid proteins
1. Core Protein
(**HBcAG**)
2. Soluble core protein
**(HBeAG)**
31
What is HBeAG?
Indicator of active HBV **replication** phase
(it is a variant of the core protein that was modified within the cell)
32
HBV envelope proteins
Surface antige (**HBsAG**)
3 forms:
1. **S** = large
2. **S2** = medium
3. **S1** - small
33
Unique feature of the DNA virus HBV
Encodes a RT enzyme
replicates through RNA intermediate
34
The first weird step of HBV replication cycle
Second and third steps?
1. After uncoating, _partially double stranded DNA genome is completed_ by host enzymes -- becomes **CCCDNA** (Covalently Closed Circular DNA)
2. _Four mRNAs_ are made (one giant one)
3. Goes to cytoplasm where the mRNAs assemble around the big one, and _NEGATIVE_ DNA is made by **Reverse Transcriptase**
35
What happens after DNA is synthesized in HBV replication?
RNA Degrades, and the POSITIVE counterpart to the negative DNA is synthesized.
The envelope forms before this completes
36
HBV released from cell via ______ after assembly
Exocytosis
37
HBV causes what kinds of infections?
Acute or chronic
38
Acute HBV incubation time
1-6 months
39
Most HBV acute patients are \_\_\_\_\_\_\_\_
asymptomatic
40
Some Acute HBV patients progress to
jaundice
41
Few patients progress to _________ during acute HBV infection
**Fulminant Hepatitis**
risks = GI bleed, coma, encephalopathy, ascites, coagulopathy)
42
Survival from acute HBV results in \_\_\_\_\_\_\_\_\_\_\_\_\_
lifelong immunity
(patients will never develop chronic infection)
43
Fulminant Hepatitis requires...
Delta agent
44
Chronic HBV patients may...
transmit infection throughout life
45
Chronic HBV is definied as
longer than 6 months
46
Infants with perinatal HBV infection will...
almost always develop CHRONIC hep B infection
47
Chronic HBV = increased risk of
cirrhosis, liver cancer, liver failure
48
HBV infects the liver but does not...
cause direct cytopathology
49
\_\_\_\_\_ is the leading cause of liver transplantation in the US
Chronic HBV
50
Titer cuves for acute HBV
1st peak = **HBsAG**
2nd peak = **IgM ant-iHBc** (Also TOTAL anti-HBc increases here)
Last = **anti-HBs**
51
Chronic HBV, _____ and \_\_\_\_\_\_last much longer in serum titer
HBeAG
HBsAG
52
\_\_\_\_\_\_ doesn't have a titer peak in chronic HBV
anti-HBs
53
HBV transmission
**Blood**, sex, contact
**Transplacental** (or perinatal)
54
Areas of highest HBV incidence
Subsaharan Afriaca, SE Asia
55
HBV treatment
Acute HBV = (None)
Chronic HBV = **Reverse Transcriptase Inhibitors**
1. Lamivudine
2. Adefovir + alpha-Interferon
56
HBV control (3)
1. Blood donation screening
2. Universal precautions
3. Passive or Active Vax
57
HBV vaccine based on \_\_\_\_. This is recommended for whom? Dosing Schedule?
_HBsAG_
recommended for young and high risk
3 injections (TwinRX = HAV + HBV together)
58
HCV genus, genome, and structure
**Hepacivirus**
**ss+RNA** (looks like Flavivirus)
59
HVC is classified into _______ genotypes. Which are the most common?
6 genotypes
Types 1-3 are most common
60
HVC Clades nucleotides differ by 25%, but difference is not correlated to...
differences in clinical disease
61
HCV displays classic _____ replication
**+RNA**
| (everything happens in the cytoplasm)
62
Acute HCV is _______ in most patients
asymptomatic
63
"Persistent HCV" definition
detectable HCV **RNA for more than 6 months** from the time of presumed infection
64
Jaundice rate in HCV patients
10-20%
65
\_\_\_\_\_\_\_\_\_\_ is responsible for HCV hepatic damage
CMI leading to inflammation of the liver
66
Hepatocellular pathogenesis of HCV (three things)
1. Miscroscopically spotted parenchymal cell degeneration
2. Necrosis of hepatocytes
3. MQ accumulate near the degenerating hepatocytes
67
Acute HCV infection shows \_\_\_\_\_\_\_\_\_\_multiplication
high, fast
68
Sx of acute HCV coincide with increase in
HCV RNA
69
\_\_\_\_\_\_\_ appears in serum after about 8 weeks post-HCV exposure
Anti-HCV (EIA-III)
70
Highest source for HCV infection
IV drug use
71
Sources (3) with least prevalence for HCV infection
nosocomial
iatrogenic
**\*perinatal**\*
72
Vertical transmission to fetus occurs in __ % of HCV cases
3-10%
73
% risk for HCV transmission from breastfeeding
0%
74
Sexual transmission of HCV is _____ than HIV and HBV
Lower
75
HCV transmission between partners may be associated with ....
shared use of Razors and toothbrushes
76
Needlestick transmission rate for HCV is _____ than HIV
HIGHER
**1.8%** versus 0.35%
77
HCV treatments (3)
1. **Interferon** + **Ribavirin**
2. Pegylated Interferon alpha + Ribavirin
(3. Bocepravir + Telaprivir (*protease inhibitors*))
78
HDV needs _____ for infection
_HBsAG_
envelope protein from other virus
79
HDV genus, genome and structure
* Deltavirus
* ss (-) RNA, Circular
* Enveloped
80
HDV RNA encodes _________ that complexes with \_\_\_\_\_\_\_
Delta agent
complexes with RNA
81
Chronic infection with HDV occurs in \_\_\_% of cases
5%
82
Two types of HDV infections:
1. Co-infection (fulminant in 1%)
2. Super-infection (fulminant in 5%)
83
\_\_\_\_\_\_\_\_ HDV infection is far more likely to develop into a chronic infection
Superinfection - 80-90% of patients
84
What is a HDV superinfection?
Infection with HDV in a patient that is **already positive** for HBsAG
85
Superinfection HDV causes rapid...
cirrhosis and hepatocellular carcinoma
86
HDV treatment
alpha interferon + lamivudine
87
HEV genome and structure
ss+RNA
icosahedral
nonenveloped
88
Number of HEV genotypes? Which cause human diseases?
Four
Only #1 causes human disease
89
Phases of HEV infection
Prodromal and icteric
90
HEV infection is \_\_\_\_\_\_\_\_\_
self-limited
91
HEV...E stands for
Enteric + Epidemic
92
HEV spread via...
fecal oral route
93
Epidemics of HEV reporded where...
fecal contamination of drinking water is common
94
Most important prevention measure for HEV is
Sanitation
95
HEV chronic infection length
HEV doesn't cause chronic infection
