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Immunology 3 > #15 Hepatitis A/B/D/E > Flashcards

#15 Hepatitis A/B/D/E Flashcards

1
Q

Structure of Hep A;
genome
how many serotypes

A

RNA Picronavirus: simular to polio in lifecycle, icosahedarl RNA virus
single serotype worldwide and has Acute disease with aysomtomatic infection

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2
Q

Spread of Hep A and most common spread

A

Fecal/oral transmission with spread from food/water/raw shellfish/poor hygeine
a. most common spread is food handlers/daycare workers and children

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3
Q

Doe Hep A have a chronic infection state?

A

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

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4
Q

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

A

we make protective antiB
lifelong immunity
only one seroteyp

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5
Q

Capsid of Hep A is stable to ________

Hep A will enter these cells bc have a lot of its receptors

A

ACID, DRYING AND DETERGENTS

LIVER

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6
Q

Hep A mRNA translated into ____ polyprotein that’s cleaved to make mature products

A

ONE
A is the first letter in the alphabet
so makes 1 polyprotein and only 1 serotype

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7
Q

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

A

cytolytic

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8
Q

Can we culture Hep A

A

NOPE.. no good tissue cultures

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9
Q

Hep A Transmision: fecal/oral
virus is steadily released from infected ______
______and _______eliminate infected cell with a little help from antiBs

A

hepatocytes
NK
cytotoxic T cell

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10
Q

Hep A liver pathology is most likely d/t

A

immunopathology (host immuen response)

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11
Q

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

A

30

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12
Q

Disease from Hep A:

Jaundice is seen by age group: more prevelent

A

as you get older (over 14 yrs old)

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13
Q

fluminant hepatitis, cholestatic hepatitis and relapsing hepatitis

A

Rare complicaitons of Hep A

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14
Q

Coures of infection for Hep A

A
  1. Ingestion and incubation for 30 days: virus is detecteable by 3 weeks
  2. 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)
  3. IgG for HAV incraeses at 8 weeks and stays high
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15
Q

At 4 weeks post ingestion of Hep A virus, we can see increase in

A

IgM specific to HAV and increase liver enZ

will stay high for 8 weeks

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16
Q

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

A

IgG

~ about time symptoms are gone

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17
Q

Preparation of inactivated HAV vaccines

who should take it

A
  1. Cell cultre adapted virus grown in human fibroblasts→ purified product inactivaed w/ formalin
  2. Recommended for: infants/people traveing to high HAV incendence areas/ ppl with chronic liver diease and peole working with HAV
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18
Q

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

A

90%

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19
Q

Take home points for Hep A

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

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20
Q

Hep E is a

A

calicivirus
E is calicEEEE
and makes you queezy

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21
Q

Genome on Hep E calicivirus

A

+ssRNA, icosahedral

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22
Q

Transmission of Hep E

A

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

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23
Q

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

A

Hep B has VERY pleomorphic lifecycle

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24
Q

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

A

Hep B

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25
Q

Distribution of Hep B

A

Distribution: seen high in africa and alaksa and norther part of S.America, low in US

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26
Q

Infants infectd with Hep B we will see

A

—see 90% will go on to have chronic virus

27
Q

bulk of reservoir of Hep B is

A

chronically infected pts that were infected young

28
Q

Acquiring Hep B older you are you see

A

resolution, less like to go chronic

29
Q

Hep B is an enveloped virus: receptor si the

A

sodium bile acid co-transporter (NTCB)

30
Q

Who has the sodium bile acid co-transporter (NTCB)

A

Hep B!!!

