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ICS/GP/ILA > HIV Symposium > Flashcards

HIV Symposium Flashcards

1
Q

How many new HIV infections per day?

A

4000

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2
Q

How many living with HIV in 2021?

A

~38.4 million

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3
Q

Which age group do 50% of all new infections occur in?

A

15-24 year olds

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4
Q

What is the UNAIDS 90/90/90 global target? and which country achieved this in 2018?

A
  1. 90% people with HIV diagnosed
  2. 90% diagnosed on ART
  3. 90% viral suppression for those on ART

UK

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5
Q

What are fast-track cities?

A

Global partnership between network of HIV burdened cities - affected communities and officals work together to accelerate local HIV responses.

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6
Q

What routes can HIV be transmitted by?

A

Blood
Sexual
Verticle (parent-child)

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7
Q

What constitutes as high risk behaviours/groups for HIV?

A
  • sexual contact with people from high prevalence groups (eg. MSM, Sub-Saharan Africa)
  • multiple sexual partners
  • rape
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8
Q

What are the main symptoms of HIV? (6)

A
  1. acute generalised rash
  2. dry cough/SOB/glandular fever
  3. indicators of immune dysfunction
  4. unexplained weight loss
  5. night sweats
  6. recurrent bacterial infections
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9
Q

What are the prevention methods for HIV?

A
  • male circumcision
  • treatment of STIs
  • microbicides and condoms
  • pre-exposire prohylaxis (PrEP)
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10
Q

Why does male circumcision help prevent HIV?

A

reduces HIV’s ability to penetrate due to keratinisation

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11
Q

When is HIV not transmittable?

A

When it is undetectable - if ART and undetectable viral load

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12
Q

What is PrEP?

A

drugs taken before sex either daily or on demand to prevent HIV transmission

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13
Q

What are the benefits of knowing HIV status?

A
  • access appropriate treatment
  • reduction in morbidity and mortality
  • reduction in transmission
  • beneficial to public health and cost effective
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14
Q

How does early diagnosis of HIV help with costs?

A

saves on social care, lost working days, benefits claimed, further onward transmission costs

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15
Q

What groups of people should be screened for HIV?

A
  • high risk
  • antenatal
  • patient-initiated request
  • diagnostic
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16
Q

What type of virus is HIV?

A

Small RNA Lentivirus - member of retrovirus family

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17
Q

What is a lentivirus?

A

characterised by long incubation period

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18
Q

What is a retrovirus?

A

uses reverse transcriptase to make DNA copies of itself

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19
Q

Why is HIV hard to recognise?

A

Not many spike projections and heavily glycosylated so makes it difficult for antibodies to bind

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20
Q

Why does HIV mutate and evolve rapidly?

A

error-prone replication and large population sizes

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21
Q

What is the mechanism of a virus infecting a cell?

A
  1. attachment - of virus to receptors/glycoproteins
  2. cell entry - ONLY viral core with nucleic acids and some proteins enters host cell
  3. interaction with host cell - uses host materials to replicate and subvert host cell defence mechanisms
  4. replication - in nucleus and/or cytoplasm
  5. assembly - in nucelus/cytoplasm/cell membrane
  6. release - burst open OR exocytosis over a period of time
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22
Q

How does HIV replicate? (long process)

A

attachment and entry –> uncoating –> reverse transcriptase RNA to DNA –> genome integration of viral DNA using integrase –> transcription of viral RNA –> mRNA spliced and translated into proteins –> new virions assemble –> budding of immature virus –> maturation protein cut by protease into individual proteins that combine into working virus

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23
Q

What is the main type of T cell that HIV infects?

A

CD4+

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24
Q

What is gp120?

A

envelope glycoprotein

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25
Q

What is the result of CD4 and gp120 binding?

A

produces conformational change in gp120

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26
Q

What makes up the structure of the CD4-gp120 co-binding site?

A

conserved bridging sheet and amino acids in V3 loop

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27
Q

How does HIV gradually damage immune system?

