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Virology > HIV > Flashcards

HIV Flashcards

0
Q

What does HIV infect?

A

CD4 positive cells: T cells, macrophages, monocytes and dendritic cells.

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1
Q

What type of virus is HIV?

A

A lentivirus, retrovirus, ssRNA.

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2
Q

What does HIV cause?

A

Progressive qualitative and quantitative decline in CD4 positive Th1 lymphocytes which leads to AIDS.

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3
Q

Where is deaths due to HIV most prevalent?

A

Sub-Saharan Africa

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4
Q

Describe the discovery of HIV?

A

Early 1900s retrovirus identified in chickens, late 1970/80 first human oncogene retrovirus HTLV-1 identified, 1982 HTLV-2 was discovered and in 1983 2 reports in science (Montagnier and Gallo) in science. The genomic sequence was published in 1985.

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5
Q

What are the distinct HIV groups?

A

M: main group which has A-K clades.
O: outlier group, confined to Cameroon/ Gabon.
N: 6 individuals confined to Cameroon.
P: 2 individuals confined to Cameroon.

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6
Q

What strand of SIV is the cause of HIV groups M and N?

A

SIVcpzPtt

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7
Q

What causes HIV groups O and P?

A

SIVgor

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8
Q

What is a zoonosis?

A

A disease of animals which may be transmitted to man under natural conditions.

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9
Q

Is HIV a zoonotic?

A

No, HIV-1 is from SIVcpz and HIV-2 from SIVmg which are zoonotic but HIV itself is not.

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10
Q

What has increased the emergence of HIV?

A

Deforestation, urbanisation, travel, unsterile needles etc.

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11
Q

Why has HIV rapidly spread?

A

International travel, blood transfusion and intravenous drug use.

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12
Q

How is HIV transmitted?

A

By contact of blood or mucosal membranes. Major route through sexual contact increase by abrasion, cuts, irritations, inflammation, high viral load, other STD and lack of proper condom use but otherwise an inefficient route as the mucosal layer is a physical barrier and the first line of the immune response. Intravenous drug use is increasing and therefore increasing infections. Mother to child infection is high however can be reduced to 2% by non-toxic, short-course antiretrovirals and not breast-feeding.

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13
Q

How can HIV be diagnosed?

A

Rapid test formats available which provide instant results however require confirmatory tests: ELISA, western blotting, RT-PCR and sequencing.

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14
Q

What are the three main proteins in the HIV genome?

A

Gag, pol and env.

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15
Q

What does gag encode for and what does this do?

A

P17- matrix protein
P24- capsid antigen
P6/7- nucleocapsid

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16
Q

What does pol encode?

A

Integrase, reverse transcriptase and protease

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17
Q

What does env encode and what do these do?

A

gp120- surface glycoprotein

gp41- transmembrane glycoprotein

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18
Q

What is the difference between HIV-1 and HIV-2 genome?

A

HIV-2 has minor protein Vpx rather than Vpu

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19
Q

What does the complexity of the HIV genome allow for?

A

Replication and persistence in adult host and cross-species transmission.

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20
Q

Give the steps of the HIV life cycle?

A

Binding, fusion, reverse transcription, nuclear import, integration, transcription, nuclear export, translation, assembly, budding, virion release.

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21
Q

How does HIV enter the cell?

A

Surface glycoprotein 120 interacts with CD4 and a conformational change allows binding of a second co-receptor. Transmembrane glycoprotein 41 then mediates fusion of cellular and viral membranes.

Chemokine receptor can also bind HIV.

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22
Q

What does reverse transcriptase do and where does it do this?

A

It converts ssRNA to dsDNA in the viral capsid.

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23
Q

What name is given to the dsDNA produced by reverse transcription and what are it’s main features?

A

Proviral DNA. It is longer than viral DNA in order to maintain its integrity and is integrated into the chromosomal DNA by integrase to produce integrated proviral DNA.

24
Q

How does the integrated proviral DNA act?

A

As a normal gene locus. The 5’ long terminal repeat (LTR) acts as an enhancer/promoter.

25
Q

What regulates transcription? Describe?

A

Tat: an 86-101 amino acid nucleolar, RNA binding protein which allows for the full length transcript to be transcribed by phosphorylation of the C-terminal tail of RNApol2 by the recruitment of TAK.

26
Q

What is the complication with transcription of gag, pol and env?

A

Gag and pol can be transcribed as usual however env requires a different orf. Therefore full length transcript is made then gag and pol are spliced to allow for env to be made separately.

27
Q

What controls expression?

A

Rev- an accessory protein produced from multiply spliced RNA. Functions by interacting on a sequence of the RNA- RRE.

28
Q

What occurs in early and late translation?

A

Early: tat, rev and nef are translated from multiply spliced RNA which has been exported.
Rev then enters the nucleus to export full length and singularly spliced RNA for translation.
Late: the remaining proteins are translated.

29
Q

What are HIV accessory genes?

A

Vif and Vpu (Vpx in HIV-2): have key roles in counteracting innate antiviral response.
Vpr: induced G2 cell cycle arrest
Nef: multiple roles

30
Q

Describe the roles of Nef in vivo?

A

Important for viral load and pathogenicity (proved with reverse genetic analysis and delta Nef, long-term non progressors). Down modulation of cell surface glycoproteins (CD4) enhancement of virus infectivity, perturbation of cell signalling.