31
Q

Hep B is what type of virus

A

hepadnovirus

32
Q

Hep B has a Circular DNA genome that is:

A

: PARTLY ds DNA

—it will go to full dsDNA inside the cell

33
Q

Hep B hepadnovirus Genome enters cell

→ DNA synthesis occurs to form fully dsDNA in the ______

A

Cytoplasm

34
Q

Once the genome of Hep B hepandnovirus has synthesized FULL dsDNA it will go to the nucleus to:

A

→ transcribes to mRNA

35
Q

Once the Hep B has transcirbed its mRNA in the NUCLEUS it will exti to cytoplasm for a special kind of translation

A

mRNA ‘reverse transcribed” to its ssDNA and DNA made partially ds
(back to the partial dsDNA.. just like it entered :)

36
Q

Hep B is a little bitch bc

A

bc it only partially does its DNA transcription

and makes all these Bull shit partial antiG it releases

37
Q

DNA is encapsidated to new virion on ___

Virons enveloped and released as well as subviral particles of _________

A 
ER
surface antiG (sAg)
38
Q

What can we do with the subviral surface antiG from Hep B

A

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

39
Q

Can we get a good tissue culture of Hep B

A

NO GOOD TISSUE cluture for hep B bc hepatocytes won’t grow in culture)

40
Q

Risk and Spread of Hep B

A
  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
41
Q

Hep V virus go to the blood

b. if not sufficent Ab prodution→

A

travels to liver and makes HBsAg which our immune system recognizes and see immune complex diseases (d/t host immune sytem)

42
Q

Hep B in liver can also go liver → viremia if

A

cell mediated immunity doesn’t work.

43
Q

Hep B viremia causes spread to m

A

milk/vaginal/semen/saliva and transmission

44
Q

Course of Hep B:

A

incuabation→ pericteric→ icteric→ convalescent

45
Q

Hep B symptoms: 2 months after infection

A

a. symtoms in the preicteric: jaundice, dark urine, malaise, anorexia, nausea, RUQ pain

46
Q

a. symtoms in the preicteric: jaundice, dark urine, malaise, anorexia, nausea, RUQ pain

A

Hep B symptoms pst 2 months of infection

may see rash or itching right away

47
Q

Of people that contract Hep B
_____ resolution
______HBsAg+ for over 6 months
_____ fulminat hepatitis

A

90% resolve
9% to HBsAg+ for 6 months
1% to fulminant hepatitis

48
Q

Of the 9% of pts that express HBsAg+ _____ will resolve, the others can be asymptomatic carriers, chronic persisant hep, or chronic acitve

A

50%

49
Q

What state would a Hep B pt need to be in to have hepatic cell carcinoma

A

they would be HBsAg +
have chrnoic active hepatitis
devo heapic cell carcinoma

50
Q

what are 3 complications of chronic active heaptitis

A

Extrahepatic disease/cirrohssis/ hepatic cell carcinoma

51
Q

Hep B; 2 months post exposure: see increase in

A

HBsAg and HBeAg

52
Q

Hep B at 3 months wee elevated

A

anit-HBe liver enZs then back down by month 6

53
Q

Once infected wth HBV the liver usually has effective _________ to eliminate the virus

A

cell medated immune response

54
Q

What happens when the liver’s cell mediated response sucks in tx HBV

A

LIMITED cell mediated immune resposne: this leads to chrnoic disease and mild symptoms

55
Q

A_____ can infect a pt with chrnoic HBV and will increase risk for fulminat hepatitis

A

delta agent

56
Q

Key is: immune control and _______can influence outcome of HBV infection

A

presence of HDV (the delta agent)

57
Q

HDV (Hep D virus) is technically a

A

viriod and only grows in Hep B infected cells

58
Q

The genome of the Dumb Hep D virus thats not really a virus

A

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

59
Q

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

A

Hep D viriod

60
Q

Hep D: Co-infection at the same time as Hep B see

A

severe acute disease and low risk of chronic infection

61
Q

Hep D: b. Superinfection: subsequent or after initial Hep B infection we see

A

chronic HepD infection and high risk of severe chronic liver disease.

62
Q

which is less risky, co infection at same time, or superinfection when D infects after B

A

duh… Co-infection is preferred

63
Q

Why does chronic HBV increase incidence of hepatocell carcinoma

A

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

64
Q

Prevention an Tx of HBV

A

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

Immunology 3 (20 decks)

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