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Flashcards in HCV/HIV Deck (36)
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1
Q

What is the rate of HCV positivity in HIV positive IVDU?

A

83% (7% in HIV-MSM)

2
Q

Why is there an overlap between HIV and HCV?

A

due to transmission routes

3
Q

How many HCV genotypes are there?

A

6

4
Q

What is the most prevalent genotype across the world?

A

genotype 1

5
Q

Where is HCV genotype 6 found?

A

south east asia

6
Q

What is the difference between the genotypes seen in general UK and HIV positive populations?

A

general- G1 and G3; HIV-positive- G1 and G4

7
Q

How many people with acute HCV infection undergo spontaneous clearance?

A

5-20%

8
Q

What are the outcomes 30 years after acute HCV in patients who have chronic HCV?

A

30% no liver disease; 40% liver fibrosis; 30% cirrhosis; HCC

9
Q

What are the major risk factors for disease progression?

A

male; older age at acuisition; alcohol

10
Q

does HIV affect the progression in HCV?

A

there is a suggestion that HIV patients can have very rapid fibrosis in acute infection but resutls are conflicting and imperfect (surrogate measures); is faster even with HAART?; increased reinfection and recurrence

11
Q

what is the rate of lvier-related deaths due to HCV in HIV patients in developed coutnries?

A

10%

12
Q

What is fibroscan?

A

ultrasound that estimates liver stiffness as a surrogate marker of fibrosis

13
Q

What are the differences in acute HCV presentation in HIV patietns?

A

often asymptomatic; antibody development can be very late so molecular testing is needed (v. expensive)

14
Q

What is a problem with fibroscan?

A

can be confounded by inflammation

15
Q

What are the risk factors for HCV acquisition in HIV positive MSM?

A

recreational drug use; higher numbers of sexual partners/ group sex; high risk sexual practices- fisting; bloody sex

16
Q

Why does HCV prevention remain crucial?

A

no sign of effective vaccine in the near future

17
Q

What are the non-viral aspects of managing HCV in HIV positive patietns?

A

co-medication; weight; HAV and HBV vaccinations; alcohol intake; optimise HAART

18
Q

Why can HBV infection not be fully eradicated?

A

persistence of viral cccDNA in host cells

19
Q

Why is cccDNA a problem if not integrated into the cellular genome?

A

has a long half-life and is able to transmit to progeny cells; reservoir for viral reactivation

20
Q

Why can a sustained virologic response be achieved in HCV?

A

has an entirely cytoplasmic life cycle and does not have a known form of persistence or latency in host cells

21
Q

What does cccDNA stand for?

A

covalently closed circular DNA

22
Q

When is HCV deemed to have achieved cure?

A

if 12 weeks after end of treatment there is no virus in the blood

23
Q

What is the effect of SVR on mortality?

A

greatly reduces mortality compared to contorl, especially when coinfected with HIV or when have cirrhosis

24
Q

What are the problems with curing HCV?

A

chance of failure; serious AE of Rx and quality of life during Rx; costs

25
Q

What is the mode of action of pegylated interferon?

A

directly hinders the replication process of the virus; enhances the immune repsonse

26
Q

What is pegylation?

A

a large molecular chain is attached to the integeron to slow the rate at which it is broken down

27
Q

What is the function of ribavirin?

A

synthetic antiviral nucleoside analogue that works with interferon but not on its own and inhibits viral growth

28
Q

What was the problem with all first generation protease inhibitors?

A

activity against genotype 1, some against 2 and 4 but no activity against 3

29
Q

What is sofosbuvir?

A

specific nucleotide analog inhibitor of HCV NS5B

30
Q

what is the benefit of sofosbuvir?

A

potent with broad genotype coverage with or without inteferon; high barriers to resistance

31
Q

What is the current rate of SVR?

A

94-99%

32
Q

What was the drug regimen for SVR in 2015?

A

peg interferon; ribavirin; protease inhibitor

33
Q

What are the 3 classes of directly acting antivirals for HCV?

A

NS5a inhibitors; protease inhibitors and polymerase inhibitors

34
Q

What are the benefits of the newer drugs for HCV?

A

shorter duration; fewer SEs; better efficacy; avoid inteferons

35
Q

How many deaths does viral hepatitis cause globally?

A

7th leading cause of death

36
Q

What type of virus is hep C?

A

RNA flavivirus