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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

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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

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3
Q

what type of virus is hiv

A

retrovirus

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4
Q

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

A

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

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5
Q

what proteins make up the gag polyprotein

A

viral core proteins matrix,capsid and nucleocaspid

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6
Q

what proteins make up the pol polyprotein

A

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

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7
Q

what proteins make up the env polyprotein

A

SU (surface), TM (transmembrane)

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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

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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

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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

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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).
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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

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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
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14
Q

what is reverse transcriptase made of

A

RT is a heterodimer of p66 and p51 subunits.

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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

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16
Q

why is viral diversification important to appreciate

A

Contribu7ons to – immune escape, drug resistance,

phenotypic changes and natural history?

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17
Q

what clades of HIV dominate

A

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

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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

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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)

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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

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21
Q

what is tat

A

potent activator of viral transcription

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22
Q

what is rev protein

A

mediates unspliced rna export

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23
Q

what is vif protein

A

critical regulator of virus infectivity

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24
Q

what is nef protein

A

immune modulator, tcell activation, virus infectivity

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25
what is vpu protein
immune modulator, virus release
26
what is vpr protein role
cell cycle, virus nuclear import, resistance modulator
27
describe the balance between a host cell and a virus in terms of the virus attempting to replicate
it is a delicate balance, host cells have measures to prevent virus from replicating but viruses have counter measures too
28
what does tetherin do and how is it opposed
tetherin stops virus from being relased from cell surface, opposed by vpu which marks tetherin for degradation
29
what does apobec3 do to protect host cell from hiv and how does virus oppose this
apobec3 changes c to u mutagenesis inhibiting reverse transcriptase, vif counteracts this
30
what does SAMHD1 do to stop hiv replication and how does the virus antagonise this process
it supress RT in myeloid cells hydrolysing dntps , countered by vpx
31
what does serinc do and how isit countered in hiv infection
serinc stops viral entry however it is countered by nef
32
draw out the typical course of hiv infection
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
describe a crucial feature of hiv1 replication
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
describe the risk of hiv transmission via sex
genrally lower significantly high in male male sex. risk is also significantly enhanced if there are other stds or epithelial lesions
35
what form of hiv transmission has the greatest estimated risk
blood transfusion, then iv drugs use needle sharing, then mother to child
36
explain how hiv is transmitted mucosally
hiv1 breaches mucosal barriers, transmitted virus are ccr5 trophic, other celles can be infected dendrites, 0.1% hiv1 exposure results in transmission.
37
what • Implies that physical barriers, and innate/intrinsic defenses are quite effective
Most transmissions result in a single | founder virus infecting the recipient
38
how does acute infection differ from chronic infection in hiv1, acute being before the adpative immune system
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
in acute hiv1 transmission what tissue is a major target
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
explain the four classes of progressors in hiv infections
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
what controls acute hiv infection
controlled by a strong CD8+ T cell | response, neutralizing antibodies arise much later
42
how does hiv affect the memory cells
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
intially viremia of hiv is controlled by cytoxic cd8 cells but not cleared why does this control eventually fail
hiv1 escapes cd8 evntually by mutations eavding adaptive immunity
44
what is the problem with continued t cell activation and general inflammation state
activates more t cells which are substrates for continued infection depleting t cells
45
how do you diagnose hiv1
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
describe in detail elisa
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
what is the significance of opportunistic infections in hiv 1
once you start getting this almost inevitably leads to death
48
name some opportunistic infections associated with aids
herpes simplex virus 1/2 oral, genital or anal, fungal pneumonia,kaposi sarcoma, toxoplasmosis, tuberculosis
49
name Classic HIV-1-associated ODs fungal ones
``` Fungus infections: Pneumocystis carinii Histoplasma Cryptococcus Coccidioidomyces ```
50
name Classic HIV-1-associated ODs bacterial ones
mycobacteria, TB, MAI etc pneumococcus non-typhoid Salmonella
51
name some beneficial genetic attributes in humans to hiv1
mhc heterozygosity, hla c, hlab57,kir,cor,ccr5 ligands
52
what is maraviroc
``` CCR5 inhibitor (Chemokine receptor antagonist) Maraviroc, prevents entry into cell ```
53
what is enfurvitide
stops viral fusion to potential host cells (tcells)
54
discuss nrti which is one of the classes of rt inhibitiors
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
discuss what nnrti stands for and what this class of rt inhibitors does give examples
Non-nucleoEde Reverse transcriptase inhibitors (NNRTI). Allosteric RT inhibitors – do not bind active site Block initiation of RT; examples: Efavirenz; Nevirapine
56
what is raltegravir
binds active site integrase blocking strand transfer reaction
57
describe the action of protease inhibitors
inhibit hiv protease to prevent cleavage of gag and gag pol to mature proteins so virus particle is non infection
58
describe Haart
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
what are the most common haart combinations
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
what are the challenges associated with hiv1 vaccine development
hiv envelope is sole target for antibodies, highly variable virus, highly glycosylated, needs to provide sterlising immunity
61
how can we try to prevent hiv
condom use, male circumcision, prep, microbicdes, vaccines
62
if bone marrow transplant appears to have cured one hiv suffeere why dont we dish it out to everyone
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

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