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Pathophysiology > HIV > Flashcards

HIV Flashcards

1
Q

When did HIV begin?

A

1981 - initially called GRID - gay related immune deficiency

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2
Q

Over 50% of new infections are transmitted by…?

A

People unaware of their HIV status

That is why it is a critical public health initiative to know your HIV status

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3
Q

What populations are most affected by HIV infections in Canada?

A

Men who have sex with men

Injection drug users

Indigenous people

**Indigenous 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 are the 3 methods of HIV transmission?

A
  1. Blood contact
  2. Sexual contact
  3. Mother to child transmission
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12
Q

What is HIV transmission a result of?

A

Exposure of bodily fluid of infected person, nature of exposure relates to risk of infection

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13
Q

Describe how HIV is transmitted through sexual contact

A
  1. Anal sex - homo or heterosexual, highest risk of tearing/injury, receptive or insertive anal sex
  2. Vaginal sex
  3. Oral sex - oral lesions & contact with infections semen/secretions
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14
Q

Which age group is most at risk for contacting HIV through vaginal sex?

A

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

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15
Q

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

A
  1. Injections/needles
    eg: sharing needles, needle stick injuries, infected tattoo/skin piercing instruments
  2. Contact with broken skin
    eg: exposure through sports, occupation hazard, developing countries
  3. Transfusions or transplants of infected organs/tissues (higher risk in developing countries)
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16
Q

When can MTCT or vertical transmission occur?

A

Pregnancy
Delivery
Breastfeeding

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17
Q

What 6 factors influence MTCT vertical transmission of HIV?

A
  1. Stage of infection
  2. Breastfeeding pattern
  3. Oral or breast lesions
  4. Gastrointestinal illness
  5. Antiretroviral therapy
  6. Invasive procedures
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18
Q

How does stage of infections influence risk of vertical transmission?

A

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

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19
Q

How does breastfeeding pattern influence vertical transmission of HIV?

A

Breastfeeding patterns: exclusive vs mixed
- Exclusive has decreased risk than mixed in developing countries because of unreliable water sources/formula

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20
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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21
Q

How do GI illnesses in babies influence vertical transmission of HIV?

A

In a baby who has a weakened gut there may
be increased portals of entry for the virus
found in breast milk

+ risk of ulcerations

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22
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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23
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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24
Q

What is HIV not transmitted through?

A

Tears, sweat, saliva, vomit, faces or urine

They may contain HIV but not in enough amounts to cause an infection

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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? (6)

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
  6. Sanctuary state in brain or CNS where ART cannot find
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29
Q

What are the sanctuary sites of the HIV?

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

What cells are a vulnerable target for HIV?

A

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

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31
Q

Describe the summary of events for IV infection

A
  1. Portal of entry
  2. Virus is taken up by macrophages or CD4 cells
  3. Virus replicates and either
    a) becomes latin or
    b) buds out of the cell
  4. IF it buds out, it increased the overall viral load in blood AND cytolysis the infected less
  5. This leads to immunodeficiency, loss of B cell function and opportunistic infection
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32
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, early stages of infection (are m-trophic)

  • CXCR4: co-receptors for binding to T-helper cells, later stages of infection (are t-trophic)
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33
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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34
Q

Why is CD4 testing useful?

A

It’s used to determine the degree of immunocompromised, the more it decreases the more further progressed the disease is

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35
Q

What is HIV staging based on?

A
  • CD4 and T lymphocyte count
  • Count takes precedence over percentage, percentage only used if count is missing
  • If no CD4 results available, stage is unknown
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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

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
38
Q

Describe the acute primary HIV infection phase.

A

Time from infection to detectable response time (6-8 weeks)

Increase in viral replication, decrease in CD4 count during first 2 weeks

S/S appear 10-25 days after exposure, last 1-2 weeks

39
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

40
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

41
Q

What is seroconversion?

A

The point in the acute phase where the immune system starts controlling viral replication = antibodies are present due to macrophages presenting HIV antigens to CD4 which triggers B cells to produce HIV antibodies

AT THE SAME time, CD8 cells are targeting infected host cells

– occurs 3 weeks to 3 months after infection (depending on health of person)
- Antibodies are present

42
Q

What is the window period or lag time

A

The time between exposure and seroconversion where the person is infected but doesnt have antibodies yet (false negative tests)

43
Q

What is viral set point?

A

Amount of virus that is present after the initial burst of viremia and the immune control that follows

44
Q

What information does the acute phase tell providers

A

Events of the primary infection including duration and intensity of symptoms, high/low viral set point gives intel into how the disease will progress

45
Q

Describe the chronic asymptomatic or latency phase of infection.

A

No signs or symptoms and/or lymphadenopathy in 2 locations

Stable viral load

46
Q

What is a stable viral load?

A

When the number of new infected cells equals the number of cells dying

Eventually, the CD4 lymphocyte replenishing system will begin to fail

47
Q

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

A

CD4 count drops by 50-90 cells/microL every year, accelerating overtime

If it changes more, should be looked into

48
Q

What is the median time for latency?

A

10 years

49
Q

What are 4 characteristics of the overt AIDS phase?

