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BDS2 - BAMS > hepatitis virus > Flashcards

hepatitis virus Flashcards

1
Q

what are the most common hepatitis viruses

A
  • hep b
  • hep a
  • hep c
  • hep d (delta agent)
  • hep e
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2
Q

what is the biology of the hep a virus

A
  • spherical non enveloped virus of 27nm
  • single stranded RNA genome
  • exceptional stability
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3
Q

what is the basic form of a virus

A
  • protein coat with either DNA or RNA

- can only grow in cells, not in an agar plate

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4
Q

what is the transmission and epidemiology of hep A

A
  • mainly transmitted through focal-oral route (can also be blood borne)
  • person-person, food borne and water borne
  • commonly follows food poisoning from sea food
  • in developed countries, 20-50% of adult’s have antibody
  • in developing countries >90% have antibody
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5
Q

what are the clinical features of hep A

A
  • incubation period is 2-7 weeks
  • many subclinical infection s
  • illness usually brief and self limiting
  • mortality <0.2% = very rarely die from it
  • no chronic disease
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6
Q

what is the diagnosis of hep A

A
  • demonstration og HAV antigen in faeces

- serology - detection of IgM and anti-HAV

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7
Q

what is serology

A

take blood from individual and look for antibodies

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8
Q

what is the immunisation of hep A

A
  • passive or active
  • passive = give preformed antibodies (short term)
  • active = give antigen and body makes antibodies
  • human normal immunoglobulin = short term protection (4 months) - passive
  • vaccine = formaldehyde inactivated, prepared from the GBM of HM 175 strain of HAV, single dose will give antibody for a year, then booster does at 6-12 month gives 10 years immunity, active
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9
Q

is hep a preventable

A

yes - it is an eminently preventable disease

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10
Q

how many people are affected with hep b worldwide

A

350 million globally

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11
Q

what age is hep b most prominent

A

70% of new cases are in 15-39 y/o

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12
Q

how much more infectious is hep b than HIV

A

more than 100x more infectious

- only take a tiny amount go blood from an infected individual to cause you infection

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13
Q

is there a curative treatment

A

no, but new antivirals suppress the viral load

- been big strides in recent years in suppressing the viral load

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14
Q

what is the viral load

A
  • nor of virus particles in 1 ml of blood

- lower load = better

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15
Q

what genome does hep b have

A
  • DNA virus

- partially double stranded DNA virus

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16
Q

what family of viruses does hep b come from

A
  • hepadnavirus
  • family of DNA viruses with a unique life cycle involving an RNA intermediate ad use of a viral polymerase with reverse transcriptase activity
  • cause liver damage
  • hep B is best known virus from family
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17
Q

what is the intact part of the hep b virus

A
  • dane particle

- viral code and genome in the centre

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18
Q

how many subtypes of hep b exist

A

8

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19
Q

what is the structure of hep b

A
  • has hep b surface antigen (HBs Ag)
  • has dna polymerase
  • has dna in centre
  • has hep b core antigen
  • has protein kinase
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20
Q

what forms the protein coat of the hep b virus

A

hep b surface antigen

- forms excessive amounts of this

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21
Q

what is the concept of the vaccine

A
  • produce antibodies against the coating to protect you
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22
Q

where is the highest prevalence of hep b

A

Africa mainly and Asia

- have >8% people have it here

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23
Q

where has an intermediate prevalence of hep b

A

russia, india, top of Africa

- 2-7% of population

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24
Q

where has low prevalence of hep b

A

uk, america, australia, netherlands

- <2% of population

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25
Q

in 2018 what were the lab reports of hep b in England

A
  • 381 acute or probable cases
  • incidence = 0.68/100,000
  • highest incidence was in London = 64.7%
  • many people do not know they have it or that they carry the virus
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26
Q

how is hep b transmitted

A
  • 3 main routes

- blood borne, sexual or perinatal

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27
Q

what are examples of people wit higher risk of hep b

A
  • iv drug users
  • sexually active people
  • children of immigrants from disease-endemic areas
  • infants born to infected mothers (perinatal)
  • healthcare workers
  • haemo-dialysis patients
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28
Q

what is perinatal spread of hep b

A
  • mother can transmit to infant
  • important in pairs of the world where hep b is endemic
  • if you are infected as a child you are more likely to be a carrier = have it for many years and will infect others
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29
Q

what is the epidemiology of hep b in non-endemic areas (UK)

