Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Inflammation > hiv/aids > Flashcards

hiv/aids Flashcards

1
Q

what is the origin of hiv-1

A

SIV chimpanzees (cpz), it is a hiv like virus haboured in oldworld primates

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

how is it believed that hiv became a pandemic

A

went from monkeys into humans via zoonotic transmission, plausible explanations are the west african bushmeat trade

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

what type of virus is hiv

A

retrovirus

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

what are the three polyproteins synthesised by a retrovirus e.g hiv

A

gag(group specific antigen)
pol(polymerase)
env(envelope glycoprotein)

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

what proteins make up the gag polyprotein

A

viral core proteins matrix,capsid and nucleocaspid

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

what proteins make up the pol polyprotein

A

enzymes: PR (protease), RT (reverse transcriptase), IN (integrase)

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

what proteins make up the env polyprotein

A

SU (surface), TM (transmembrane)

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

what is definition of retrovirus

A

viraL GENOME IS STORED as rna so reverse transcriptase needed to make dna. then integration occurs in which there is covalent insertion of viral cdna into genome of infected cell, using integrase

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

what is the consequence of integration in an infected cell

A

to cure retroviral infection you need to kill all cells containing viral genome, however cells go into latent phase, not producing any viral proteins so can’t be spotted by immune system

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

describe structure of mature hiv-1 particle

A

hiv is envelope virus, has a lipid bilayer with protruding env spikes, inside the envelope there are shells of gag proteins. MA associates with the membrane, ca forms conical caspid, and nc coats viral rna genonome, the core has two rna stands, about 50 copies of viral enzymes.

cellular factors can also be packaged. like cylclophillin

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

how does mature hiv1 particle differ to immature one

A 
In	the	mature	par7cle,	MA	associates	
with	the	membrane,	CA	forms	the	
conical	capsid,	and	NC	coats	the	viral	
RNA	genome.	The	core	contains	two	
genomic	RNA	strands	(plus	strand),	
tRNALys3,	and	about	50	copies	of	each	
viral	enzyme	(PR,	RT	and	IN).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what does hiv require to enter the host cell and what cells is hiv trophic for

A

two receptors cd4 and chemokine receptor (CCR5/CXCR4), trophic for cd4 and macrophages

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

what are the three distinct enzymatic activities of reverse transcriptase

A
  1. RNA-dependent DNA polymerase
  2. RNAasH (cleaves RNA from RNA/DNA hybrid)
  3. DNA-dependent DNA polymerase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is reverse transcriptase made of

A

RT is a heterodimer of p66 and p51 subunits.

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

describe some modes of hiv sequence diversification

A

copy errors, reverse transcriptase has no error checker, recombination(shift), drift plus shift, these factors all accelerate viral diversification

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

why is viral diversification important to appreciate

A

Contribu7ons to – immune escape, drug resistance,

phenotypic changes and natural history?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what clades of HIV dominate

A

HIV-1 Sequence Diversity (B & C clades predominate)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what is a clade

A

different subtypes of related viruses called clades, nucleotide sequence cant differ by more than 30 per cent, clades don’t have sig phenotype diff, but big implications for hiv vaccination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how does CDNA produced by reverse transcriptase integrate in cell genome

A

integrase cleaves 3’ end 2 nucleotides gone, triggers host repair mechansims which then integrates the foreign material into the host genome randomly (some areas are favoured)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

why are scientist interersted in hiv1 regulatory/acessory proteins

A

diverse functions all essential, adapters that facilitate molecular interactions, contribute to evasion of host control mechanisms such as immune system, can they be targeted with therapeutics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is tat

A

potent activator of viral transcription

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is rev protein

A

mediates unspliced rna export

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is vif protein

A

critical regulator of virus infectivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is nef protein

A

immune modulator, tcell activation, virus infectivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what is vpu protein

A

immune modulator, virus release

26
Q

what is vpr protein role

A

cell cycle, virus nuclear import, resistance modulator

27
Q

describe the balance between a host cell and a virus in terms of the virus attempting to replicate

A

it is a delicate balance, host cells have measures to prevent virus from replicating but viruses have counter measures too

28
Q

what does tetherin do and how is it opposed

A

tetherin stops virus from being relased from cell surface, opposed by vpu which marks tetherin for degradation

29
Q

what does apobec3 do to protect host cell from hiv and how does virus oppose this

A

apobec3 changes c to u mutagenesis inhibiting reverse transcriptase, vif counteracts this

30
Q

what does SAMHD1 do to stop hiv replication and how does the virus antagonise this process

A

it supress RT in myeloid cells hydrolysing dntps , countered by vpx

31
Q

what does serinc do and how isit countered in hiv infection

A

serinc stops viral entry however it is countered by nef

32
Q

draw out the typical course of hiv infection

A

viral load is high initially, cd4 drop from 100 to around 600, immune system takes some control and viral load drops to a set load, there is a latency period and then progression to aids where viral load rises and cd4 decrease. this is where you can get opportunistic infections

33
Q

describe a crucial feature of hiv1 replication

A

obligate formation of the provirus , one of the biggest hurdles to devloping a cure, SO IF WE CAN “WAKE UP” ALL OF THE PROVIRUS IN
LATENTLY
INFECTED CELLS IN PRESENCE OF ONGOING DRUG
THERAPY

34
Q

describe the risk of hiv transmission via sex

A

genrally lower significantly high in male male sex. risk is also significantly enhanced if there are other stds or epithelial lesions

35
Q

what form of hiv transmission has the greatest estimated risk

A

blood transfusion, then iv drugs use needle sharing, then mother to child

36
Q

explain how hiv is transmitted mucosally

A

hiv1 breaches mucosal barriers, transmitted virus are ccr5 trophic, other celles can be infected dendrites, 0.1% hiv1 exposure results in transmission.

