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Intersystems > HIV > Flashcards

HIV Flashcards

1
Q

What does the HIV gag gene code for?

A

Structural proteins of the capsid, matrix, core and nucleocapsid.

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2
Q

What does the HIV pol gene code for?

A

Viral enzymes: protease, reverse transcriptase, RNase H and integrase enzymes. Expressed as a Gag-Pol polyprotein before autocleavage.

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3
Q

What is the structure of HIV’s genome?

A

+ sense ssRNA

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4
Q

What are the co-receptor sites involved in HIV binding to T cell?

A

CCR5 and CXCR4

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5
Q

Outline the general steps involved in HIV becoming disseminated throughout the body.

A

Mucosal exposure to HIV-1
Selective infection by R5 strains
HIV binds to dendritic cell by DC-SIGN
Transport of virus to regional lymph nodes
Spread of infection to activated CD4 T lymphocytes
Entry of virus infected cells into the bloodstream
Widespread dissemination

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6
Q

What is the most common drug target against HIV?

A

Reverse transcriptase

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7
Q

What does the Long Terminal Repeat do?

A

Assists the virus in integrating its reverse-transcribed DNA into the host DNA by binding to HIV integrase.

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8
Q

What does HIV integrase do?

A

catalyses the random integration of HIV cDNA into cell DNA

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9
Q

What is integration required for?

A

Production of new virus.

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10
Q

What does 5’LTR do?

A

Acts as HIV gene promotor

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11
Q

How does 5’LTR respond to viral Tat protein?

A

It is greatly increased in expression.

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12
Q

What does the Tat protein do?

A

Binds to TAR RNA to promote transcriptional elongation

Downregulates MHC-1 gene transcription

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13
Q

Which two regulatory proteins are essential for HIV replication?

A

Tat and Rev

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14
Q

Which proteins interfere with MHC-I and why?

A

Tat, Nef and Vpu

Prevents MHC-I presenting HIV particles to Cytotoxic Lymphocytes

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15
Q

What does vif protein do?

A

Promotes infectivity of cell-free virus, blocks cell defences targeting single stranded cDNA.

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16
Q

What is the function of nef?

A

Multifunctional -> important for in vivo pathogenesis

Down-modulates cell MHC-1 and CD4.

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17
Q

What is the ‘Natural combination therapy’ developed by humans before HAART therapy?

A

TRIM5a: destabilisation of the viral capsid
APOBEC3G: induces lethal hypermutations in viral genome (G-> A)
Tetherin: inhibition of virus release

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18
Q

What were the Counter-measures developed by HIV to counteract the ‘natural combination therapy’ developed by the human immune defense?

A

HIV-1 Vpu: Degrades CD4, antagonises tetherin, inhibits surface expression of CD1d, facilitates the release of fully infectious virions and counteracts innate immunity factors

HIV-1 VIf protein: Degrades APOBEC3

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19
Q

Where is the main latent HIV reservoir?

A

in the Central and transitional memory cells

20
Q

What is acute HIV characterised by?

A

Rapid and massive loss of the body’s CD4+ T-cells

21
Q

Generally, how long is clinical latency period in untreated and undiagnosed HIV? i.e. before the patient starts to develop constitutional diseases.

A

~7 years

22
Q

What are the effects of HIV on the Gut?

A

Massiv eloss of memory T-lymphocytes in Gastric Associated Lymphoid Tissue (GALT)
Gut Epithelial cell apoptosis

23
Q

What is the HIV viral load?

A

Amount of HIV RNA in the plasma

24
Q

Why is there limited effectiveness of IgG specific for HIV envelope?

A

Most antibody to Env does not neutralise HIV.

High levels of Env glycosylation means that immunogenicity of virus-bound gp120 is reduced

25
Q

Give three reasons why an HIV-1 vaccine has been so difficult.

A

High error rate of Reverse transcriptase -> huge diversity
Envelope gp120 timers have highly variable regions exposed on the outer surface.
Envelope trimer: evolved to resemble self antigens
Glycans mask Env and provide greater evolutionary diversity and antibody evasion.

26
Q

What are the two causes of CD4+ depletion in HIV?

A

CD4+ T cell destruction
Chronic immune-activation
Impaired T-cell production by thymus

27
Q

How does chronic immune-activation lead to CD4+ T-cell destruction?

A

Integrity of gut mucosal barrier lost, which leads to microbial products leaking into systemic circulation, which results in stimulation of immune cells and elevation of pro-inflammatory cytokines -> CD4+ T-cells enter cell-cycle and die/

28
Q

What type of pneumonia is considered an AIDS related illness?

A

Pneumocystis jirovecii

29
Q

What are the host factors that may determine disease progression?

A

Genetic
HLA type
Immunology
Age

30
Q

What immunological features of a host may determine disease progression?

A

High titre of neutralising antibody
High level of CD8+ HIV-I specific T cells
High level CD4+ HIV-1 specific proliferative responses

31
Q

What are four types of inhibitors used in HIV-1 antiviral chemotherapy?

A

Fusion/entry inhibitors
Reverse transcriptase inhibitors
Protease inhibitors
Integrase inhibtors

32
Q

What is a nucleoside?

A

Nucleotides without a phosphate group

33
Q

What are nucleotides?

A

mono, di and tri-phosphate forms of the nucleosides

34
Q

What is acyclovir? How does it work?

A 
Herpesvirus drug (prodrug - activated by herpesvirus thymidine kinase)
Nucleoside (guanosine) analogue - lacks the 3' hydroxyl group required to form DNA polymer
35
Q

What is Valacyclovir?

A

A proprodrug derived from acyclovir.

Improved bioavailability

36
Q

What is Ribavirin?

A

Guanosine analogue
Inhibits many RNA and DNA viruses in vitro.

Influenza, haemorrhagic fevers, Hep C, Respiratory syncitial virus, bronchiolitis, pneumonia

37
Q

What does NRTI stand for?

A

Nucleoside Reverse Transcriptase Inhibitors for HIV-1.

38
Q

How do NRTIs work?

A

Viral reverse Transcriptase uses them in preference to cellular nucleosides; prevent chain elongation.
Reduces infection of new cells but cannot eliminate virus completely.

39
Q

What is Zidovidine (AZT)?

A

Thymidine analogue (NRTI)

40
Q

What does NNRTI stand for?

A

Non-nucleoside Reverse transcriptase inhibitor

41
Q

What are NNRTIs NOT?

A

Do NOT bind nucleotide bindign site of RT
Are NOT DNA analogues
Directly inhibit the Reverse Transcriptase inhibitors by other mechanisms
Do NOT have close structural similarity to the nucleotides

42
Q

What is Raltegravir?

A

Integrase inhibitor

43
Q

What to protease inhibitors prevent?

A

maturation of virus

44
Q

What mechanisms drive ongoing immune activation in an HIV-infected person?

A

HIV replication/virion production
HIV gene expression
Co-infections (CMV, HCV)
Homeostatic mechanisms following T-cell loss
Dysregulation of Type 1 interferon and other cytokines due to loss of Tregs

45
Q

What are the co-morbidities to which chronic immune activation and inflammation may contribute?

A 
Cardiovascular disease
Cancer
Bone fractures/osteoporosis
Liver failure
kidney failure
cognitive decline
frailty

Intersystems (16 decks)

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