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FAMILY, COMMUNITY AND PUBLIC HEALTH > HIV RELATED LECTURES[129/130][127/128][074][075][073][126] > Flashcards

HIV RELATED LECTURES[129/130][127/128][074][075][073][126] Flashcards

1
Q

What happens to the CD4 count and the viral load as HIV progresses?

A

CD4 count: decreases
HIV viral load: increases

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2
Q

What is a low CD4 count associated with?

A

An increase in opportunistic infections and tumors

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3
Q

Below what CD4 count do most AIDS diagnoses occur?

A

CD4 less than 200

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4
Q

what interventions can be done to prevent mother to child transmission?

A

Antiretroviral therapy
avoidance of breastfeeding
post exposure prophylaxis for baby (4 weeks on HAART - Highly active antiretroviral therapy)

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5
Q

what cancer is associated with HIV?

A

Kaposi’s sarcoma

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6
Q

what do we mainly use for monitoring and follow up of an HIV patient?

A

CD4 count and viral load every 3 months

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7
Q

what is the main aim of HAART?

A
  • does not cure, but extend life and increase QOL
    -suppresses HIV replication enough to have undetectable plasma viral load by 24weeks of treatment. Undetectable= untransmissible.
  • immune system is able to recover well on HAART, hence CD4 count increases which reduces opportunistic infections and certain malignancies
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8
Q

What family and genus does the HIV virus belong to?

A

Family: Retroviridae
Genus: Lentiviruses (lenti: slow, denoting slow progression of disease)

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8
Q

What family and genus does the HIV virus belong to?

A

Family: Retroviridae
Genus: Lentiviruses (lenti: slow, denoting slow progression of disease)

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8
Q

What family and genus does the HIV virus belong to?

A

Family: Retroviridae
Genus: Lentiviruses (lenti: slow, denoting slow progression of disease)

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9
Q

what enzyme does HIV possess that allows it to transcribe from ssRNA to DNA in order to integrate its genetic material into host cells?

A

Reverse transcriptase.

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10
Q

what are the 3 major structural genes possessed by HIV virion?

A
  1. env gene, coding for:
    env gp120: responsible for viral binding to host cells
    env gp41: mediates fusion of virus with host cell membrane
  2. gag gene, coding for gagp24 (core protein)
  3. Pol genes (polymerase) coding for:
    reverse transcriptase, protease, integrase
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11
Q

in what year was HIV identified?

A

1985

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12
Q

what is another name for HAART

A

CART (Combined antiretroviral therapy)

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13
Q

name a few conditions that happen as a result of immunodeficiency from the HIV infection

A
  • cryptococcal meningitis
  • kaposi’s sarcoma
    -oesophageal candida
  • herpes (Shingles)
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14
Q

How many types of HIV viruses are there?

A

HIV-1: INFECTS HHUMANS. the most widespread type is group M (can also be split into subgroups A-J, B being predominant in the west)

HIV-2: Simian immunodeficiency virus, infects non-humans (non pathogenic in their host species of origin)

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15
Q

Name the 3 clinical stages of an HIV infection

A
  1. Early, acute stage: primary HIV infection. inital rapid rise in plasma viremia, massive decrease ofCD4 cells in tissue, with only a slight decrease in blood.High levels of innate immune activation and inflammation. Non specific, flu like symptoms: myalgia, headache, rash, fever, fatigue, lymphadenopathy, GI symptoms. Self limiting, 2-4 weeks. Resolution of symptoms correlates with increase in blood CD8+ count, and a decline of plasma viremia coincides with it.
  2. Clinical latency stage:
    minimal to know symptoms. CD4 count slowly decreases. Towards the end of this period, patient gets constitutional symptoms of immunodeficiency start to show.
  3. OVERT AIDS:
    severe constitutional symptoms, opportunistic infections, neoplasms, and eventually, death.
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16
Q

state the steps of replication of HIV in CD4 cells

A
  1. binding to CD4
  2. fusion
  3. reverse transcription
  4. integration of viral DNA into human DNA
  5. Replication
  6. Assembly to form cell with HIV genetic material
  7. Budding, goes to infect more and more cells.
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17
Q

HIV gp120 uses what on the T cell as a receptor to bind to it?

A

CD4.

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18
Q

What on the T cell is used as a coreceptor for HIV?

A

CCR5 (Chemokine receptor 5), however some HIV viruses use CXCR4 (chemokine receptor 4 instead).
HIV tends to use CCR5 early in the course of the disease then use CXCR4 as the patient progresses to AIDS.

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19
Q

Name the 6 classes of anti-HIV drugs.

A
  1. entry inhibitors
  2. fusion inhibitors
  3. Nucleoside/ Nucleotide reverse transcriptase inhibitors
  4. Non Nucleoside/ Nucleotide reverse transcriptase inhibitors
  5. Integrase inhibitors
  6. Protease inhibitors
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20
Q

give an example of entry inhibitors and its mechanism of action. in which patients would this drug be ineffective?

A

Maraviroc, works by blocking the CCR5 (HIV co receptor on T cells). This drug would not work on people with HIV viruses that use CXCR4 as a coreceptor. Therefore, virus must be tested for tropism prior to prescription of maraviroc.

21
Q

give an example of fusion inhibitors

A

enfuvirtide

22
Q

give an example of Nucleoside/ Nucleotide reverse transcriptase inhibitors

A

Nucleoside RTI: Zidovudine (AZT)
Nucleotide RTI: Tenofovir

23
Q

give an example of Non- Nucleoside/ Nucleotide reverse transcriptase inhibitors

A

Efavirnez/ nevirapine/ etravirine

24
Q

give an example of integrase inhibitors

A

raltegravir

25
Q

give an example of protease inhibitors

A

ALL ARE BOOSTED WITH RITONAVIR, MOST POTENT PROTEASE INHIBITOR:
lopinavir, darunavir, saquinavir, fosamprenavir, tipranavir

26
Q

why is monotherapy not recommended? what should we use instead?

A

high rate of mutation, leading to drug resistance. a combination of antiretroviral drugs is required (HAART or CART).
Antimicrobial prophylaxis should be given to AIDS patients.

27
Q

which HIV patients should be given prophylaxis against pneumocystis pneumonia? when can it be stopped?

A

cotrimoxazole should be given to patients with a CD4 count below 200. it can be stopped whenwhen CD4 count is stable above 200

28
Q

how long should HIV patients be on HAART for?

A

lifelong, no breaks.

29
Q

what happens if patient decides to take a break from HAART?

A
  • Fall of CD4 below 200, development of AIDS
  • generating drug resistant virus
  • increased cardiovascular risk.
30
Q

when should antiretroviral drug resistance testing be performed?

A

prior to HAART and at each HAART switch if previous medication failed.

30
Q

when should antiretroviral drug resistance testing be performed?

A

prior to HAART and at each HAART switch if previous medication failed.

31
Q

Name the 3 HIV target cells

A
  1. MAINLY CD4 LYMPHOCYTES (CCR5 and
    CXCR4 coreceptors are also required for entry)
  2. macrophages
  3. APCs
32
Q

what are the 3 types of cells making up the CD4 pool?

A

Naive (prior to antigen exposure)
- central memory (log lived memory cells that recirculate among secondary lymphoid tissue)
- effector memory: reside in mucosal sites, mainly intestinal, primarily responsible for fighting infection

32
Q

what are the 3 types of cells making up the CD4 pool?

A

Naive (prior to antigen exposure)
- central memory (log lived memory cells that recirculate among secondary lymphoid tissue)
- effector memory: reside in mucosal sites, mainly intestinal, primarily responsible for fighting infection

33
Q

out of the 3 types of cells making up the CD4 pool, which contains CCR5 and therefore makes up the majority of HIV infected T cells?

A

Effector memory cells

34
Q

Describe the mechanisms by which HIV is able to evade the immune system

A
  • antigenic diversity, so escape CTL and neutralizing antibody responses
  • immunodominant epitopes hidden within gp41
    -down regulates antigen recognition on cell surface, so evades innate and adaptive immune responses
  • the virus finds a passage through dendritic cells and macrophages
  • HIV codes for negative regulatory factor, which manipulates the host’s cellular machinery to allow for infection.
35
Q

what happens to CD4 cells if HIV infection is not controlled in PHI stage?

A

CD4 are rapidly infected and killed by the virus. With chronic immune activation, memory cells become depleted. lack of CD4 cells impairs CTL responses, massive loss of effector memory cells in the gut. A tropism switch happens from CCR5+ to CXCR4+

36
Q

What does initial control of viremia during PHI stage indicate?

A

it is predictive of long term prognosis (slow progression to AIDS)

37
Q

Who are elite controllers?

A

A subgroup of HIV infected indivuals with chronic infection and levels of viremia less than 50 copies per ml

38
Q

name a few serological markers during HIV infection

A

p24 antigen, anti surface and antigp120 IgM during acute stage
anti=p24, antigp41, anti-gp 120 IgG

39
Q

how many drugs are given in HAART/ CART?

A

2 NRTI + 1 drug from other class (usually protease?)

40
Q

which bodily fluids could be potentially infectious for HIV?

A

Blood, bloody fluids
cerebrospinal/amitotic fluid
pericardial/ peritoneal
pleural/ synovial
semen/ vaginal/ breast milk

41
Q

single most effective mechanism to reduce HIV transmission?

A

male circumcision (reduces HIV target cells)

42
Q

what are other ways to prevent HIV transmission?

A

condoms, microbicides, pre and post exposure prophylaxis by giving ART (antiretroviral therapy) to HIV negative induvial

43
Q

how many hours post exposure will PEP be effective? what drug should be given?

A

72 hours only. after that there is no use in taking post exposure prophylaxis. post exposure prophylaxis with zidovudine(NucleosideRTI) is protective. British guidelines recommend 1st line:
Truvada (2NRTI) and Kaletra( a PI)

Four week course of 3 antiretroviral drug therapy (e.g., zidovudine and lamivudine

44
Q

What should mothers take to prevent transmission of HIV to baby?

A

3 drugs, start by week 24 (however if viral load is above 30,000, start by 2nd trimester). Transmission occurs mostly during delivery.
If the mother has undetectable VL by week 36, deliver vaginal. Avoid breast feeding.

45
Q

What are the two most effective TB drugs?

A

Isoniazid and rifampicin

46
Q

What class of HIV-1 M is predominant in the west?

A

B

47
Q

What does the gp120 of an HIV viral cell act on in the human body?

A

CD4 on T cells.

48
Q

How do we determine anti retro viral drug resistance? And when should we do it?

A

Before starting HAART, we should do anti retro viral drug resistance by performing GENETIC SEQUENCING (test for reverse transcriptase and protease gene). This should also be done upon switching drugs.

49
Q

In the UK, when is HIV tested for during pregnancy?

A

At the 12tg week, and again at the 28th week if there is a continuing risk of infection.

50
Q

What is the dictator of the possibility of transmission?

A

Plasma viral load

FAMILY, COMMUNITY AND PUBLIC HEALTH (10 decks)

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