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40 Cards in this Set
- Front
- Back
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Hepatitis A
___virus 27 nm, naked icosahedral capsid + sense, single-stranded RNA 1 serotype |
Picorna
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Characteristics of Hepatitis A
Stable to: Acid at pH 1 Solvents (ether, choloroform) Detergents Salt water, ground water (months) Drying Temperature 4°C: weeks 56°C: 30 minutes: stable 61°C: 20 minutes: partial inactivation Inactivated by: ___ Formalin (0.35%, 37ºC, 72hrs) Peracetic acid (23%, 4 hrs) Β-Propiolactone (0.25%, 1 hr) Ultraviolet radiation (2 μW/cm²/min) |
Chlorine treatment of drinking water
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Hepatitis A
Virus reproduces in hepatocyes and Kupfer cells, released Bile Stool Shed 10 days then Jaundice Antibodies T-cells activated Immunity – lifelong Pathology – immune response No chronic infection No association with ___ |
hepatic carcinoma
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TIME COURSE OF HEPATITIS A
Symptoms appear abruptly with immune response (15-50 days) Fever Fatigue Nausea Loss of appetite Abdominal pain ___ (4-6 days later) Viral shedding precedes sxs, stops before cessation of sxs __% complete recovery 1-3% fulminant→80% mortality Liver failure w/ encephalopathy |
Jaundice
99 |
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EPIDEMIOLOGY OF HAV
40% of acute hepatitis Contagious before ___ Spread fecal-oral, contaminated water, dirty hands High concentration in stool Shellfish – filter feeders → concentrate virus Water supply, restaurants, daycare centers Over-crowding Seropositive Sweden – 13% USA – 44% Taiwan – 88% |
symptoms
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raw oysters think ___
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hep A
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Hepatitis B
Hepadnavirus 42 nm, enveloped,circular, partially double-stranded DNA Encodes reverse transcriptase, replicates through RNA intermediate Enveloped Virion (=___ surface antigen that helps avoid detection like flares) – very resistant Ether Low pH Freezing Moderate heating |
Dane Particle
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HEPATITIS B
Hepatitis B core antigen(___) surrounds Polymerase Reverse transcriptase Ribonuclease H Hepatitis B surface antigen (___) In envelope Released into serum ___ actual virion in serum Spherical or filamentous Immunogenic |
HBcAg,
HBsAg, Outnumber |
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___ is a DNA virus that replicates via an RNA intermediate using reverse transcriptase
Integrated viral DNA found in ___ |
hep B,
hepatocellular carcinomas |
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PATHOGENESIS AND IMMUNITY DETERMINATES OF ACUTE AND CHRONIC HBV INFECTION
Virus in ___ secretions IV → most efficient Acute or chronic w/ or w/o sxs -Based upon immune response initiated by interferon --Cell mediated --Inflammatory response Presence of HBsAg, HBeAg indicative of active infection Replicates in hepatocytes with integration of HBV genome; minimum cell damage |
every (Blood, semen, saliva, milk, vaginal secretion)
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hep B with ___ will always result in fulminant hepatits
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delta agent
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walk through HBV infection
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when you hear immune complex diseases think (4 things)
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Vasculitis
Arthralgia Rash Renal Damage |
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___ is associated with Primary Hepatocellular Carcinoma (PHC)
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HBV
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Time Course of HBV
Less severe children<adults Incubation ___ days Symptoms Fever Malaise Anorexia Followed by- Nausea Vomiting Abdominal discomfort Chills ↑ liver enzymes Icterus Jaundice Dark urine Pale stools 1% of icteric pts.→fulminant(ascites, bleeding) |
45-160
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OUTCOMES OF ACUTE HBV
Chronic Infection 5-10% 10% cirrhosis, liver failure Major source of spread If co-infected with HDV → Fulminant disease Primary Hepatocellular Carcinoma __% 2ª to chronic HBV HBV genome incorporated into PHC cells → cell growth directly, or cycles of tissue damage and repair with eventual mutation? Taiwan 15% of population are HBV carriers 50% die form PHC or cirrhosis |
80
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HBV
Treatment, Prevention, and Control (for chronic disease) Hepatitis B ___ within 1 week of exposure ___ for Chronic HBV HIV reverse transcriptase inhibitor? Famciclovir? Blood screening Lifestyle changes Universal blood and body fluid precautions Vaccination Genetically engineered 95% effective 1 serotype |
immune globulin,
Interferon-α |
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Hepatitis C
Originally named non-A,non-B Hepatitis Has not been isolated ID’d by ELISA ___virus 30-60nm, + sense single stranded RNA Enveloped Humans, chimpanzees |
Flavi
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___
Chronic infection -Inhibits cell death (apoptosis) -Inhibits Interferon-α action (persistant infection) -Remains cell associated CMI → tissue damage PHC(Primary hepatocellular carcinoma) -Induction of cell growth -Continual liver repair Antibody not protective |
