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MultiSystems 1 > HIV > Flashcards

HIV Flashcards

1
Q

What type of virus is HIV? Other features

A

Retrovirus

  • single stranded
  • positive-sense
  • enveloped
  • genus: Lentivirus
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2
Q

What is the main effect of HIV?

A

CD4+ T cell depletion

<500 = AIDS

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3
Q

What is HIVs mechanism of attacking CD4+ T cells?

A
  1. CD4 binding
  2. Co-receptor binding on chemokine receptor:
    - CCR5 OR
    - CXCR4
  3. Fusion, including integration of proviral DNA
  4. Budding
  5. Maturation
  6. New HIV virion

Usually first infect cells like dendritic cells, which will take virus to lymph nodes and cause immune reaction. Infects CD4 T cells and monocytes in lymphoid tissue which go everywhere else.

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4
Q

What are the key types/subtypes?

A 
HIV1:
Group M (A-K)
Group N
Group O
Group P

HIV2
- less virulent/infective/prevalent

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5
Q

Transmission

A
  • Sex - rectal or vaginal
  • IV drugs
  • IV infected blood/blood products
  • Vertical
  • Others
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6
Q

Most common symptoms of primary HIV infection (in descending order)

A
  • fever
  • fatigue
  • rash
  • headache
  • lymphadenopathy
  • pharyngitis
  • myalgia/arthralgia
  • diarrhoea
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7
Q

How many cases asymptomatic?

A

40-90%

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8
Q

How soon can HIV anti-body be detected?

A

22-27 days post infection

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9
Q

How soon can HIV RNA be detected in plasma?

A

1-3 weeks before antibody

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10
Q

What is the difference between early (Acute) vs chronic infection?

A

Early:

  • CD4+ T cell depletion, especially in gut
  • This will then recover quickly
Chronic:
Immune activation and inflammation in lymphoid tissues caused by:
- Macros/monos
- Dendritic cells
- CD4+ T cells
Slow decrease over time
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11
Q

What are the different stages/symptoms?

A
  1. Seroconversion
    - Fever
    - Myalgia
    - Arthralgia
    - Adenopathy
    - Malaise
    - Rash
    - Meningitis
  2. Asymptomatic or non-OI disease
    - Thrombocytopenia
    - Reactive arthritis
    - Polymyositis
    - Bell’s Palsy
    - CIDP
  3. Mucutaneous OIs
    - Deb. dermatitis
    - Warts
    - Molluscum
    - HZV
    - HSV
    - Candidiasis
    - Hairy Leukoplakia
    - TB
  4. Severe OIs (AIDS, stage IV)
    - Pneumocystosis
    - Toxoplasmosis
    Cryptosporidosis
    - Cryptococcosis
    - MAC
    - CMV
    - Kaposi’s Sarcoma
    - Lymphoma
    - Cervical Cancer
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12
Q

Other pathogens causing disease as a result of HIV-induced immunodeficiency

A
  • herpes
  • Heps
  • HPV
  • TB
    • Strep pneumoniae
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13
Q

What cancers are HIV patients more prone to?

A
  • Kaposi’s sarcoma - HHV-8
  • Lymphoma - EBV

  • Primary cerebral lymphoma - EBV

  • Carcinoma of cervix/anus – HPV
  • Smooth muscle tumours – EBV

Note: infection-related cancers higher in HIV than transplant recipients

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14
Q

Why does HIV make them more prone to these viruses?

A

CD4 T cells – interferon gamma (chronic interferon activation, therefore chronic inflammatory disease) – activate macrophages etc.

If no CD4s, macrophages can’t work Also CD8s can’t work properly – therefor viral infections such as EBV, CMV. Therefore more prone to cancers relating to viruses.

Path:

  • HIV Replication
  • CD4+ depletion, particularly in GALT (gut associated lymphoid tissue)
  • Transloctaion of microbial products from gut AND HIV replication cuases immune activation and inflammation in lymphoid tissue
  • This results in depletion of naive T cells, memory B cells and NK cells. B cells persistently stimulated and less likely to deal with pathogens.
  • Immune activation/inflammation also results in non AIDS HIV disease:
  • atherosclerosis
  • osteoporosis
  • Type 2 diabetes
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15
Q

What neuro diseases can HIV cause?

A

Encephalopathy (brain)
- HIV-associated neurocognitive defect (HAND)
• Dementia when severe

Myelopathy (spinal cord)
- Spastic parapareisis

Neuropathy (peripheral nerves)

  • Distal symmetric polyneuropathy (DSPN)
  • Mononeuropathy multiplex
  • Chronic inflammatory demyelinating polyneuropathy (CIDP)
  • Progressive lumbosacral polyradiculopathy
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16
Q

MISC HIV diseases:

A
  • Thrombocytopaenia
  • Nephropathy
  • Primary pulmonary HT
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17
Q

What is the problem of HIV latent reservoir?

A

Latent infected CD4+ T cells

They aren’t replicating so can’t be targeted by treatments

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18
Q

Effects of smoking and HIV?

A

HIV significantly affects mortality in HIV patients

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19
Q

Treatment interruption

A

Results in more hIV and non-HIC associated disease outcomes and death

Meds even reduce things like CVD risk:

  • frailty and bone disease
  • liver disease
  • diabetes
  • cognitive decline and dementia risk
  • CVD
  • Cancer risk
  • Immune Senesence
20
Q

Why does HIV affect bone aging?

A

Twice rate of osteopenia and OP due to high bone turnover

Osteoclasts driven by B cell s which are persistently activated in HIV infection.

NOT entirely stopped by treatment

21
Q

How does HIV increase CVD risk?

A

Chronic inflammatory state - vascular and endothelial dysfunction:

  • HT
  • Atherosclerosis
  • MI

This risk is reduced hugely by cessation of smoking but still higher than background population.

22
Q

How does HIV result in poorer fat profile?

A 
Due to virus, environment, genetics.
Adipose tissue and liver dysfunction:
- lipodystrophy
- insulin resistance
- dyslipidaemia
23
Q

Biomarkers

A
  • CD4 T cell counts
  • sCD163 - reduced only with aviremic HIV RNA level
  • sCD14 - not influenced by any level of HIV RNA level
  • CXCL10
24
Q

How effective is HIV treatment?

A

Effectively prevents AIDS

Limitations in preventing systemic inflammation and long term morbidities

25
Q

How due CD4 T cell counts change as disease progresses?

A

Stage I: Asymptomatic

  • Acute phase
  • Weeks 0-9
  • Large dip and then started ro recover

Stage II: Minor symptoms

  • Weeks
  • slight recovery in count

Stage III: Moderate symptoms

  • Over years
  • Count slowly declines
  • Stage IV: AIDS
  • 8+ years
  • faster CD4 Depletion

NOTE: viral load is the inverse of CD4 count

26
Q

What are the indications for HIV testing?

A

HIV Indicator disease (i.e. test for HIV if they have these diseases):

  • Any AIDS defining condition
  • TB
  • STI
  • HBV,HCV
  • Lymphomat5
  • Head and neck cancer
  • Anal and cervical CIN 2+
  • Unexplained thrombocytopenia, lymphopenia, neutropenia >4 weeks
  • Recurrent/multidermatomal Shingles
  • Severe psoriasis
  • Severe Dermatitis
  • Extensive warts/molluscum contagiosum
  • Florid/difficult fungal infections
  • Oral candida
  • Oral hairy leukoplakia
  • Necrotizing gingivitis
  • Constitutional symptoms with no other apparent cause
  • Mononucleosis type syndrome
  • Any unexplained retinopathy

Other indictaions:

  • IV drug users
  • Partners of these people
  • Men who have sex with men, and their female partners
  • People from high prevalence countries
  • Pregnant women
  • Blood products before 1985
27
Q

All asymptomatic MSM (men who have sex with men) should be tested for:

A

Pharyngeal swab, anorectal swab, first void urine:
- CT and GN

Serology:

  • Syphilis
  • HIV
  • Hep A,B,C
28
Q

How frequently should men be tested?

A

If any sexual activity in last 12 months:
- At least once a year

If unprotected anal sex, >10 partners in 6 months, group sex, drug use in sex, HIV positive:
- Up to 4 times a year

29
Q

How should anal swab/urine be collected?

A
  • Self collection of anal swab and urine sample is sufficient for asymptomatic patients
30
Q

How is HIV tested?

A

Combined p24 antigen and HIV 1/2 antibody test on blood

31
Q

Facts about p24 testing:

A
  • The p24 antigen test may become negative 2-6 weeks after exposure, /peaking around 3-4 weeks
  • Positive tests are subject to confirmatory tests and sometimes repeat blood collection may be needed e.g. Western blot Rapid test
  • It may take 2-3 weeks for symptoms to occur and the p24 and antibody test to become positive
  • The great majority of HIV infected patients will return a positive test by 6 weeks post exposure,
  • 3 months post exposure remains the recommended time for final testing
32
Q

Patterns of various markers

A
  • /HIV antibodies start to appear in small quantities around 2-3 weeks. Remain elevated forever
  • CD4s increase again and then decrease steadily over time
  • HIV RNA in blood peaks within first year and then drops, increading again slowly over time
  • P24 Ag similar to HIV RNA - peaks within first few weeks (2-3 weeks), then declines sharply, then increases steadily over time again
33
Q

Window periods for serum markers?

A

HIV RNA:
- 10 days (7-21)

p24 Ag:
-17 days (13-28)

HIV Ab:
- 22 days (18-34 days)

34
Q

/Pre-test counselling for HIV?

