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Infectious diseases (Den 303) > HIV and AIDS > Flashcards

HIV and AIDS Flashcards

1
Q

What does HIV stand for?

A

Human Immunodeficiency Virus

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2
Q

What does AIDS stand for?

A

Acquired Immune Deficiency Syndrome

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3
Q

Why type of virus is HIV?

A

Lentivirus (slow)

-HIV and AIDS both retroviruses

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4
Q

HIV transmission

A 
Sexual contact
Blood
-blood contact
-IVDU
Infected blood products
In utero
Breast milk
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5
Q

Major route of HIV infection in developed countries

A

Male - homo/bisexual

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6
Q

Major route of HIV infection in developing countries

A

Male and female - heterosexual

Child - infected via in utero transmission

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7
Q

HIV types

A

HIV 1 - most common

HIV 2 - less easily transmitted and less pathogenic

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8
Q

Main groups of HIV 1

A

Main (M) - pandemic strains
New (N)
Outlier (O) - confined to Cameroon area
Many subtypes

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9
Q

HIV mutates readily

A

Reverse Transcriptase does not proofread

  • ***** diagram
  • infected individuals contain a heterogenous viral population
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10
Q

HIV evolution and origins

A

Likely chimp co-infection with 2 SIV strains
-viral crossover creates new strain
-how did it transfer to humans?
Origin of HIB-1 in Cameroonian Chimps –> Congo in 1920s –> urbanisation –> diamonds –> rail travel –> indipendence 1960s
HIV-2 confined to west Africa

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11
Q

HIV shape (DIAGRAM)

A

Lipid membrane of envelope, envelope glycoproteins, host proteins
Matrix protein
Major structural (core) protein
Single-stranded RNA, p7^gag, p9^gag, reverse transcriptase

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12
Q

Infection of CD4 positive cells (DIAGRAM)

A

E.g. Th-cell, gp120

  • initial attachment via gp120 binding to CD4
  • followed by co-receptor (CCR5/ CXCR4) binding
  • attachment followed by membrane fusion and internalisation (gp41 dependent)
  • when cells are activated viral proteins are produced and 1000s of new virus progeny synthesised
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13
Q

Resistance to co-receptor binding

A

People with CCR5 mutations are resistant

  • occurs in 2-14% of Europeans (caucasian), and 15% of Icelandic
  • heterozygous: < susceptibility to infection
  • homozygous: resistance
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14
Q

Why so much resistance in Caucasian Europe?

A 
Mutation is 3000 years old
Evidence suggests not selection pressure
Unlikely that it was Vikings
Maybe Founder effect
-spread from smaller population in which high frequency occurred
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15
Q

Virus variation during HIV infection

A 
Isolates from early infection - CCR5 (M)
-macrophage tropic and low cytopathic effect
-more transmissable
Isolates from late infection - CXCR4 (T)
-high cytopathic ability 
-less transmissable
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16
Q

Infection and dissemination

A

Blood stream –> macrophage

  1. –> virus reservoir and transport –> dysfunction, virus release, cytokine release and dysregulation of immune functions
  2. –> CD4 cell, T cell –lymph node (increased viral load in blood–> CD4 cell cytolysis –> AIDS, dementia, immunodeficiency, loss of B-cell control (lymphadenopathy and hypergammaglobulinaemia), loss of DTH function (cutaneous infections, intracellular pathogens) –> loss of T-cell function –> severe systemic opportunistic infections, Kaposi’s sarcoma, lymphoma
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17
Q

Disease progression

A 
Primary infection - 1000 CD$+ cells/ μl
3-6 weeks: acute HIV syndrome
-dissemination of virus
Clinical latency 12 weeks - 10 years
10 years: constitutional symtpoms, opportunistic infections
11 years: death
18
Q

Opportunistic bacterial infections and AIDS

A

Mycobacterium tuberculosis
Salmonella
Haemophilus, Streptococcus, Pneumococcus- Pyogenic infections (pus formers)
-recurrent

19
Q

Opportunistic protozoal infections and AIDS

A

AIDS-defining:

  • Cryptosporidium (chronic diarrhoea)
  • Toxoplasma gondii (disseminated, including CNS - from cats)
20
Q

Opportunistic fungal infections and AIDS

A 
Aspergillus - pneumonia
AIDS-defining
-Candida - oral presentation
-Crytococcus neoformans - CNS
-Pneumocystis jiroveci/ carinii - pneumonia
21
Q

Opportunistic viral infections and AIDS

A

AIDS-defining:

  • HSV: chronic oral infection
  • EBV: hairy leukoplakia and B-cell lymphomas
  • HHV-8: Kaposis sarcoma
22
Q

Some oral manifestations of HIV infection

A

Thrush
Erythematous candidosis
Gingival erythema
Hairy leukoplakia

23
Q

Progression to AIDS - untreated

A

10% of HIV-infected subjects progress within 2-3 years
5-10% clinically asymptomatic after 10 years
Remaining subjects progress to AIDS within 10 years - DEATH
Situation drastically improved by antiretroviral therapy
-low rates of AIDS and death compared to diagnoses in ART area

24
Q

The AIDS epidemic

A

In UK most new infections among homosexual community (57.5%)
-39% hetero
-3% IVDU
-0.5% mother-child
Asian and African epidemic more heterosexual
-may be due to associated high level of STDs - ulceration

25
Q

Global estimates

  1. people living with HIV 2016
  2. AIDS related deaths 2016
  3. No. new HIV infections per day
A
  1. 36.7 million
    - numbers going up per year
  2. 1 million
    - numbers going down
  3. 5000
    - 64% sub-Saharan Africa
26
Q

2011 World AIDS day aims

A
  1. Focused interventions for key populations at higher risk
  2. Elimination of new HIV infections among children
  3. Behaviour change programmes
  4. Condom promotion and distribution
  5. Treatment, care and support
  6. Voluntary medical male circumcision in countries with high HIV
    - improves hygiene
    - lwoers underlying STDs
27
Q

Ending AIDS targets by 2020

A

90% of people living with HIV know their status
90% of people living with HIV who know their status are on treatment
90% of people on treatment are virally suppressed

28
Q

Stigma

A

Discrimination in health-care settings, eastern Europe

29
Q

Botswana

A

Recent success
Number of new infections dramatically lowered to 10,000
Treatment coverage increased to around 90%
Almost at 90 90 90 targets

30
Q

HIV drug targets

A 
Fusion inhibitors
*NRTIs (nucleoside reverse transcriptase inhibitor)*
NNRTI (non-)
Integrase inhibitors
PI (Protease inhibitors)
CCR5 entry inhibitors
31
Q

NRTI mechanism (DIAGRAM)

A

Nucleotide analogues cause chain termination when RT builds DNA from RNA

32
Q

Treatment

A

Highly Active Anti-Retroviral Therapy
First line regimen
-2NRTIs (side-effects must be managed)
-e.g. zidovudine (AZT), lamivudine (3TC), embricatabaine (FTC), stavudine (d4T)
-1NNRTI - inactive against HIV-2
-e.g. Efaviren, Nevirapine
OR
Protease inhibitor (PI): high turnover in body = many pills
-boosted with Ritonavir to improve efficacy
-e.g. Indinavir (IDV), Fos-amprenavir (FPV)
OR
Integrase inhibitor

33
Q

Side-effects of NRTIs

A

AZT- headaches and nausea, anaemia, neutropenia
Stavudine-lactic acidosis, lipoatrophy (loss from face and limbs – gain to neck and tummy) and peripheral neuropathy- possibly via mitochondrial toxicity
Rashes

34
Q

Side-effects of NNRTIs

A

Stevens Johnson Syndrome: a severe disorder of mucous membranes
Teratogenecity

35
Q

Side effects of PIs

A

Lipodystrophy

  • fat loss from legs
  • fat gain - pot belly
36
Q

Resistance to HIV drugs

A

Increasing problem
Drug holidays
-ineffective
-compliance also an issue

37
Q

Alterative first line

A

DTG or dolutegravir used with tenofovir disoproxil fumarate (NtRTI) & lamivudine (NRTI)
DTG – Integrase inhibitor, first used in 2014 but becoming more and more widely used

38
Q

Vaccine prospects

A

Still some way off
-mutation rates high
But best prospect for eradication?

39
Q

Dental transmission control

A

Very low risk, even with risk contact only 1/300 chance of infection
Normal infectious control procedures
-gloves
-sterilise instruments
-dispose of sharps
-suction
-care if blood spillage
If at risk: contact Occy health physician for prophylactic HAART and HIV testing
If needlestick with HIV+ pt - PEP administration ASAP within 72hrs
-no NHS emplyee infected in last 10y

40
Q

HIV testing

A

ELISA based blood test
-detects HIV antibodies in blood
Antibody takes 6-12 weeks to develop
Most reliable testing at 3 months (re-test at 6 months)
Babies may test positive from maternal antibody - PCR test
Home test kits exist but blood test most reliable

Infectious diseases (Den 303) (3 decks)

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