#15 Hepatitis A/B/D/E Flashcards
Structure of Hep A;
genome
how many serotypes
RNA Picronavirus: simular to polio in lifecycle, icosahedarl RNA virus
single serotype worldwide and has Acute disease with aysomtomatic infection
Spread of Hep A and most common spread
Fecal/oral transmission with spread from food/water/raw shellfish/poor hygeine
a. most common spread is food handlers/daycare workers and children
Doe Hep A have a chronic infection state?
NO CHRONIC infection: protecteive antiB devo in response to infection and confers lifelong immunity
**A ≠cause chronic infection bc only 1 sero we make antiB to
Why don’t se wee a chronic infection with Hep A
we make protective antiB
lifelong immunity
only one seroteyp
Capsid of Hep A is stable to ________
Hep A will enter these cells bc have a lot of its receptors
ACID, DRYING AND DETERGENTS
LIVER
Hep A mRNA translated into ____ polyprotein that’s cleaved to make mature products
ONE
A is the first letter in the alphabet
so makes 1 polyprotein and only 1 serotype
Unlike other picornaviruses, Hep A virus is not ______ but is shed from cells
cytolytic
Can we culture Hep A
NOPE.. no good tissue cultures
Hep A Transmision: fecal/oral
virus is steadily released from infected ______
______and _______eliminate infected cell with a little help from antiBs
hepatocytes
NK
cytotoxic T cell
Hep A liver pathology is most likely d/t
immunopathology (host immuen response)
Incubation period for Hep A is ____ days and you can start to shed virus before you show symptoms. Also makes it difficutly to identify source of infection
30
Disease from Hep A:
Jaundice is seen by age group: more prevelent
as you get older (over 14 yrs old)
fluminant hepatitis, cholestatic hepatitis and relapsing hepatitis
Rare complicaitons of Hep A
Coures of infection for Hep A
- Ingestion and incubation for 30 days: virus is detecteable by 3 weeks
- At 4 weeks see increase in IgM specific to HAV(lasts for 8 weeks then decreases)
a. aslso see elevated liver enZ and icteric symptoms (if present) - IgG for HAV incraeses at 8 weeks and stays high
At 4 weeks post ingestion of Hep A virus, we can see increase in
IgM specific to HAV and increase liver enZ
will stay high for 8 weeks
At 8 weeks post infection, we see incraese _______ for Hep A
IgG
~ about time symptoms are gone
Preparation of inactivated HAV vaccines
who should take it
- Cell cultre adapted virus grown in human fibroblasts→ purified product inactivaed w/ formalin
- Recommended for: infants/people traveing to high HAV incendence areas/ ppl with chronic liver diease and peole working with HAV
Since Hep A vaccine liscensed we’ve seen a ____decrease in HAV
90%
Take home points for Hep A
Key points for HAV: hepatotropic, picornavirus, acute, 1 sero, time course and incubation contricute to spread, fecal/oral and have vaccine to specific people
Hep E is a
calicivirus
E is calicEEEE
and makes you queezy
Genome on Hep E calicivirus
+ssRNA, icosahedral
Transmission of Hep E
drinking fecal contaminated water
if seen in US… d/t travel outside of US
endemic in africa/russia/S.america
You see a culture of pleomorphic looking cells with rods and shit… what could it be?
Hep B has VERY pleomorphic lifecycle
Has wide varitey of organisms when EM=== rods, pleomorphic structures d/t lifecycle
Hep B
Distribution of Hep B
Distribution: seen high in africa and alaksa and norther part of S.America, low in US
Infants infectd with Hep B we will see
—see 90% will go on to have chronic virus
bulk of reservoir of Hep B is
chronically infected pts that were infected young
Acquiring Hep B older you are you see
resolution, less like to go chronic
Hep B is an enveloped virus: receptor si the
sodium bile acid co-transporter (NTCB)
Who has the sodium bile acid co-transporter (NTCB)
Hep B!!!
Hep B is what type of virus
hepadnovirus
Hep B has a Circular DNA genome that is:
: PARTLY ds DNA
—it will go to full dsDNA inside the cell
Hep B hepadnovirus Genome enters cell
→ DNA synthesis occurs to form fully dsDNA in the ______
Cytoplasm
Once the genome of Hep B hepandnovirus has synthesized FULL dsDNA it will go to the nucleus to:
→ transcribes to mRNA
Once the Hep B has transcirbed its mRNA in the NUCLEUS it will exti to cytoplasm for a special kind of translation
mRNA ‘reverse transcribed” to its ssDNA and DNA made partially ds
(back to the partial dsDNA.. just like it entered :)
Hep B is a little bitch bc
bc it only partially does its DNA transcription
and makes all these Bull shit partial antiG it releases
DNA is encapsidated to new virion on ___
Virons enveloped and released as well as subviral particles of _________
ER surface antiG (sAg)
What can we do with the subviral surface antiG from Hep B
c. these are non-infectious and have been KEY in our devo of vaccine for Hep B—make recombinant forms in yeast cells to prime our immune system
Can we get a good tissue culture of Hep B
NO GOOD TISSUE cluture for hep B bc hepatocytes won’t grow in culture)
Risk and Spread of Hep B
- highest risk is heteroxesual spread; as well as man to man, IDU and other
Blood/IV drug/sex/neonatal infection: see virus go to the blood
Hep V virus go to the blood
b. if not sufficent Ab prodution→
travels to liver and makes HBsAg which our immune system recognizes and see immune complex diseases (d/t host immune sytem)
Hep B in liver can also go liver → viremia if
cell mediated immunity doesn’t work.
Hep B viremia causes spread to m
milk/vaginal/semen/saliva and transmission
Course of Hep B:
incuabation→ pericteric→ icteric→ convalescent
Hep B symptoms: 2 months after infection
a. symtoms in the preicteric: jaundice, dark urine, malaise, anorexia, nausea, RUQ pain
a. symtoms in the preicteric: jaundice, dark urine, malaise, anorexia, nausea, RUQ pain
Hep B symptoms pst 2 months of infection
may see rash or itching right away
Of people that contract Hep B
_____ resolution
______HBsAg+ for over 6 months
_____ fulminat hepatitis
90% resolve
9% to HBsAg+ for 6 months
1% to fulminant hepatitis
Of the 9% of pts that express HBsAg+ _____ will resolve, the others can be asymptomatic carriers, chronic persisant hep, or chronic acitve
50%
What state would a Hep B pt need to be in to have hepatic cell carcinoma
they would be HBsAg +
have chrnoic active hepatitis
devo heapic cell carcinoma
what are 3 complications of chronic active heaptitis
Extrahepatic disease/cirrohssis/ hepatic cell carcinoma
Hep B; 2 months post exposure: see increase in
HBsAg and HBeAg
Hep B at 3 months wee elevated
anit-HBe liver enZs then back down by month 6
Once infected wth HBV the liver usually has effective _________ to eliminate the virus
cell medated immune response
What happens when the liver’s cell mediated response sucks in tx HBV
LIMITED cell mediated immune resposne: this leads to chrnoic disease and mild symptoms
A_____ can infect a pt with chrnoic HBV and will increase risk for fulminat hepatitis
delta agent
Key is: immune control and _______can influence outcome of HBV infection
presence of HDV (the delta agent)
HDV (Hep D virus) is technically a
viriod and only grows in Hep B infected cells
The genome of the Dumb Hep D virus thats not really a virus
small RNA copied by host RNA pol II and catalytically active ‘ribozyme’ processes itself
encodes 1 antiG and becomes packatged in Hep B sAg’s
small RNA copied by host RNA pol II and catalytically active ‘ribozyme’ processes itself
encodes 1 antiG and becomes packaged in Hep B sAg’s
Hep D viriod
Hep D: Co-infection at the same time as Hep B see
severe acute disease and low risk of chronic infection
Hep D: b. Superinfection: subsequent or after initial Hep B infection we see
chronic HepD infection and high risk of severe chronic liver disease.
which is less risky, co infection at same time, or superinfection when D infects after B
duh… Co-infection is preferred
Why does chronic HBV increase incidence of hepatocell carcinoma
injured liver has sustained cell proliferation, more genetic errors
injuection of HBV into DNA = genomic instability
Virally encoded ‘X’ proteins is oncogenic~ decreaes p53
this ‘X’ product also increaes experssion of surface antigen to cauase inflammation
Prevention an Tx of HBV
screen blood supply and vaccination is KEY to prevent high-risk ind and infants.
a. subunit vaccine—recombiant HBsAg produced in yeast which self assembles into immuegenic particles
universal blood/body fluid precautions and lifestyle precautions
