HIV Symposium Flashcards

1
Q

Where did HIV come from?

A

HIV 1 from Chimpanzees and HIV2 from sooty managebeys

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2
Q

When did the start calling it AIDS?

A

1982

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3
Q

HIV was discovered in?

A

1983- Pasteur

Gallo- 1984

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4
Q

Which drug was primarily given to HIV patients?

A

Zidovudine

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5
Q

Prophylaxis in 1989 was?

A

Nebulised pentamidine

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6
Q

AZT could reduce transmission by?

A

25 to 8%

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7
Q

Lazarus syndrome?

A

Blood circulation return spontaneously after your heart stops beating and fails to restart despite CPR.

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8
Q

What is highly active anti-retro viral therapy, HAART?

A

Combination therapy- usually at least 3 anti retro viral drugs

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9
Q

Side effects of HAART?

A

Wasting of face
Lipodystrophy (gain fat some places and lose in other)
Gain of weight

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10
Q

HIV life cycle?

A

Attaches to CD4, require cofactors CCR5
Fuses with membrane and releases 3 enzymes
Uses reverse transcriptase to turn rna strand to dna
DNA integrated to host nucleus , integrase
Produces proteins
Protease to snip proteins and buds off

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11
Q

Anti- retro viral classes?

A

Fusion inhibitors
Coreceptor inhibitors
Nucleoside reverse transcriptase inhibitors
Non nucleoside reverse transcriptase inhibitors
Integrate inhibitors
Protease inhibitors

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12
Q

How many viruses produced per person per day?

A

10 billion

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13
Q

Mutations in HIV happen every?

A

10,000 bases

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14
Q

Normal values of CD4?

A

> 500

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15
Q

If diagnosed for CD4 was less than 350 then increased risk of death is by?

A

10 fold

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16
Q

Combination prevention?

A

Treatment as prevention TasP
Pre-exposure prophylaxis- PrEP
Expansion of HIV testing

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17
Q

U=U?

A

Undetectable is untransmittable

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18
Q

PrEP?

A

Truvada (tenofovir)

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19
Q

When was PrEP allowed to be given?

A

Oct 2020

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20
Q

How many people living with HIV globally?

A

37.7 million

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21
Q

How much reduction in infections since 1997?

A

52%

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22
Q

What happens initially in HIV?

A

Mucosal infection keeps developing, HIV specific CD8 T cells rise sharply and reduce viral load, gradual loss of CD4 t lymphocytes

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23
Q

Where does the virus undergo lyric replication?

A

CD4 t helper cells

24
Q

Examples of opportunities diseases?

A

Tuberculosis
PCP, pneumonia
Kaposi sarcoma

25
Q

What is the main receptor for HIV?

A

CD4 via gp120

26
Q

What are the stages of HIV?

A
Fusion
Viral genome is released
Reverse transcription 
Integration
Replication and protein synthesis 
Budding
New mature vision
27
Q

What co receptors are present when HIV tries to invade a cell?

A

CXCR4 or CCR5

28
Q

What is CCR5?

A

Receptor for RANTES, MIP 1 alpha

29
Q

What are rantes and MIP 1 alpha and SDF 1?

A

Molecules involved in lymphocyte chemotaxis and HIV suppression

30
Q

Where are high levels of HIV entry co-receptor CCR5 expressed?

A

Lamina propria and intraepithelial CD4 T cells

31
Q

What happens to the co-receptors during HIV infection and and why is their role important?

A

Depleted

Prevention of invasive infection
Killing infected epithelial cells
Immune regulation

32
Q

The viruses using CCR5 co receptors are called?

A

R5 viruses

33
Q

Which strains are most commonly transmitted sexually?

A

R5

34
Q

When are viruses able to use CXCR4?

A

5 years into infection

35
Q

When they are able to use CXCR4 what are the viruses called?

A

X4, if use both then called

R5X4

36
Q

How are CD4 T cell destroyed after HIV infection?

A

Death by cytoplasmic effects

Activation induced cell death apoptosis

Killing of infected cells by cytotoxic t lymphocytes

37
Q

What are the mucosal HIV transmission routes?

A

Genitourinary, rectal and oral mucosa

38
Q

What percent of CD4 cells are in gut?

A

60%

39
Q

Lamina propria CD4 T cells express high levels of?

A

CCR5

40
Q

Depletion of CD 4 t cells in the gut leads to?

A

Increased translocation of gram negative lipopolysaccharide positive bacteria

41
Q

Rise of LPS systemically causes?

A

Immune activation and TNF production, which drive HIV replication and upregulation of CCR5

42
Q

Whe did antibody test for HIV come out?

A

1985

43
Q

In 1989 what was the treatment for HIV?

A

Nebuliser pentamidine

44
Q

What was the mono therapy for HIV?

A

AZT- zidovudine

45
Q

What is current practice?

A

Combination therapy 3 drugs

Normal vaginal delivery f viral load less than 40

Transmission rates less that 1

46
Q

In early replication what are the levels of virus?

A

More than 10 million copies/ml

47
Q

Aim for viral load to be?

A

Less than 40

48
Q

Significant risk of morbidity and mortality if CD4 count is less than?

A

350cells/mm

49
Q

Over 200 CD4 you are prone to?

A

TB, Kaposi’s Sarcoma,
shingles, oral thrush,
seborrhoeic dermatitis

50
Q

Between 50 and 200 you are prone to?

A

Pneumocystis pneumonia,

toxoplasmosis, lymphoma

51
Q

Under 50 CD4 you are prone to?

A

MAC, CMV, PML, CNS lymphoma

52
Q

What is treatment as prevention?

A

Taking ART to prevent

53
Q

What are the aims?

A

All new diagnosis on ARVs by 30 days
98-100% to be taking effective treatment
100% have undetectable viral loads

54
Q

Event based PrEP?

A

2 tablets 2-24 hours before sex
1 tablet 24 hours later
1 tablet 48 hours later

55
Q

AIDS related death reduced by?

A

64%