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Patho > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

1
Q

When did HIV begin?

A

1981 - initially called GRID - gay related immune deficiency

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2
Q

Who are over 50% of new infections transmitted by?

A

People who are unaware of their HIV status
** why encouraging the public to know their HIV status is a critical public health initiative

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3
Q

What populations are most affected by HIV infections in Canada?

A
  1. Men who have sex with men
  2. Injection drug users
  3. Aboriginal people
    **Aboriginal people overrepresented in Canada’s HIV epidemic = rate of new infections 2.7x higher than other groups
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4
Q

What is the largest population of people living with HIV?

A

Globally 38.4 million people living with HIV
Largest population is sub-Saharan Africa = 69% of all global HIV infections

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5
Q

Compare and contrast HIV-1 and HIV-2.

A

Similarities: both have similar structure and function
Differentiated by: envelope glycoproteins, point of origin, latency period

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6
Q

Where is HIV-1 found? Where was it believed to have originated?

A

Central Africa **origin
North America,
Europe,
Australia

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7
Q

What are the major classes of HIV-1?

A

M = main
N = new
O = outlier
+/- P = newest class

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8
Q

Where is HIV-2 found and what are the diseases general characteristics?

A

Found primarily in West Africa
1. milder disease
2. less virulent
3. longer latency period,
4. no clades

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9
Q

What are clades?

A

Distinctive branches or subtypes that HIV can be further divided into
- HIV has lots of clades due to the rapid rate of mutation
* individuals can be infected with more than one clade of HIV

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10
Q

How many clades are within HIV-1?

A

9 clades within the 3 main classes

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11
Q

What fluids can HIV be transmitted by? (5)

A
  1. Blood
  2. Semen
  3. Pre-ejaculate
  4. Vaginal secretions
  5. Breast milk
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12
Q

HIV transmission is a result of what?

A

Exposure to body fluids of infected individuals
Nature of exposure = risk of infection

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13
Q

What are the 3 main modes of HIV transmission?

A
  1. Sexual contact
  2. Blood contact
  3. Vertical/mother-to-child transmission (MTCT)
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14
Q

What are the 3 types of sexual contact that can result in HIV transmission?

A
  1. Anal sex - homo or heterosexual, higher risk of tearing/injury
  2. Vaginal sex
  3. Oral sex - oral lesions & contact with infections semen/secretions
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15
Q

What age group is more vulnerable to contacting HIV through vaginal sex and why? (3)

A

Young women, 13-25 yr are more vulnerable due to:
1. immature genital tract mucosa = less reliable mucous production = higher risk of injury
2. More likely to practice unsafe sex
3. Less likely to seek out or access healthcare

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16
Q

What are 3 categories of transmission under blood contact? Give examples of each.

A
  1. Injections/needles - sharing needles, needle stick injuries, infected tattoo/skin piercing instruments
  2. Contact with broken skin - sports, occupational hazard, developing countries
  3. Transfusions or transplant of infected organs or tissues - higher incidence in developing countries
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17
Q

When can MTCT or vertical transmission occur?

A

Pregnancy
Delivery
Breastfeeding

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18
Q

What 6 factors influence vertical transmission of HIV?

A
  1. Stage of infection
  2. Breastfeeding pattern
  3. Oral lesions in baby or breast lesions in mother
  4. GI illness
  5. Antiretroviral therapy
  6. Invasive procedures
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19
Q

How does stage of infections influence risk of vertical transmission?

A

Higher viral load occurs early in infection = increased risk of transmission = if an infection occurs during of just before pregnancy

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20
Q

How does breastfeeding pattern influence vertical transmission of HIV?

A

Breastfeeding patterns: exclusive vs mixed
- Exclusive has decreased risk than mixed
- Risk of transmission increases with duration of breastfeeding

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21
Q

How do oral or breast lesions influence vertical transmission of HIV?

A

Oral lesions in baby or breast lesions in mother = increase risk due to:
- increased portals of entry
- increased exposure to blood

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22
Q

How does GI illness in baby influence vertical transmission of HIV?

