#15 Hepatitis A/B/D/E Flashcards by Meghan May

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Why don’t se wee a chronic infection with Hep A

we make protective antiB
lifelong immunity
only one seroteyp

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Unlike other picornaviruses, Hep A virus is not ______ but is shed from cells

cytolytic

How well did you know this?

Not at all

Perfectly

Can we culture Hep A

NOPE.. no good tissue cultures

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Hep A liver pathology is most likely d/t

immunopathology (host immuen response)

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Disease from Hep A:

Jaundice is seen by age group: more prevelent

as you get older (over 14 yrs old)

How well did you know this?

Not at all

Perfectly

fluminant hepatitis, cholestatic hepatitis and relapsing hepatitis

Rare complicaitons of Hep A

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

At 8 weeks post infection, we see incraese _______ for Hep A

IgG

~ about time symptoms are gone

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Since Hep A vaccine liscensed we’ve seen a ____decrease in HAV

90%

How well did you know this?

Not at all

Perfectly

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

How well did you know this?

Not at all

Perfectly

Hep E is a

calicivirus
E is calicEEEE
and makes you queezy

How well did you know this?

Not at all

Perfectly

Genome on Hep E calicivirus

+ssRNA, icosahedral

How well did you know this?

Not at all

Perfectly

Transmission of Hep E

drinking fecal contaminated water
if seen in US… d/t travel outside of US
endemic in africa/russia/S.america

How well did you know this?

Not at all

Perfectly

You see a culture of pleomorphic looking cells with rods and shit… what could it be?

Hep B has VERY pleomorphic lifecycle

How well did you know this?

Not at all

Perfectly

Has wide varitey of organisms when EM=== rods, pleomorphic structures d/t lifecycle

Hep B

How well did you know this?

Not at all

Perfectly

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

1. 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

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

#15 Hepatitis A/B/D/E Flashcards

(64 cards)