Hepatitis C
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percentage of HCV recovery and clearance
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___ is the only viroid-like agent to infect humans, depends on ___ specifically ___ for packaging
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hepatitis D (delta agent),
hepatitis B, HBsAg |
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HDV
Transmission Blood Semen Vaginal secretion Infection, Replication only with concurrent HBV Can be co-infected, same routes of transmission More rapid, severe infection if HBV ___ with HDV, results in ___ HDV→ cytotoxic to liver Antibodies to HBsAg protective (attachment) |
superinfected,
fulminant hepatits |
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Hepatitis E is similar to ___
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HAV
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MHC presentation is central to ____
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adaptive immunity (specific immunity)
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Why bother with antigen processing for T-cells, why not just have them recognized the pathogen directly like antibodies? (2 reasons)
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Intracellular pathogens such as viruses cannot be reached.
MHC makes sure the decision to destroy is not made by one cell only. For example, helper T induces macrophage to release cytokines. |
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What is the component that can be used to differentiate between MHC class 1 and class 2
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Beta2-microglobulin is only on class 1
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MHC class I molecules are expressed on ___
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all nucleated cells
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MHC class __ present extracellular pathogens and apoptotic cells
MHC class __ present poorly folded, damaged or unwanted proteins and intracellular pathogen-derived proteins |
II,
I |
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Describe the key differences between MHC class I and II peptide loading
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class 1 starts with intracellular pathogen processed by proteasome, and binding occurs in ER
class 2 starts with endocytic vesicle, and binding occurs in phagolysosome |
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Proteins that aid peptide transport and loading of MHC class I in ER
In the ER lumen ___ first binds to MHC class I. Later, ___ binds which also allows peptide fragments to enter lumen. Patients with a defect in this protien suffer from ___ |
calnexin,
TAP, chronic viral infections |
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Proteins that aid peptide loading of MHC class II in acidified vesicle:
___ fills the peptide-binding groove while in the ER (preventing binding by intracellular pathogens) ___ continues to fill the peptide groove once in the vesicle. ___ catalyzes the release of above protein allowing the binding of the endocytosied antigen |
invariant chain,
CLIP, HLA-DM |
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MHC class I can accommodate peptides of ___ amino acids
MHC class II can accommodate peptides of ___ amino acids the reason for this is that class II is open ended and the amino acids can overhang |
8-10,
13-25 |
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T-cells bind to specific antigens and specific MHCs. This is known as ___
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MHC restriction
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CD8 binds the ___ domain of MHC class I
CD4 binds the ___ domain of MHC class II |
alpha3,
beta2 |
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What are the MHC isotypes that mostly present pepdites and are higly polymorphic?
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Class 1:
HLA-A, HLA-B, HLA-C Class 2: HLA-DP, HLA-DQ, HLA-DR |
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Which chromosome has most of the MHC genes?
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chromosome 6
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How many different MHC isoforms can an individual express?
How are they expressed? |
6 class I and 6 class II
codominant expression |
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If individuals could make only one MHC isotype, then a pathogen could wipe out the population by avoiding detection.
So why are the genes encoding for MHC isotypes increased ad infinitum? Because every APC has only a certain number of MHCs plus you need more than just one to activate a T cell. MHCs would be too dilute. But MHC ___ increases the resistance of the population from rapidly mutating or newly encountered pathogens without increasing the number of MHC isotypes |
polymorphism
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describe the difference between direct allorecognition and indirect allorecognition
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3 ways drugs can suppress immune system:
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Block gene expression: prednisone
Block DNA replication: Methotrexate, etc. Inhibit T-cell activation: Rapamycin, etc. |