A

GI illness = weakened gut = increased portals of entry for virus in breastmilk

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23
Q

How does antiretroviral therapy (ART) influence vertical transmission of HIV?

A

ART significantly decreases risk during of transmission during pregnancy & labour/delivery

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24
Q

How do invasive procedures influence vertical transmission of HIV?

A

Ex. of invasive procedure = use of forceps during delivery
– can cause increased portals of entry and increase blood exposure

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25
Q

What virus family does HIV belong to?

A

Retrovirus family: viruses that carry their genetic material in the form of RNA and use the reverse transcriptase enzyme to convert RNA into viral DNA

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26
Q

What genus does HIV belong to?

A

Lentivirus genus: viruses (within the retrovirus family) that
- affect the nervous and immune systems
- have long latency periods
- have persistent viremia
- have more complex genome structure than other retroviruses

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27
Q

Describe the main elements of HIV’s structure.

A
  1. Envelope - gp120 spikes with gp41 stems
  2. Core - bullet shaped, surrounded by the capsid
  3. Within the core
    - 2 identical strands of RNA
    - 3 critical enzymes: reverse transcriptase, integrase, protease
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28
Q

Where can HIV be found at any given time? (5)

A
  1. Mucous membranes - macrophages & dendritic cells
  2. Actively infected CD4 lymphocytes
  3. Latently infected CD4 lymphocytes (can be latent for 2 years)
  4. Memory CD4 cells
  5. Floating or “free” virus
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29
Q

What are the ‘sanctuary sites’ of HIV? (2)

A
  1. Brain & CNS
  2. Immune system
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30
Q

What are the vulnerable target cells for HIV?

A

Uninfected but activated CD4 cells - they become infected when they arrive at the site of injury

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31
Q

Describe HIV’s summary of infection and what the result of that is.

A
  1. Portal of entry
  2. Virus taken up by macrophages +/- T-helper cells
  3. Virus replicates
  4. Either become latent or is released
  5. If released (cytolysis of infected cell facilitates virus release)
    - increased viral load in blood,
    - loss of B cell function
    - immunodeficiency – opportunistic infections
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32
Q

What are the target cells for HIV?

A

** any cell that has CD4 receptors – T-helper cells, dendritic cells, microglia

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33
Q

Explain the receptors and co-receptors that are required for HIV to bind to host cells.

A

gp120 protein spike binds to CD4 receptors
co-receptors are required for different cell types:
- CCR5: co-receptors for binding to macrophages (are m-trophic)
- CXCR4: co-receptors for binding to T-helper cells (are t-trophic)

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34
Q

When do certain cell types become infected?

A

Macrophages become infected during early stages of infection
T-helper cells become infected during later stages of infection

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35
Q

What are the three phases of the HIV course of infection?

A
  1. Acute primary HIV infection phase
  2. Chronic asymptomatic or latency phase
  3. AIDS phase
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36
Q

How long is the progression of infection in an untreated person?

A

8-12 years

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37
Q

Define the acute primary HIV infection phase.

A

–> the time from initial infection to development of a detectable antibody response
usually 6-8 weeks

38
Q

What lab results occur early in the acute infection phase?

A

In first 2 weeks:
- large amount of viral replication = increased viral load
- decreased CD4 count

39
Q

What is peak viremia?

A

The mild flu-like symptoms (most experience rash to trunk) that occur 10-25 days after exposure and last 1-2 weeks

40
Q

What is seroconversion?

A

The point in the acute phase where the immune system starts controlling viral replication = antibodies are present
– occurs 3 weeks to 3 months after infection (depending on health of person)

41
Q

What is the window period or lag time?

A

The time between exposure and seroconversion where the person is infection but doesn’t have antibodies yet
- would give a false negative test

42
Q

What is the viral set point?

A

The amount of virus that’s present after initial viremia and seroconversion (immune control) after

43
Q

What important information does the acute phase tell providers?

A

The events of the primary infection = duration & intensity of symptoms –> important indicators of the individual’s disease course

44
Q

Describe the chronic asymptomatic or latency phase of infection.

A

Where individual has stable viral load and doesn’t have signs or symptoms

45
Q

What does ‘stable viral load’ mean?