31
Q

What are the three stages of HIV infection?

A

Primary phase illness: (aka acute infection), many virus particles being produced, possible flu-like symptoms, immune response works to suppress viraemia to a set point.
Asymptomatic phase: depending on set point reached (lower the longer) 10+ years with no sign of infection or symptoms.
AIDS: loss of CD4 cells and high vareamia.

32
Q

Is HIV latent?

A

No, shows clinical latency but not cellular.

- long asymptomatic phase but continuous virus replication and rejuvenation of CD4 cells to remain “latent”.

33
Q

What is the virus vs. host battle?

A

Virus: CD4 destruction and loss of function, lymph node destruction, viral variation and mutation.
Host: cytotoxic T-cell response, antibody response, CD8 antiviral factors, chemokines.

34
Q

What are probable symptoms in the primary phase?

A

Fever, malaise, rash, diarrhoea and lymphadenopathy.

35
Q

During the asymptomatic phase what could be possible symptoms?

A

Fatigue, weight loss, thrush or shingles.

36
Q

What determines the types of symptoms?

A

The levels of CD4 cells.
Normal: ~2000/uL
200-500/uL: Generalised lymphadenopathy, oral lesions, shingles, reactivation of latent, mycobacterium tuberculosis – Basal cell carcinoma of skin, poxvirus, papillomavirus
<200/uL: Protozoal infections, bacterial infections, fungal infections, viral infections

37
Q

What are the target cell types of HIV infection?

A

T-lymphocytes; CD8+ (cytotoxic T-cells) and CD4+ (T helper cells). CD4+ divide into Th1 (activate and drive the toxicity of cytotoxic T- cells) and Th2 (produce soluble molecules to help B lymphocytes).
Primarily affects Th1.

Monocytes derived mononuclear phagocytes, macrophages and dendritic cells.

38
Q

What does Fv1 stand for?

A

Friend virus susceptibility factor-1

39
Q

What do the two alleles of Fv1 do?

A

Fv1-N and Fv1-B block the dsDNA entering the nucleus on their opposite cell types.

40
Q

What can restrict HIV-1 replication?

A

A protein, TRIM5alpha, present in non-human primate cells.

41
Q

What is TRIM5alpha?

A 
A HIV-1 restriction factor. Consists of a ring domain and B-box domains (for autoubiquitinylation), coiled coil (for trimerisation) and SPRY domain (for binding to capsid). 
Mechanism of action: 
1. Virus binding and membrane fusion
2. Proteasomal degradation 
3. Capsid disruption 
4. Block of reverse transcriptase.
42
Q

Why is human TRIM5alpha not a HIV-1 restriction factor?

A

As it has a mutation in SPRY domain which prevents interaction with the HIV capsid

43
Q

What is Vif?

A

A protein which increases infectivity by inhibiting the antiviral factor APOBEC3G

44
Q

What is Vpu?

A

81 amino acid integral membrane protein. Which binds to and induces degradation of CD4 by ubiquitin-proteasome pathway and allows Env to escape trapping in ER. Increases virion release.

45
Q

What is tetherin?

A

Blocks enveloped virion release by tethering the virus to the membrane for endocytosis and degradation.

46
Q

What does SAMHD1 do?

A

Acts to block HIV-1 replication in myeloid cells by forming an active dimer and removing the 3 phosphate groups from the dNTP inhibiting the reverse transcriptase.

47
Q

What blocks nuclear uptake or chromosomal integration?

A

MxB

48
Q

What are the two types of therapies for HIV?

A

Standard and HAART

49
Q

What are the three classes of drugs in standard therapy?

A

Nucleoside analogue reverse transcriptase inhibitors (NRTIs), non-nucleoside reverse transcriptase inhibitors (NNRTIs) and protease inhibitors

50
Q

What is the usually set-up of HAART?

A

Triple therapy: 2 NRTIs and 1 NNRTI or PI.

Sometimes quadruple therapy.

51
Q

What do the drug classes block?

A

Protease inhibitors block maturation, NNRTIs and NRTIs block reverse transcription. Also entry inhibitors and an integrase inhibitor.

52
Q

Where to NNRTIs bind reverse transcriptase?

A

In a specific site other than the active site

53
Q

What do all NRTIs have in common? Give an example?

A

All analogues of nucleosides but lack 3’OH and are therefore chain terminators.
Azidothymidine: a deoxythymidine inhibitor.

54
Q

Give an example of some NNRTIs?

A

Efavirenz, nevirapine, etravirine

55
Q

Give an example of a protease inhibitor?

A

Saquinavir and nelfinaver

56
Q

What are the pros and cons of HAART therapy?

A

Pros: can be manipulated to avoid resistance, treatm interruptions possible, effective at reducing viral load and disease progression.
Cons: cost, compliance (effects on lifestyle), side effects, drug-drug interactions, post-therapy reversion.

57
Q

What is the new drug that prevents interaction of the virus with CCR5 and therefore blocks entry?

A

Maraviroc

58
Q

What is T-20?

A

A peptide that blocks conformational change involved on fusion of viral and cellular membranes by gp41 fusion domain. Limited evidence of genetic resistance. Licensed for clinical use as Enfuvirtide.

Virology (3 decks)

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