Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Virology > Hepatitis > Flashcards

Hepatitis Flashcards

1
Q

Symptoms

A

Inflammation of liver Acute: older people, non-specific, flu like symptoms, jaundice, dark urine Haem from RBCs broken down into billirubin, cleaved by bile, but liver not working –> jaundice Chronic: younger people General malaise Cirrhosis of liver, liver cancer Fulminant: sudden disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hepatocytes

A
  • Infected by hepatitis virus Some products drian into bile duct
  • Hepatocytes damaged –> can’t secrete bilirubin
  • Virus released into bile duct in polarised manner - capsid, naked viruses
  • Hep B and C - enveloped virus, secreted into venous system
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Jaundice

A

Immune response to hepatitis virus causes liver damage, not virus intself Virus is cytopathic, but not cytolytic Blistering effects in damaged liver Hepatocellular carcinoma = cancer

Acute form causes jaundice = hyperbilirubinemia

Chronic: cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hepatitis pathogenesis

A
  • Cytopathic Not cytolytic
  • Most disease is immune-mediated
  • Age-related outcomes
  • Exposure early in life - less severe acute disease, higher rates of chronic infection (hep not cleared)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Many hepatitis viruses

A

All belong to different families

No cross protection HBV and HCV cause chronic infection

A: infectious hepatitis

B: serum hepatitis

C: non A, non B

D: viroid, not virus, dependant on HBV

E: enteric non-A, non-B

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Type of viral hepatitis

A

A and E - enteric, acute B, C, D - blood/body fluids, chronic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Prevention

A

A: pre-post exposure immunization E: ensure safe drinking water, hygiene

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Diagnosis acute hepatitis

A

Past vs. chronic vs. acute infection

Acute easier to distinguish

ELISA tests: IgM antibody (all antibodies start as IgM) - acute, sensitivity >90%, Specificity >99% I

gG antibody to viral proteins: rising titre confirms acute infection

Nucleic acid tests: PCR from blood/faeces, inferior to ELISA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hep A distribution

A
  • Prominent in developing countries
  • Northern territory - indigenous communities
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hep A

A
  • Picornaviridae - related to polio, rhino
  • non-enveloped (+) ssRNA
  • resistant to stomach acid
  • Codes a single polyprotein
  • Single serotype worldwide - 1 vaccine will protect
  • Infects man, many higher primates
  • Replicates in cell culture
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Life cycle of Hep A and E

A
  • 2 points of replication (not seen in B and C)
  • Ingestion from contaminated water and food –> REPLICATION 1 in intestinal epithelia –> blood –> REPLICATION 2 in liver –> bile/faeces
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hep A clinical features

A
  • IP: average 30 days (15-50 days)
  • Symptoms: More acute infections with increase in age
  • Symptoms: jaundice, vomiting, pale faeces, dark urine
  • Complications: fulminant hepatitis, cholestatic hepatitis (prevention of release of bile)
  • No chronic seen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

ALT liver enzyme peak

A

See symptoms and IgM reduction, IgG increase, increase Total anti HAV Also see HAV in faeces

Secreted into faeces before any symptoms seen

When immune response begins –> see antibodies

Damage to liver measured by ALT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hep A pathogenesis

A

Ingested orally —> reaches liver after replication in intestine Replicates in cytoplasm Secreted in bile and excreted in faeces Symptoms: 2-3 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

HAV prevention and treatment

A

Sanitation Travellers to endemic countries get vaccination Post exposure - intimate contacts Treatment: rehydration and nutrition Inactivated vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Hep A vaccine

A

Grown in cell culture Inactivate whole virus with formulin Alum adjuvant 2-3 doses - need boosters HIghly effective: >95% after 1 dose 100% after 2 doses

Expensive to produce - need diploid cells (limited replication cycles, not tumour cells), testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Hep E

A
  • Hepeviridae, formerly Caliciviridae
  • Non enveloped - more fragile Icosahedral + ssRNA
  • Not as widley distributed
  • Mostly associated with faecally contaminated drinking water
  • Minimal person-person transmission
  • Asia >African countries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Hep E clinical features

A

40 days, 2 - 10 weeks

Case fatality rate: 1-3%, pregnant women: 15-25% ; compared to v.low Hep A fatality rate

Symptoms increased with age –> more immune response

No chronic disease identified Vaccine approved in China. GSK candidate vaccine being stalled (we don’t have one)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ALT HEV

A

At its peak –> symptoms Virus becomes present in stools Increase in igM and IgG antibodies Eventually virus is cleaved

Doesn’t replicate as efficiently as Hep A

Symptoms coincide with increase in antibodies + spike in ALT

20
Q

Transmission risk for HA/EV

A

food/water contamination: +++ Sexual: + Intravenous drug users: +

No perinatal complications

21
Q

Transmission risk HBV, HCV

A

sexual: ++ Intravenous drug: +++ Perinatal without resistance: 30% Perinataal with Rx: 1-2%

22
Q

Prevent of B, C, D

A

B: pre/post exposure immunization C: blood donor screening, risk behaviour modification (sexual partners, sharing needles) D: pre/post exposure immunization: risk behaviour modification, co infect with hep B

23
Q

Hepatitis prevalence

A

Hep C >B> HIV 16x more hepatitis than HIV in Aus

Large proportion are injecting drug users: 50% IDUs = HCV+

24
Q

Hep B virus

A

Hepadna family double walled structure with outer envelope and inner capsid Makes decoy molecules that form only envelope proteins - long filamentous structures, just has HbsAg particles