A

Depletes CD4 T cells

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28
Q

Why is HIV a lifelong disease?

A

Once viral integration has occured, infection persists in reservoir of latently infected cells

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29
Q

HIV symptoms at CD4 count of 200-500?

A
  • vaginal/oral candidasis
  • skin disease
  • fatigue
  • bacterial pneumonia
  • herpes zoster
  • fever/diarrhoea/weight loss
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30
Q

HIV symptoms at CD4 count of 50-200?

A
  • kaposi’s sarcoma, non-hodgkins lymphoma
  • pneumocystis carinii pneumonia
  • toxoplasmosis, oesophageal candidiasis, cryptococcosis
  • CNS lymphoma
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31
Q

HIV symtpoms at <50 CD4 count?

A

CMV and mycobacterium avium complex

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32
Q

What does Pol gene encode?

A

reverse transcriptase, protease, integrase

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33
Q

What does Env gene encode?

A

envelope proteins, eg. gp120

34
Q

What does Nef gene increase?

A

infectivity

35
Q

What does Tat gene contribute to?

A

viral replication, production of host transcription factors

36
Q

What does Gag gene encode?

A

structural proteins, polyproteins

37
Q

What does Rev gene bind to and allow?

A

binds to viral RNA and allows exit from nucleus. also regulates splicing

38
Q

What is the consequence of HIV being able to pass directly from cell-to-cell?

A

inaccessible to antibodies in blood

39
Q

When and where is the loss of CD4 cells the biggest in HIV infection?

A

Early acute HIV in lymphoid tissue in the gut

40
Q

What is the consequence of loss of CD4 cells in the gut?

A

Makes gut mucosa leaky, so bacteria can pass through and stimulate immune cells. Leads to chronic immune activation that exhausts immune system

41
Q

What other factors contribute to immune activation?

A

directly through inflammatory cell death and co-infections

42
Q

Why can’t the HIV strains be neutralised quickly enough?

A

key responses (CD4 T cell) are infected by HIV first

43
Q

What do CD8 cells use to control viral replication?

A

HLA class 1 molecules

44
Q

What is the function HLA class 1 molecules?

A

present peptides with different characteristics that can come from any part of the pathogen (can include conserved structural and functinal internal proteins).

45
Q

What does HLA 1 recognition trigger?

A

release of soluble anti-viral factors and the death of the infected cells

46
Q

There are critical parts of the viral envelope which are needed to enter CD4 cells. Where are these located?

A

deep pockets overhung by sugar molecules - only reveald when virus docks onto CD4

47
Q

What can change without affecting virus function?

A

the envelope (gp120) proteins

48
Q

What is the role of cytotoxic T lymphocytes in response to HIV infection?

A

appear early and exert pressure on the virus so variants emerge which can escape recognition and cause rise in viral road

49
Q

What is the differene between HLA A/B and C expression?

A

A/B are down-regulated to undermine CTL killing of infected cells, but C are maintained to prevent NK cell killing

50
Q

Why is life expectancy still reduced in people with HIV despite medication?

A
  • issues of adherence, side effects, and drug resistance
  • increase in non-AIDS defining illness, eg. lung and CVD
  • reservoir of latently infected cells persist even with ART
51
Q

What does life expectancy relate to?

A
  • size of latent HIV reservoir
  • persistent immune activation
  • co-infection
52
Q

Who is most at risk of HIV?

A

MSM, heterozexual women, injecting drug users, commercial sex workers, heterosexual men, truck drivers, migrant workers

53
Q

What requirements would you have to meet to be cured from HIV?

A
  1. absence of viral replication without ART
  2. viral load remains below detection
  3. no CD4 decline
  4. no risk of onward transmission
54
Q

How does male circumcision reduce HIV transmission?

A

reduces ability of HIV to penetrate due to keratinisation. foreskin also contains langerhans cells which are prime targets for HIV and can also have abrasion/inflammation which would facillitate passage of HIV

55
Q

What are the 2025 <10% targets?