A
  1. CD4 count below 200
  2. Opportunistic infection
  3. Secondary neoplasms
  4. Wasting syndrome
50
Q

What is wasting syndrome?

A

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

51
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)
52
Q

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

A

< 200 cells/microL

53
Q

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

A
  • CD4 count
  • symptoms (more in developing countries
54
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
55
Q

What are 3 methods of screening for HIV?

A
  1. POC rapid testing - looks for antibody presence (seroconversion)
  2. 3rd gen EIA (enzyme immunoassay)
  3. Home test kit
56
Q

What confirmatory tests are used for HIV SCREENING?

A
  1. Screen using 4th gen EIA

if positive:

  1. Western blot (GOLD standard)

This test is expensive + more sensitive for detecting presence of antibodies

Can still have false negative in lag time

57
Q

Who is a long term non-progressor?

A

Someone who develops normal immunity without ART
* Remains AIDs free/symptoms free
* Stable CD4 count
* Survival longer than 25 years

58
Q

How is Acute HIV infected tested for?

A

P24 antigen test diagnoses acute infection by checking for RNA in plasma, can detect 2-3 days after symptoms starts

  • used for high-risk exposures, high risk populations, infants
59
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

60
Q

What 4 important lab values are monitored?

A
  1. CD4 count
  2. CD8 count
  3. CD4/CD8 ratio
  4. Viral load
61
Q

What happens to CD4 count 6 months after seroconversion?

A

CD4 count drops by ~30%

62
Q

What happens to CD8 count after 6 months of seroconversion?

A

Rises by 40%

63
Q

What is the normal CD4 : CD8 ratio?

A

In someone without HIV
4 : 1

64
Q

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

A

Ratio is usually less than 1

Usually 0.08 meaning LESS CD4 than CD8

Meaning less able to activate cell mediated immunity (less effective)

65
Q

What is viral load reported as?

A

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

66
Q

What 3 tests measure viral load?

A
  1. HIV RNA amplication test (RT-PCR)
  2. Branced chain DNA (bDNA)
  3. Nucleic acid sequence based amplifcation assay (NASBA)
67
Q

How is baseline viral load measured?

A

2 measurements 2-4 weeks apart after positive serology test

Monitor every 3-4 months

68
Q

What does baseline viral load determine?

A
  • When to start antiretrovial therapy
  • Adjustments to ART
69
Q

What does the viral load tell us?

A
  1. Relationship between virus and rate of disease progression
  2. Rate of viral turnover
  3. Relationship between immune system activation and viral replication
70
Q

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

A

CD4 decreases
CD8 increases

71
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
72
Q

When should ART be offered?

A

Immediately during ACUTE phase of primary HIV infection regardless of symptoms or CD4 count

73
Q

How do fusion inhibitors work?

A

Inhibotrs ability of viral to fuse to host cells by binding to gp41 and making it rigid (can’t conform)

Acts like the lock

74
Q

How do protease inhibitors work?

A

Blocks protease enzyme which blocks viral assembly

** atazanavir (Reyataz)
side effects: lipodystrophy & hyperglycemia

75
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
76
Q

How do nucleoside reverse transcriptase inhibitors work?

A

Blocks reverse transcriptase = premature termination of DNA strand

Side effects: lactic acidosis, severe hepatomegaly
** AZT or ABC

77
Q

How do NON-nucleoside reverse transcriptase inhibitors work?

A

Drug binds directly to the enzyme RT and prevents conversion of RNA to DNA

S/E: rash

78
Q

How do integrase inhibitors work?

A

Stops transfer of viral RNA into host DNA

79
Q

How do co-receptor inhibitors work?

A

Prevent fusion of virus and host cell membrane by blocking CCR5 receptors

80
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. Older than 50
  3. HIV associated kidney disease
  4. Pregnancy
  5. Risk of HIV transmission
81
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

OR

If asymptomatic and CD4 count > 500 BUT have risk factors

82
Q

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

A

Decrease in viral load

83
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 supression is acheived, then every 3-4 months for the first year
84
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

85
Q

What is the combo of initial regimen that is reccommended?

A

A nucleoside reverse transcriptase inhibitor and a NON nucleoside reverse transcriptase

86
Q

When would someone receive PrEP

A

Pre-exposure prophylaxis is given when someone is deemed clinically at risk

87
Q

Why might ART fail to suppress viral replication?

A
  1. Incomplete adherance
  2. Poor absorption
  3. Toxicity/SE (lowered or missed dose)
  4. Pharmokinetic interaction
  5. Infected with resistent virus
88
Q

What are the long term side effects of ART (list 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 is HIV resistance testing useful to determine?

A
  1. What drugs to not use in patients with increasing viral loads despite ART
  2. Used in previosuly untreated individuals who may be infected with resistant HIV strain
90
Q

What do we know about curing HIV?

A
  1. Only 5 people have been cured
  2. Cure is difficult to decide on since there is a long latency period
  3. Cure ex: person had blood cancer and had stem cell transplant from someone with a CCR5 mutation

Pathophysiology (9 decks)

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