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PM3A > HIV & Anti-Retroviral therapy > Flashcards

HIV & Anti-Retroviral therapy Flashcards

1
Q

What is UNAIDS 90-90-90?

A

A global target set for countries to have:
(1) ≥90% HIV+ to be diagnosed
(2) ≥90% HIV+ to be on ART
(3) ≥90% HIV+ to have viral load depressed

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2
Q

What is the cause of HIV and the pathogenesis?

A

Lentivirus - a type of retrovirus, infecting the immune cells:
(1) CD4+ T helper cells
(2) Macrophages
(3) Dendritic cells

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3
Q

What type of virus is lentivirus?

A
  • Group IV
  • ssRNA
  • Positive sense
  • Enveloped
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4
Q

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

A

(1) HIV-1

(2) HIV-2 - less virulent and less infective

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5
Q

How does the infection of immune cells by lentivirus lead to low levels of helper T cells?

A

(1) Direct viral killing of infected cells

(2) Increased apoptosis of infected cells

(3) Killing of infected CD4+ T cells by CD8 cytotoxic lymphocytes

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6
Q

What does a CD8 cytotoxic lymphocyte do?

A

Kills infected CD4+ (Helper) T cells

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7
Q

What effect does increased death of CD4+ (Helper) T cells have?

A

(1) Increased susceptibility to opportunistic infections

(2) Susceptibility increases as CD4+ (Helper) T cell count falls below critical level

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8
Q

What are the stages of the HIV life cycle?

A

Lentivirus binds to CD4 receptor to fuse with host cell membrane

Virus uncoats and viral RNA + proteins enter host cell

Viral DNA is transcribed via reverse transcriptase

Viral DNA enters nucleus
Integrates into host genome using viral integrase

New viral DNA is used as genomic RNA
This is used to make new viral proteins

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9
Q

How can HIV enter the body?

A

Into the bloodstream
or
mucus membranes (vaginal/penis/anus)

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10
Q

Where is HIV present in the body once contracted?

A

semen
vaginal fluids
breast milk
blood
rectal excretions

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11
Q

How can HIV be transmitted?

A

Unprotected sex
mother to baby
IV drug use - needle sharing/needle stick injury
blood transfusions

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12
Q

How can HIV spread be prevented?

A

HIV testing
condoms
post exposure phrophylaxis PEP
pre-exposure phrophylaxis PrEP
Needle exchange programmes & clean needles
blood screening

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13
Q

How is HIV diagnosed

A

ELISA-immunoassay
detection of antibodies for HIV
detection of p24 antigen

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14
Q

What is the period for which HIV+ patients may test negative with older tests?

A

3 months

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15
Q

Where can tests be accessed by the public

A

sexual health clinics
hospitals
GP surgeries
community pharmacies

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16
Q

What tests are undertaken by the patient following an HIV positive diagnosis?

A

-Immunoassay (ELISA) to differentiate between HIV-1 and HIV-2

-HIV NAT (nucleic acid test)

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17
Q

When do AIDS symptoms occur following HIV infection?

A

7.5 years post infection

18
Q

How does HIV lead to death if left untreated?

A

Progressively destroys all CD4+ (helper) T cell lymphocytes

19
Q

what is seroconversion?

A

the acute infection stage of HIV infection, flu-like symptoms: fever, headache, rash

20
Q

What is clinical latency?

A

chronic infection (asymptomatic) stage of HIV infection

21
Q

When does the body’s CD4+ (helper) T lymphocyte count begin to decline in an HIV infection?

A

Seroconversion, acute infection stage

21
Q

Are HIV antibodies present in seroconversion?

A

No, they are only starting to be made

22
Q

When can common infections be seen in an HIV infection?

A

chronic latency stage

23
Q

What characterises AIDS

A

Immune system can no longer fight infection
Low CD4+ (helper) lymphocyte count
High viral load

24
Q

When are opportunistic infections observed in HIV infections?

A

AIDS stage of infection

25
Q

What happens if an HIV infection (AIDS) is left untreated?

A

DEATH

26
Q

How does AIDS develop?

A

Untreated HIV infection

27
Q

What is ART and its aims?

A

antiretroviral therapy

Increase CD4+(helper) T lymphocyte count
Increase quality of life + life expectancy
decrease risk of infections
decrease transmission
decrease viral load
decrease risk progression

28
Q

What are the types of ART?

A

Entry/fusion inhibitors
these drugs block HIV from getting inside healthy cells.

RT inhibitors
bind to a specific protein so the HIV virus can’t make copies of itself.

integrase inhibitors
These stop HIV from making copies of itself by blocking a key protein that allows the virus to put its DNA into the healthy cell’s DNA.

protease inhibitors
These drugs block a protein that infected cells need to put together new HIV virus particles.

29
Q

What stage of the HIV-life cycle does an entry/fusion inhibitor affect?

A

Stage 1: virus receptor binding
stage 2: virus uncoating and entry of RNA and proteins into CD4+ (helper) lymphocyte t cell

30
Q

What stage of the HIV-life cycle does an RT inhibitor affect

A

Stage 3: viral DNA transcription using reverse transcriptase

31
Q

What stage of the HIV-life cycle does an integrase inhibitor affect?

A

stage 4: prevents integration of viral DNA into host genome

32
Q

Which stage of the HIV life cycle does a protease inhibitor affect?

A

stage 5
prevents generation of new viral proteins

stage 6
prevents assembly of viral proteins and RNA at the CD4+ (helper) T lymphocyte cell membrane

33
Q

What are the two types of RT inhibitor?

A

NRTIs
causes DNA chain termination, analogue of dNTPs

NNRTIs
direct inhibitor of HIV reverse transcriptase

34
Q

How can the formation of mature viral particles be prevented?

A

protease inhibitor drugs

35
Q

What is the first line treatment for HIV

A

combination therapy
2 NRTIs
1 NNRTI/PI/INI

36
Q

How can viral load be decreased in HIV infections in pregnancy?

A

Integrase inhibitor drug

37
Q

How is transmission of an HIV infection from mother to child prevented?

A

Antenatal screening

38
Q

Who is PrEP medicine intended for?

A

HIV negative individuals who are at risk of HIV infection, currently only TRUVADA available

39
Q

How much as a % does PrEP treatment reduce HIV infection by?

A

> 90%

PM3A (36 decks)

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