25
Q

Heb B genome

A
  • 2 direct repeats (12 bp) Short AT nucleotide - binding site to recruit viral DNA polymerase
  • RNA primer at 5’ end Not closed covalent circular DNA -one strand left open Has viral DNA polymerase attached
  • Relaxed circle
  • Can make 4 different mRNA - all have same termination site but different start X: integrated form - potentially causing cancer C: core, Pre C: HbeAg important for making replication competent expression, P: polymerase
  • Coding potential:
  • Pregenomic RNA: more than 1 time around, codes for core protein and polymerase and pre core region
26
Q

Hep B replication

A

Non-close covalent genome enters nucleus –> pre genomic RNA –> exported out of cell and recruits vesicle –> reverse transcription 5-10% reverse replication on other side 90-95%: second template exchange, DR stick to each other, –> randomly terminates –> 5’ RNA cap

27
Q

Life cycle of B, C, D

A

Sex, injection –>penetration of mucosal epithelia but DOES NOT REPLICATE –> blood –> replication in liver –> blood, semen, fluids

28
Q

Hep B modes of transmission

A

Sexual - sex workers, homosexuals

Parenteral: health workers, Intravenous drug addicts

Perinatal: mothers who are HbeAg positive (replicating virus) more likley to transmit to offspring (important for replication)

Body fluids:

High - blood, serum, wound exudates

Moderate - semen, vaginal fluid, saliva

Low/not detectable - urine, faeces, sweat, tears, breastmilk

29
Q

Hep B clinical features

A

IP: average 60-90 days, range: 45-180 days

Jaundice: >5 yrs old much more common

Acute case-fatality: 1%

Chronic: <5 years, recognised as self if born with it

Premature mortality from chronic liver disease: 20%

30
Q

HBV infection

A

Acute infection (resolution) –> chronic carrier –> chronic hepatitis (stabilisation) –> progression –> cirrhosis (compensated chirrhosis)–>decompensated cirrhosis (death) –> liver cancer –> death 30-50 years

31
Q

Recovery of Acute hep B

A

Increase in HBsAg HBeAg present - required for replcation Peak of symptoms when immune response developing - IgM HBc = core, HBs = surface proteins Anti-HBe produced which stops HBeAg –> virus cleared

32
Q

Chronic Hep B

A

HBsag, total anti-HBc increase and remain stable IgM eventually decreases Chronic carrier: HBsag+ Most common cause of liver cancer 30% chronic infection - eventually die from it

33
Q

Liver disease progression

A

NOrmal liver –> acute/chronic hep B –> cirrhosis –> end state liver disease –>hepatocellular carcinoma Pre and post prevention: vaccine Chemoprevention: treat acute/chronic with cytokines IFN-a and Peg IFN, a + antivirals Cancer screening: tumour marker, ultrasound, transplantation

34
Q

Hep carcinoma

A

HCC is 100 x more likely in HBV carriers Repeated hepatocyte destruction and regeneration –> chromosomal mutations –> cancer Possible role for HBV X-gene

Partially integrated into hepatocytes

35
Q

Heb B diagnosis

A

HBsAg: general marker of infection Anti-HBs Ig: recovery/immunity to HBV anti-HBc IgM: acute infection anti-HBc IgG: chronic infection HBeAg: active replication of virus, effectiveness of therapy (record at start and end of therapy) Anti-Hbe Ig: virus not replicating , sign that patient has cleared virus but can still be positive for hBsAg HBV-DNA: active replication of virus, more accurate than HBeAg because of escape mutants - monitor response to therapy

36
Q

Hep B vaccine

A

Originally subviral particles, purified from blood, inactivated 3 times Now grown in yeast - alum adjuvant, 2-3 doses Protects against HDV post - exposure vaccination possible

37
Q

Hep D virus

A

deltavirus Viroid element ssRNA - 70% self complementarity, binds to itself

38
Q

Hep D clinical features

A

Coinfects with HBV - severe acute disease, low risk of chronic infection (if both start at same time) Superinfecion: Start with HBV, introduce HDV later –> usually develop chronic HDV infection and severe chronic liver disease

39
Q

Hep C

A

Flavivirus family: ss + RNA

70% have lifelong chronic infection,

30% clear virus 80% of infections through IDU

No vaccine, no small animal model

Poor immunity - carriers can be superinfected

High mutation rate

Infection in cell culture is very difficult Viral enzyme functions - protease

40
Q

Hep c virus

A
  • Has capsid Encodes polyprotein that is cleaved
  • Virus encodes own resistance to innate response - IFN Viroporin
  • RDRP highly error prone –> mutations
  • Envelope proteins E1 and E2 form heterodimer
  • Cholesterol included in viral particle - difficult to distinguish by electorn microscopy
  • Structural: nucleocapsid, E1 and E2 envelope glycoproteins
  • Nonstructural: viroporin, transmembrane protein, RNA helicase - cleaves polyprotein, cofactors - replication, IFN-resistance proteins, RdRNAP
41
Q

Hep C clinical features

A

IP: 6-7 weeks Chronic: 70% 70-90%: chronic carriers Immunity: no protective antibody response Leading cause of liver transplantation

42
Q

Hepadnavirus replication

A

+dsDNA –> + RNA –> -DNA –> dsDNA

43
Q

Hepadnavirus genome

A

Very small genome - used with great economy Replicate using reverse transcription

44
Q

Hepadna DNA

A

Genome made of 2 strands of DNA 1 strand is incomplete Short sequence is triple-stranded because of complementary sequence at 5’ ends

45
Q

Hep B - polymerase protein domains

A

Domains: terminal domain Spacer Reverse transcriptase Rnase H Also has DNA-dependent DNA polymerase

46
Q

Transmission risk for hepatitis

A
47
Q
A

Virology (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions