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Semester 1 > HIV > Flashcards

HIV Flashcards

1
Q

Origins of HIV

When was it rife

A

evolved from SIV, simian immunodeficiency virus, from apes in Africa, jumped to humans around 1920

1980s massive global spread (air traffic accessible to all)

peak epidemic 2004

to date over 40 million deaths

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2
Q

HIV is what type of virus and what is that/ how work briefly

A

HIV is a retrovirus, has RNA genome

uses reverse transcriptase to convert viral RNA to DNA

viral DNA is integrated into host cell’s DNA, allowing retrovirus to replicate

may endogenous or exogenous

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3
Q

endogenous vs exogenous retrovirus

A

endogenous:

  • stably integrated into human genome, forms normal genetic elements
  • transmit vertically like a mendelian gene

exogenous
- transmit horizontally, human to human

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4
Q

structure of HIV

A

external lipid bilayer and glycoprotein envelope
internal protein core

Gp120
Gp41

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5
Q

what is Gp120 on HIV

A

Gp120 has docking glycoprotein function

for binding to host cell receptors

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6
Q

what is Gp41 on HIV

A

Gp41 has transmembrane protein function

mediates fusion process

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7
Q

Gp120 binds to what type of receptors

A

Gp120 binds to CD4 receptors

mostly on lymphocytes, also on monocytes, macrophages, any cell with CD4 receptors

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8
Q

how does HIV infect target cell? brief

A
  • Gp120 binds to CD4 receptors
  • Gp41 virus-cell fusion
  • virus loses membrane within cell, viral genome free in cell
  • reverse transcriptase into single stranded proviral DNA, then double stranded
  • HIV integrase integrates proviral DNA into host DNA, programmes to make copies of virus (replication
  • viral assembly, facilitates by HIV protease
  • released from cell via budding
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9
Q

how does HIV infect target cell? more detail

A

Gp120 binds to CD4 receptor on host cell
(ie T helper cell)

Gp41 enables virus-cell fusion

virus loses its membrane once within cell (capsid and matrix digested), genetic material now free in cytoplasm

reverse transcriptase transcribes 1 SS viral RNA to SS proviral DNA, reverse transciptase turns to double stranded proviral DNA

HIV integrase integrates proviral DNA into host DNA

host cell programmed to make copies of viral genome, replication

viral assembly- viral genome packaged into mature virion with a membrane, facilitated by HIV protease

once mature released from cell via budding into blood to infect other

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10
Q

name enzymes involved in HIV infecting target cells, what do they do

A

reverse transcriptase- transcribes viral RNA into proviral DNA and single to double stranded

HIV integrase- integrates proviral DNA into host DNA

HIV protease- facilitates viral assembly

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11
Q

what happens to the cell once virus has infected, been replicated and left cell

A 
host cell death, usually by apoptosis
or CD8+ may recognise virus being expressed alongside MHC class 2 and kill the T helper cell, destroying immune function
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12
Q

what cell population does HIV infection affect most, what do we see in this population after infection

A

HIV causes progressive decline in CD4+ T helper cells

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13
Q

what is normal range for CD4+ count?

at what point see signs immunosuppression
at what point serious opportunistic infctions
at what point severe immunosuppression

what unit is this

A

normal range CD4+ count >500-1500

<350 signs of immunosuppression
<200 serious opportunistic infections
<50 severe immunosuppression

cells per mm3

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14
Q

timeline of HIV infection

HIV copies vs CD4+ copies

A

when first infected (first 12 weeks or so):
CD4 plummets, recovers as body makes more
viral load rises lots and rapidly, highly infectious

clinical latency period:
CD4 count slowly decreases, see progressive decline
viral load stable, slowly rises towards end as CD4 reduces

immunological exhaustion:
CD4+ cells ran into ground, HIV copies rocket
see opportunistic diseases, eventually death

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15
Q

when are the most infectious periods/ when most likely transmitwhen someone has HIV

A

when first infected when CD4 plummets and HIV rockets. Person has no/ few symptoms so likely time of transmission

immunological exhaustion very infectious but very weak so unlikely to transmit

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16
Q

how long does it take to get from HIV to AIDS if no treatment

A

could be 3-5 years, could be 20 years

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17
Q

in HIV, what does risk of opportunistic infection depend on

A

CD4 count

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18
Q

what are the most common opportunistic infections in HIV

A 
herpes
salmonella
cerebral toxoplasmosis (protozoal infection, presents like a stroke)
candidiasis
varicella zoster
kapose sarcoma
19
Q

what is the leading cause of HIV+ death worldwide

A

TB

20
Q

How is HIV contracted

A

sexual transmission (unprotected sex)

  • facilitates by co-existing STDs
  • risk incr by number partners
  • most common method transmission

contact with infected blood/ bodily fluids
- dirty needles, bad blood transfusion

mother to baby

  • birth and breastmilk
  • can give baby short course ART before birth to prevent transmission, use formula
21
Q

HIV prevelance worldwide

A

70% of world HIV+ population sub saharan africa

low in EU, USA

22
Q

do some people have natural immunity to HIV

A

yes, most prevelant in EU population as mutation arose during black plague

mutation in CCR5 gene, a co-receptor for HIV

if both alleles have mutation, cannot be infected with HIV
if 1 mutated allele have delayed disease progression

23
Q

HIV UK epidemiology, risk groups

A

highest risk groups:
MSM
black african
IV drug users

40% are late diagnosed

20 LAs with >5/1000 people HIV=

  • highest HIV prevelance London, 18/20
  • Manchester
  • Brighton
24
Q

when to offer HIV test

A

if have risk factors:

  • have a blood borne virus eg hep b and c
  • has an opportunistic infection

if an emergency admission in a high prevelance area

exposed

25
Q

what do HIV blood tests look for

A

HIV antibody presence indicated infection

4th gen tests test for HIV antibody and p24 antigen, shorter window period

3rd gen tests just HIV antibody

26
Q

why window period HIV

A

takes time to make antibodies, up to 3 months, so may be too soon to detect

at 4 weeks 95% will have antibodies
at 3 months 99.9% have antibodies

27
Q

how long after exposure is HIV testing offered

A

test at 4-6 weeks with 4th gen, repeat at 12 weeks

28
Q

if test positive for HIV, what else is tested

A

HIV viral load count
CD4+ count
HIV drug resistance test

29
Q

is there a chance of transmitted resistance to HIV drugs

A

yes, 10-20% chance

30
Q

an opportunistic infection?

A

only affects those with impaired immune system. Healthy people wouldn’t be affected

31
Q

pneumocystis pneumonia is?

A

an opportunistic fungal infection
seen in HIV pts off ARTs, w CD4 under 200/ml

symptoms:
increasing SOB, hypozaemia, fever, dry cough

progresses over time, can die from resp failure

inflamm, damage, failure due to inflamed cells and inflamm debris

give oral steroid course

32
Q

How do ARTs work

A

antiretroviral drugs. suppress HIV replication, preventing CD4+ cell death and immunological exhaustion, allows for immune reconstitution

drugs that block every step of retrovirus lifecycle

  • fusion/entry inhibitors
  • reverse transcriptase inhibitors
  • integrase inhibitors
  • protease inhibitors

give AT LEAST 3 drugs in combi

33
Q

why is it important to give at least 3 types of ART in combi

A

to prevent replication

if only 1/2 types of ART virus mutates and drugs become ineffective, viral resistance

34
Q

nb mixing other meds with ART

A

ART can inhibit/ induce an enzyme in liver (cytochrome P450)

this leads to toxic or sub-therapeutic levels of co-administered meds, must always check drug interactions so not to reduce their efficacy

eg statins, oral contraceptives, older anti epileptics

35
Q

after 6 months ART onwards

A

irrespective of CD4 count, :
not at risk for HIV assoc opportunistic infections
CANNOT TRANSMIT to sex partner
as long as not diagnosed late have same life expectancy as HIV-

U=U
undetectable= untransmissable

36
Q

HIV disclosure to partner etc against consent

A

no legal obligation, but GMC allows and ethically should

if cannot convince HIV+ to disclose and are NOT undetectable on ART, not taking ART, unsafe sex, the partner is at high risk of serious communicable disease. then disclose

37
Q

procedure for disclosing HIV status to partner without consent

A

encourage PLHIV, allow time
make them aware of the law on this area
tell them you will inform

38
Q

what is the law on reckless transmission of HIV

A

reckless transmission= knowingly infecting another is a criminal offence

in England and Wales, transmission must occur

in Scotland, only risk of transmission needed

could end up being GBH

39
Q

discrimination and stigma HIV today

A

2010 equality act protects HIV+

1 in 3 PLHIV fear being rejected by partner
1 in 5 have been

1 in 5 have been excluded from family events

only 45% of public can correctly identify how it is transmitted

for gay men, fear and shame seeps over from past

40
Q

prevention measures HIV

A

safe sex- condom and lube
PrEP
PEP

41
Q

how do LGBT foundation help w condoms

A

free postal delivery condoms and lube
distributed to barbers, clubs etc in gay village

also do loads to support and inform

42
Q

PrEP

A

used by HIV- at risk of HIV+ to prevent getting
86% effective
can be bought online, recently made NHS
dosage depends on method of sex
need full -ve screen first and full STD screenings regularly

43
Q

PEP

A

post exposure prophylaxis
must be started within 72 hours
28 day course
available GUM and A+E

44
Q

what is HIV wasting syndrome

A

seen in late HIV
over 10% unintentional weight loss
malabsorptionm weakness, deficiencies, diarrhoea, fever
exacerbates illness, incr risk death

Semester 1 (18 decks)

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