A
  1. < 10% of people living with HIV and key populations experiencing stigma and discrimination
  2. < 10% of people living with HIV and women/girls experiencing gender-based inequalities or violence
  3. < 10% of countries having punitive laws and policies
56
Q

What are the 2025 > 95% targets?

A
  1. 95% of people at risk using combination prevention
  2. 95/95/95 HIV testing, treatment, and viral suppression
  3. 95% of women access sexual health services
  4. 95% coverage of services for eliminating verticle transmission
  5. 90% of those with HIV receiving TB prevention treatment
  6. 90% with HIV and those at risk linked to other integrated health services
57
Q

What global factor has big impact on containment and spread of HIV?

A

poverty and socio-political factors

58
Q

Why can HIV affect both high risk groups and general population?

A

epidemic at different stages in different regions

59
Q

Why are people with HIV 30-50% more likely to die from covid?

A

covid vaccine doesn’t reach countries with highest HIV prevalence

60
Q

WHat percentage of people in sub-Saharan Africa do not know HIV status?

A

~20%

61
Q

What are consequences of high HIV prevalence in sub-Saharan Africa?

A

significant impact on life expectancy and distortion of healthcare spending

62
Q

What are the 3 routes of transmission in paediatric HIV infection?

A
  1. in utero - transplacental
  2. intra partum - exposure to maternal blood/secretions in delivery
  3. breast milk - ingestion of contaminated milk
63
Q

Why is untreated HIV infection particularly aggressive in African infants?

A
  1. abundance of HIV target cells
  2. immaturity of immune system
  3. genetic similarity to virus donor
  4. high incidence of co-infections
64
Q

What kinds of comorbidities can children with delayed diagnosis of perinatal HIV experience?

A

heart muscle abnormalities, chronic lung disease, growth failure, osteoporosis

65
Q

Which two markers are used to monitor HIV infection?

A
  1. CD4 cell count
  2. HIV viral load
66
Q

A patient comes in with fever, rash, and other non-specfic symptoms. What should you ask about?

A

sexual history and HIV seroconversion

67
Q

What 3 signs should you test for HIV for?

A
  1. unexpected patient with common problem
  2. no clear underlying cause
  3. recurrent infections
68
Q

What type of rash is HIV?

A

symmetrical maculopapular rash that can involve the whole body

69
Q

What is a differential diagnosis for HIV rash?

A

syphilis

70
Q

When do symptoms usually begin in acute HIV?

A

2-4 weeks then undergo period of clincal latency which is usually asymptomatic.

71
Q

What are the main non-specific symptoms of HIV?

A
  • mouth ulcers and sore throat
  • fever and headache
  • lymphadenopathy
  • myalgia
  • vomiting/diarrhoea
  • weight loss
72
Q

What infections should prompt a HIV test?

A

shingles, thrush, oral leucoplakia (caused by EBV), molluscum contagiosum

73
Q

At what CD4 count are you diagnosed with AIDS?

A

CD4 <200

74
Q

What is the most common AIDS defining illness/opportunistic infection?

A

pneumocystis pneumonia (PCP)

75
Q

What are the symptoms of PCP?

A

fever, SOB, dry cough, pleuritic chest pain, drop in o2 sats

76
Q

What is PCP treated with?

A

co-trimoxazole (and prednisolone if hypoxic)

77
Q

What cancers are increased in risk with HIV?

A

Kaposi’s sarcoma, lymphomas, cervical/penile/anal, hepatocellular carcinoma

78
Q

What CNS presentations can occur with HIV?

A
  • TB
  • CNS lymphoma
  • cytomegalobirus retinitis
  • ocular toxoplasmosis
  • cryptococcal meningitis
79
Q

What is there a low threshold for in patients with HIV and a headache?

A

lumbar puncture

80
Q

What is HAART?

A

highly active antiretroviral therapy, usually 3+ drugs that act on different points in viral replication cycle

81
Q

Why is good adherence and avoiding drug interactions key in HIV prognosis?

A
  • suppresses replication
  • avoids drug resistance

ICS/GP/ILA (9 decks)

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