A
  • 80% inapparent disease, 20% acute hepatitis
  • 95% recovery, 5% chronicity (most are adults)
  • can lead to cirrhosis and liver cancer
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30
Q

what is the epidemiology of hep b in endemic areas (Asia)

A
  • mostly inapparent disease
  • 5-20% recovers, 80-95% chronicity (most are infants)
  • can lead to cirrhosis and liver cancer
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31
Q

what is the risk of chronic hep b by the age of acquisition and immune status

A
  • neonates = 90-100%, very high risk of becoming a carrier
  • children = 20-40%
  • immunosuppressed = 21%, high risk of becoming a carrier
  • adults = <5%
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32
Q

what are possibly outcomes of exposure to hep b

A
  • infection (65% subclinical)
  • this can the lead to :
  • death from fulminant hepatitis (1%)
  • persistent infection HBs Ag for >6 months (5-9%)
  • recovery with immunity (90-95%)
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33
Q

what happens if you are given the antigen of hep b and don’t develop antibodies in first 6 months

A
  • you are likely to be a carrier = chronic
34
Q

if someone is making a normal recovery from hep b what antibodies will they have

A
  • IgG anti HBc
  • IgM anti HBc
  • Anti HBe
  • Anti HBs
  • amount of antigens of these will decrease and eventually there will be none (within 2-3 months)
35
Q

what antibodies show you are making recovery from hep b

A

HBe and HBs

36
Q

what happens if you are a chronic carrier of hep b

A
  • will only form antibodies IgG anti HBc and IgM anti HBc

- no anti HBe or anti HBs ( so antigens HBe and HBs do not disappear an are still present month or years later

37
Q

what people are risks to others in hep b

A

chronic carriers

38
Q

what is passive immunisation of hep b

A
  • hep b immunoglobin (give if person not responding to vaccine)
  • from pooled plasma
  • main use is single acute exposure in non-immune individual
  • administer within 48hrs of infection
  • highly immunogenic
39
Q

what is the HBV vaccine

A
  • highly immunogenic
  • no booster dose is required for persons who have responded to HBV vaccine (if responded once and have antibody, you will be protected even if antibody amount decreases)
40
Q

what did the WHO recommend in 1992 which helped hep b

A
  • they suggested that the HBV vaccine become integrated into national immunisation programmes of all highly endemic countries
  • was done in Taiwan and it had a good response
  • in theory if this vaccine was universally given, hep b could be eradicated
41
Q

what is the active immunisation of hep b

A
  • vaccine = hep b surface antigen absorbed on aluminium hydroxide adjuvant
  • produced by recombinant DNA technology
  • protection = good
  • response = not always good, need to check antibody levels
  • vaccine administration =intramuscular
  • 3 doses required = time zero, one month and six months
  • post immunisation = test for antibody response 2-4 months after vaccine course completed
42
Q

what is the average volume of blood inoculated in needle stick injury and how many virus particles could that contain of hep b

A
  • with a 22 gauge needle, 1microlitre of blood is inoculated
  • this can contain 100 infectious doses of HBV
  • a non-responder to the vaccine had a 1 in 3 chance of becoming infectious from this injury
43
Q

what is the risk of hep b post exposure prophylaxis

A
  • in vaccine responders there is no risk
  • in vaccine non-responders = in the occupational setting, hep b immune globin provides estimated 70-75% protection from HBV infection
44
Q

how can you treat chronic HBV infection

A
  • goal of therapy = sustained viral suppression
  • agents available = immunomodulatory agents (inferon alpha and pegylated interferon
    = nucleoside analogues - telbivudine, entecavir
    = nucleotide analogues - adenovirus and tenofovir, suppers viral load to level at which they’re not deemed to be a risk
45
Q

when was hep c discovered

A

in 1989 and was originally called non-a non-b hepatitis

46
Q

what type of virus is hep c

A
  • flavivirus family = related to these

- blood borne

47
Q

how many genotypes does hep c have

A

6

- not just one virus, 6 genotypes behave differently

48
Q

how many people worldwide are infected with hep c

A

200 million

- fro every 1 person with HIV, 4 have hep c

49
Q

is a vaccine available for hep c

A

no

  • can be seen as a bigger is than hep b
  • treatments have improved but are expensive
50
Q

what genome is hep c

A

RNA virus

51
Q

how big is the hep c virus

A

30-38nm

- morphology unknown

52
Q

can hep c be grown in culture

A

no, needs serology to diagnose

53
Q

what is the global prevalence of hep c

A
  • high in Asia, top of Africa = >3.5%
  • moderate in UK, Europe, most of Africa = 1.5-3.5%
  • low in USA, Canada = <1.5%
54
Q

how is the prevalence of chronic infection of hep c changing

A
  • decreasing steadily

- 143,000 in 2015 in England, 113,000 in 2018

55
Q

what is the main risk factor for hep c in developed countries

A

intravenous drug use

- significant number of people with hep c don’t know they have it

56
Q

when is someone no longer infectious with hep c

A

once they have been treated, doesn’t cure them but means they are no longer infectious to others

57
Q

how is hep c diagnosed

A
  • serologically
  • anti-HCv test = detects presence of antibodies, indicates exposure to HCV
  • HCV-RNA test = identifies presence of virus in blood, indicates active infection, main test
  • viral load/quantitative HCV test = measures number of viral particles in peripheral blood
  • viral genotyping = additional test, determines type of HCV present, treatments needs to be focused around type
58
Q

what is the clinical course of hep c

A
  • incubation = average incubation is 6-12 weeks, average seroconversion period =15 weeks
  • acute infection = clinically mild (sub-clinical, high amount of chronic carriers), jaundice in 25% of patients
  • chronic hep c = high frequency (60% of the infected), most cases preceded by clinically apparent infection, slowly progressive over 20 years
59
Q

what is seroconversion

A

time a specific antibody develops and become detectable in the blood

60
Q

what is the long term risks of hep c

A

like hep b, long term risks could be liver cancer and cirrhosis
- link with hepatocellular carcinoma

61
Q

what is the natural history of hep c

A
  • exposure (acute phase) = 25% become resolved
  • 75% non resolved become chronic = 80% of those stay stable
  • other 20% who didn’t stay stable develop cirrhosis = 75% of those become slowly progressive
  • other 25% the have liver failure, transplant and death
62
Q

what can help hep c disease get worse

A

HIV and alcohol

63
Q

how long does it take from exposure of hep c to liver failure

A
  • could take up to 25 years

- is often called the silent disease

64
Q

what is the treatment of hep c

A
  • interferon alpha in combination with ribavarin
  • plus boceprevir or telaprevir (HCV protease inhibitors)for genotype 1
  • self injected
65
Q

what were the problems with interferon alpha alone as a treatment of hep c

A
  • caused depression in patients
66
Q

what has improved by adding rubivarin and protease inhibitors to the interferon in hep c treatment

A
  • depression in patients was massively reduced
67
Q

what do protease inhibitors do in hep c treatment

A

stop proteases breaking up protein chains to make viral chains so new chains couldn’t be made

68
Q

what are second generation protease inhibitors used in hep c treatment

A
  • sofosbuvir

- ledipasvir

69
Q

how many people are cured from hep c

A
  • 98%
  • these newer drugs begin formed for treatment means the long term risk fo hep c aren’t a risk anymore
  • also means health workers infected can go back to work
70
Q

what is another name for hep d

A

delta agent

71
Q

what type of genome does hep d have

A

rna virus

72
Q

when can hep d replicate

A

only with hep b present

73
Q

why can hep d only replicate when hep b is present

A
  • as delta agent relies on hep b producing the protein coat as it can’t do it itself = the coat allows it to attach to liver cells
74
Q

how is hep d transmitted

A
  • blood borne virus
  • parental and sexual routes
  • co-infection or supra-infection with hep b
75
Q

what is supra infection

A

when you already have hep b and then hep d then cause infection
- has a low chance of recovery compared to co-infection which has a high recovery

76
Q

how do you treat hep d

A

if have hep b vaccine then cant get hep d

77
Q

what are the risks of hep d

A

same risks as in hep b

78
Q

what is hep e like

A

largely mimics hep a

- transmitted focal-orally

79
Q

what is the biology of hep e

A
  • spherical non-enveloped virus (32-34nm)
  • single stranded RNA genome
  • calcivirus like
  • can’t grow in tissue culture
80
Q

what is the transmission and epidemiology of hep e

A
  • epidemic and sporadic forms

- mainly in India, Africa, Asia (not really in UK)

81
Q

what are the clinical features of hep e

A
  • incubation period is 2-9 weeks
  • mainly young adults affected (15-40)
  • usually self-limiting acute disease
  • high mortality in pregnancy (205) due to lower immunosuppression
  • no chronic disease

BDS2 - BAMS (18 decks)

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