A

When the number of newly infected cells equals the number of cells that die from infection

46
Q

What happens to the CD4 count during the chronic asymptomatic phase?

A

CD4 count drops by 50-90 cells/microL per year = this accelerates over time

47
Q

What is the median time for the latency phase?

A

In an untreated person = 10 years

48
Q

What does the AIDS phase typically present with? (3)

A
  1. Opportunistic infections
  2. Secondary neoplasms/cancer
  3. Wasting syndrome
49
Q

What are examples of opportunist infections that can occur during the AIDS phase?

A
  • Karposi’s sarcoma
  • lymphoma
  • varicella
  • bacterial & pneumocystis pneumonia
  • TB
  • toxoplasmosis
  • cytomegalovirus (frequently occurs at end of life for AIDS patients)
50
Q

Define wasting syndrome.

A

Unintended weight loss of >10% body weight – resulting in weakness, diarrhea, nutritional deficiencies

51
Q

What is the CD4 count of a person in the AIDS phase?

A

< 200 cells/microL

52
Q

What diagnostic information does the CDC use for staging HIV infections?

A
  • CD4 count
  • symptoms (more in developing countries)
53
Q

What is a normal CD4 count?

A

1000-1200 cells/microL

54
Q

What are the 3 stages and their CD4 counts that the CDC uses?

A

Stage 1: no significant immunocompromise = CD4 > 500
Stage 2: advanced immunocompromise = CD4 200-499
Stage 3: severe immunocompromise (AIDS) = CD4 < 200

55
Q

Why is CD4 count useful in HIV staging?

A

** determining degree of immunocompromise
- can be used to reinforce clinical decision-making
- long-term prognosis is related to lowest measured CD4 count

56
Q

What is important to note about CDC stages?

A

They can be downgraded but not upgraded – aka you can get worse but not better

57
Q

What factors influence the time it takes for the immune system to create HIV antibodies? (4)

A
  1. genetics
  2. how transmission occurred
  3. the amount of virus person was exposed to
  4. if post-exposure prophylaxis occurred
58
Q

What are 3 methods of screening for HIV?

A
  1. Point of care (POC)/rapid HIV testing = looks for antibody presence (seroconversion)
  2. 3rd generation EIA (enzyme immunoassay)
  3. Home test kit
59
Q

What confirmatory tests are used for HIV?

A

Is a 2-step process
Step 1: 4th generation EIA - if positive = proceed to next step
Step 2: western blot - gold standard

60
Q

What test is used for acute HIV infection testing? Who is it used for?

A

P24 antigen test to diagnose acute infection - detects viral RNA in plasma
- used for high-risk exposures, high risk populations, infants

61
Q

When can the p24 antigen test be used?

A

As early as 2-3 days after symptoms start
Peaks at 3-4 weeks after exposure

62
Q

What is the P24 antigen test called in BC?

A

RNA NAAT

63
Q

What are 4 important lab values that are monitored

A
  1. CD4 count
  2. CD8 count
  3. CD4/CD8 ratio
  4. Viral load
64
Q

What happens to CD4 count 6 months after seroconversion?

A

CD4 count drops by ~30%

65
Q

What happens to CD8 count 6 months after seroconversion?

A

CD8 count rises by ~40%

66
Q

What is the normal CD4/CD8 ratio?

A

Person without HIV, ratio > 1 = usually 4:1

67
Q

What is the CD4/CD8 ratio in HIV positive individual? What is the result?

A

ratio < 1 – usually 0:08
Result – less CD4 cells to activate CD8 cells = less able to activate cell-mediated immunity = it’s less effective

68
Q

What is viral load reported as?

A

** the actual amount of free virus in the plasma
Reported as # of virus copies detected in 1ml

69
Q

What are 3 tests that can measure viral load?

A
  1. HIV RNA amplification (RT-PCR) test
  2. Branched chain DNA (bDNA) test
  3. Nucleic acid sequence based amplification assay (NASBA)
70
Q

How is baseline viral load measured?

A

2 measurements 2-4 weeks apart after positive serology test
- continue monitoring every 3-4 months

71
Q

What is baseline viral load used to determine?