37
Q

what • Implies that physical barriers, and
innate/intrinsic defenses are quite
effective

A

Most transmissions result in a single

founder virus infecting the recipient

38
Q

how does acute infection differ from chronic infection in hiv1, acute being before the adpative immune system

A

primary target in acute phase are cd4 cells, majority are mucosal, up to 60% can be lost due to cytopathicity of hiv1, apoptosis + ctls

39
Q

in acute hiv1 transmission what tissue is a major target

A

galt tissue, hiv spreads rapidly to the cd4 cells here, the immune integerity of the gut never recovers and you can get chronic immune activation there

40
Q

explain the four classes of progressors in hiv infections

A

viral load predicts survival time, normal progressor will have aids 8-10 years, rapid progressors will have aids in 1-3 years, long term non progressors and elite controllers

41
Q

what controls acute hiv infection

A

controlled by a strong CD8+ T cell

response, neutralizing antibodies arise much later

42
Q

how does hiv affect the memory cells

A

cd4 t cells deplete due to cytoxi killing or apoptosis, immune hyperactivity results in more tcells being activated and this makes them more susceptable to destruction. results in loss of cd4 t cell memory pool and thymic bone marrow dysfunction

43
Q

intially viremia of hiv is controlled by cytoxic cd8 cells but not cleared why does this control eventually fail

A

hiv1 escapes cd8 evntually by mutations eavding adaptive immunity

44
Q

what is the problem with continued t cell activation and general inflammation state

A

activates more t cells which are substrates for continued infection depleting t cells

45
Q

how do you diagnose hiv1

A

either elisa which detects individuals who have seroconverted after 3 months, or rtpcr which is ONLY test that can diagnose before 3 months, looks at virus particles per millitre of blood

46
Q

describe in detail elisa

A

only detects hiv1 infections in those who have seroconverted after 3 months, so if done before 3 months a negative test may not be conclusive, a positive sample will be retested using elisa or western blot

47
Q

what is the significance of opportunistic infections in hiv 1

A

once you start getting this almost inevitably leads to death

48
Q

name some opportunistic infections associated with aids

A

herpes simplex virus 1/2 oral, genital or anal, fungal pneumonia,kaposi sarcoma, toxoplasmosis, tuberculosis

49
Q

name Classic HIV-1-associated ODs fungal ones

A 
Fungus	infections:	
Pneumocystis carinii
Histoplasma
Cryptococcus	
Coccidioidomyces
50
Q

name Classic HIV-1-associated ODs bacterial ones

A

mycobacteria, TB, MAI etc
pneumococcus
non-typhoid Salmonella

51
Q

name some beneficial genetic attributes in humans to hiv1

A

mhc heterozygosity, hla c, hlab57,kir,cor,ccr5 ligands

52
Q

what is maraviroc

A 
CCR5 inhibitor (Chemokine receptor
antagonist) Maraviroc, prevents entry into cell
53
Q

what is enfurvitide

A

stops viral fusion to potential host cells (tcells)

54
Q

discuss nrti which is one of the classes of rt inhibitiors

A

1.Nucleoside-analogue reverse transcriptase inhibitors (NRTI)
Incorporated into elongating DNA chain; no 3’OH leads to chain termination
Examples: Zidovudine/AZT; Lamivudine/3TC; Abacavir; Tenofovir

55
Q

discuss what nnrti stands for and what this class of rt inhibitors does give examples

A

Non-nucleoEde Reverse transcriptase inhibitors (NNRTI). Allosteric RT inhibitors – do not bind active site
Block initiation of RT; examples: Efavirenz; Nevirapine

56
Q

what is raltegravir

A

binds active site integrase blocking strand transfer reaction

57
Q

describe the action of protease inhibitors

A

inhibit hiv protease to prevent cleavage of gag and gag pol to mature proteins so virus particle is non infection

58
Q

describe Haart

A

Highly Active Anti-Retroviral Therapy (HAART)
(Combination therapy)
3 is the magic number – Difficult for HIV to
Simultaneously mutate to avoid combinations
of drugs
All resistance mutations in HIV enzymes comes with a fitness cost
(mutants replicate less efficiently that wildtype often requiring 2nry
Mutations to cope

59
Q

what are the most common haart combinations

A

2 nrti one nnrti or protease inhibitor, rmeber haart is not a cure, it controls hiv replication below detectable, but stop treatment and hiv will rebound back

60
Q

what are the challenges associated with hiv1 vaccine development

A

hiv envelope is sole target for antibodies, highly variable virus, highly glycosylated, needs to provide sterlising immunity

61
Q

how can we try to prevent hiv

A

condom use, male circumcision, prep, microbicdes, vaccines

62
Q

if bone marrow transplant appears to have cured one hiv suffeere why dont we dish it out to everyone

A

bone marrow transplant is dangerous surgery and impractical when ind can take haart and live indfinetly, rather focus on finding specifc drugs that activate latent infected cells while taking haart

Inflammation (23 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions