HIV Flashcards

1
Q

How many people living with hiv

A

37m

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

HIV closely related to

A

SIV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Efffect of SIV on chimps

A

No harm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Humans got HIV from animals how

A

Bushmeat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

HIV is a

A

Retrovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

3 parts of a retro virus

A

Gag: group specific antigen
viral core proteins: MA (matrix), CA (capsid), NC (nucleocapsid)

Pol: polymerase
enzymes: PR (protease), RT (reverse transcriptase), IN (integrase)
Env: envelope glycoprotein
SU (surface), TM (transmembrane)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Retrovirus is

A

Virus using reverse transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Process of retrovirus

A

Reverse transcrip7on: copying of an RNA template (the viral
genome) into a double-stranded DNA copy.

2.  Integration on: covalent insertion of viral cDNA into the genome of the
infected cell, to form the provirus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

HIV1 is tropic for

A

CD4 expressing cells: helper T cells and macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Modes of HIV sequence diversification

A

Copying error(drift)
Recombination(shift)
Drift plus shift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Diversification results in

A

Immune escape drug resistance and phenotypic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Different subtypes of related viruses are called

A

Clads

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Regulatory/ accessory protein

A

•  Tat – potent ac7vator of viral transcrip7on
Rev – mediates unspliced RNA nuclear export
• Vif – cri7cal regulator of virus infec7vity
Nef – immune modulator, T-cell ac7va7on, virus infec7vity
• Vpu – immune modulator, virus release
• Vpr – cell cycle, virus nuclear import, resistance modulator

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HIV resistance factors internally

A

Tetherin inhibits release of virus on cell surface

APOBEC3 catalysts C to U mutagenesis and inhibits RT

SAMHD1 suppresses RT in myeloid cells by hydrolysing dNTPS

SERINC interferes with viral entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Inexorable fall of CD4 cells causes

A

AIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Risk of acquisition by exposure to HIV

A

Sexual transmission 0.5% (increased by other STDs)

IV drug use (0.67% per needle)

Blood transfusion (90%)

Mother to child: breast milk or at birth (25%)

17
Q

Main target for acute HIV1 infection

A

Gut associated lymphoid tissue (GALT)

18
Q

Normal progresser ?

A

Most people progress to AIDS in 8-10 years

19
Q

Rapid progressor

A

1-3 years progress to aids

20
Q

Long term nonprogressors

A

Maintain low level of detectable viral RNA in blood

AIDS free indefinitely

21
Q

Elite controller

A

<50 copies of viral RMA

AIDS free indefinitely

22
Q

Acute in controlled by

A

Strong 8+ T cell

Neutralising antibodies arise later

23
Q

T cell responses: solutions + problems

A

Initial viremia controlled by CD8 cytotoxic T cells, but not cleared

HIV1 mutates and escapes adaptive immunity

Continued T cell activation lead to inflammation

Inflammation leads to immune dysfunction and pathology

24
Q

Diagnosis of HIV

A

ELIZA test for anti-p24

Only detects those who are seroconverted (3 months)

25
Best diagnosis
RFPCR
26
Aids cancers and opportunistic infections
Kaposis sarcoma human herpes virus 8 Fungal pneumonia Toxoplasmosis Reactivation of oral herpes simplex virus 1/2 Cytomegalovirus induced retinitis Tuberculosis
27
Types of virus specific inhibitors
Entry Reverse transcriptase Intergrase Protease
28
Entry inhibitors + example Fusion inhibitors
Works with host cell to stop entry, however virus can evolve and come in through a different protein Prevents a confirmational change/rearrangement
29
Reverse transcriptase nRTI NNRTI
Integration is stopped before whole protein can be formed NNRTI is a non competitive inhibitor that stops initiation
30
Intergrase stops?
Intergration in the nucleus
31
Protease does what
Virus produced but cleaveage stopped
32
HAART IS
Highly active antiretroviral therapy
33
Is HAART a cure
No if you stop taking it you will relapse
34
How many drugs prescribed in HAART
3
35
Barrier to curing HIV
Latent viral reservoirs
36
Bone marrow to cure HIV
Dangerous and impractical for patients that can live on HAART
37
HUV prevention
Effective condom use Male circumcision Pre exposure prophylaxis Topical micro ideas