A
  • when to start antiretroviral therapy
  • making adjustments to ART
72
Q

What does viral load tell us?

A
  1. relationship between the virus & rate of disease progression
  2. rate of viral turnover
  3. relationship between immune system activation & viral replication
73
Q

What happens to CD4 and CD8 counts as viral load increases?

A

CD4 decreases
CD8 increases

74
Q

What are the 5 categories of antiretroviral drugs?

A
  1. Fusion inhibitors
  2. Protease inhibitors
  3. Reverse transcriptase inhibitors
  4. Integrase inhibitors
  5. Co-receptor inhibitors
75
Q

How do fusion inhibitors work?

A

Inhibits ability of virus to fuse with host cells by binding to gp41 - becomes rigid & can’t make configurational change
** enfuviritide (fuzeon) or T20

76
Q

How to protease inhibitors work?

A

Blocks protease enzyme which blocks viral assembly
** atazanavir (Reyataz)
side effects: lipodystrophy & hyperglycemia

77
Q

What are the two types of reverse transcriptase inhibitors?

A
  1. Nucleoside reverse transcriptase inhibitors (NRTIs) = nukes
  2. Non-nucleoside reverse transcriptase inhibitors (NNRTIs) - non-nukes
78
Q

How do nucleoside reverse transcriptase inhibitors work?

A

Blocks reverse transcriptase = premature termination of DNA strand
Side effects: lactic acidosis, hepatomegaly
** AZT or ABC

79
Q

How do non-nucleoside reverse transcriptase inhibitors work?

A

Bind to reverse transcriptase = prevents conversion of RNA to DNA
side effects: rash
** delaviridne (rescriptor)

80
Q

How to intgrase inhibitors work?

A

Stops transfer of viral RNA into host DNA
** kaltegravir (isentress)

81
Q

How do co-receptor inhibitors work?

A

CCR5 Antagonist - blocks co-receptor to prevent fusion of virus to host cell
** maraviroc (celsentri)

82
Q

What are the treatment recommendation and clinical stages from the BC centre for excellence in HIV/AIDS?

A
  • if symptomatic or have CD4 < 500 = start treatment
  • if asymptomatic with CD4 > 500 but have risk factors = start treatment
83
Q

What 5 risk factors are considered by the BC Centre for Excellence in HIV/AIDS when starting treatment?

A
  1. Increased risk of disease progression
  2. Age > 50
  3. HIV-associated kidney disease
  4. Pregnancy
  5. Risk of HIV transmission
84
Q

What is the first indication of success HIV treatment via antiretrovirals?

A

Decrease in viral load

85
Q

How is the efficacy of HIV ART monitored?

A

Regular assessment of viral load and CD4 count
– checked at 4 weeks, then every 4-8 weeks until suppression is achieved, then every 3-4 months for the first year

86
Q

How is the ART concentration in the blood monitored and what is it used for?

A

Peak & trough values
Used to:
- predict toxicity
- max efficiency
- evidence of adherence

87
Q

What are some of the reasons why ART may fail to suppress viral replication? (5)

A
  1. Incomplete adherence
  2. Poor absorption
  3. Toxicity/side effects = pts lowering or missing doses
  4. Pharmacokinetic interactions
  5. Infected with resistant viruses
88
Q

What are some of the long-term side effects of ART? (7)

A
  1. Kidney problems
  2. Liver problems
  3. Decreased bone density
  4. Skin rash
  5. Nerve problems
  6. Pancreatitis/diabetes
  7. Changes in fat metabolism
89
Q

What information do we know about ‘curing’ HIV?

A
  1. Only 5 people globally have been cured
  2. Difficult to determined if ‘cured’ due to long latency period
  3. Cure was: person had blood cancer, underwent stem cell transplant from donor with CCR5 mutation
90
Q

What is HIV resistance testing useful to determine?

A
  1. What drugs not to use in patients with increasing viral loads despite therapy
  2. Used in previously untreated individuals who may be infected with resistant HIV strain
    ** similar to C&S testing for bacteria

Patho (9 decks)

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