A
  • Reason for testing and risk assessment
  • Timing of risk and option of post-exposure prophylaxis (PEP)
  • Need for other STI and blood-borne virus testing
  • History of previous HIV testing
  • Confidentiality and privacy issues
    o Notifiable disease
    o Contact tracing if positive
  • Natural history of HIV and transmission info
  • Prevention of transmission and risk reduction through behavior change
  • Implication of a positive test result, including availability of treatment
  • Implications of a negative result
  • Explanation of the window period
  • General psych assessment and assessment of social supports in event of positive result
  • Logistics of tests – time taken for results to become available and method of delivering results
35
Q

Factors contributing to rapid RNA virus evolution?

A
  • Error-prone polymerases
  • Lack of proof-reading mechanisms
  • Magnitude of replication:
    o large burden of infected cells
    o generation time
  • Selective pressures
    o Drugs
    o Cellular and anatomic compartments
36
Q

Constraints on RNA virus evolution?

A
  • Requirements for adaptation to multiple tissues or hosts (eg, arboviruses)
  • Overlapping reading frames (eg, HBV)
  • RNA structure
  • Restriction of replication
    o Fitness
    o Latency
37
Q

Describe HIV1 Drug resistance:

A
  • Bell shaped curve – does not occur at 0 antiviral drug activity or 100% activity – so big problem with missed doses – adherence is a huge problem – literally can’t have any viral replication
  • Emergence of drug-resistant virus is an inevitable consequence of the failure to fully suppress HIV-1 replication.
  • Drug resistance leads to failure of antiretroviral therapy.
  • Using combination therapy prevents drug resistance
  • Requirement for high life long adherence
38
Q

What are the most common drug combos?

A 
o	2 (NRTI) RT inhibitors (reverse transcriptase) + integrate inhibitor 2 (NRTI)
o	RT inhibitors + NNRTI
o	2 (NRTI) RT inhibitors + boosted protease inhibitors
39
Q

What are the toxic effects of ART therapies?

A 
o	Pancreatitis 
o	Lactic acidosis 
o	Neuropathy 
o	Renal calculi
o	Subcutaneous fat wasting
o	Metabolic syndrome 
o	Hyperlipidemia
o	Systemic drug hypersensitivity syndromes
40
Q

Individual patient considerations when choosing antiretroviral drugs

A

o Adherence potential

o Risk factors for adverse drug effects
• HLA-B5701+ (if this genetic marker is present, then risk) (abacavir hypersensitivity syndrome)
• Renal dysfunction (tenofovir nephropathy)

o Other medical conditions
• TB, liver disease, cardiovascular disease, recreational drug use, pregnancy

o Pregnancy potential in women
o Co-infection with Hepatitis B virus
o Potential for infection by drug resistant HIV
o Potential for interactions between ART and other medications

41
Q

How effective are ART therapies?

A
  • > 80% of patients achieve suppression of HIV RNA to undetectable levels in plasma

Only need outpatient care 2-4 times/year

42
Q

ART for prevention?

A

96% in partners

43
Q

PrEP?

A

> 90%

Reverse transcriptase inhibitors

44
Q

Who are PrEP candidates?

A

• Men who have sex with men (MSM), transgender individuals, heterosexual men and women, IVDUs At Substantial risk of acquiring HIV infection:

  • HIV-positive sexual partner, pre-conception for women
  • Recent bacterial STI
  • High number of sex partners
  • History of inconsistent/no condom use
  • Commercial sex work
  • High-prevalence area or network
45
Q

Categories of treatment?

A
  • Integrase Inhibitors (Viral DNA needs to integrate)
  • Protease Inhibitors (Needed for budding to mature HIV virion)
  • Reverse Transcriptase Inhibitors
  • Fusion/entry inhibitors (i.e. virus needs to enter cell)
46
Q

What is the SOAP system in reference to HIV?

A 
-	Subjective
o	1.Does he understand the diagnosis?
o	2.When transmitted?
o	3.Primary HIV?
o	4.AIDS symptoms?
o	5.Past medical issues?
o	6.Current or recent sexual relationships? Mental state
-	Objective
o	1.Vital signs
o	2.Organ systems: - significant positives and negatives
o	3.Mental state
o	4.Results to date
  • Assessment
    o Individual – diagnosis, stage/severity, comorbidities
    o Public health implications
-	Plan
o	1.Further Ix
o	2.Referrals
o	3.Public health
o	4.Mental state
47
Q

SPIKES for breaking bad news

A
  • Setup
  • Perception – what do they already know? How were they prepared for the test?
  • Invitation – Ask if its okay to talk about it (readiness), or in front of their guests
  • K knowledge – plain English
  • Emotion – be empathetic
  • Summarize/strategy

MultiSystems 1 (1 decks)

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