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Patho II > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

1
Q

Retrovirus

A

An RNA virus that replicates by inserting a DNA copy of their genome into the host cell

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2
Q

HIV structure

A
  • Enveloped RNA retrovirus
  • Capsid: core that contains the RNA ( med research on interference with capsid)
  • Enzymes in the capsid carry out steps in the life cycle
  • Glycoproteins: spikes embedded in the envelope - they have an affinity for binding on CD4 receptors
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3
Q

Steps of viral replication

A
  1. HIV binds to CD4 cell. RNA, proteins & enzymes released
  2. HIV reverse transcriptase converts viral RNA into DNA.
  3. HIV DNA moves to nucleus & spliced into host’s DNA.
  4. HIV RNA moves out of the nucleus into cytoplasm & makes long chains of viral proteins & enzymes.
  5. Immature viral particle forms containing cellular & HIV proteins. Chains cut into smaller pieces by protease.
  6. Infectious viral particle ready to be released containing HIV RNA, viral proteins & enzymes.
    * *produce billions of new virus particles which can stay latent in the host DNA – undetectable unless they’re actively replicating
    * *copies “seed”: disseminate w/o detection
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4
Q

HIV and CD4 cells

A
  • Helper (CD4) cells coordinate & activate both B lymphocytes [antibody mediated] & cell-killing cytotoxic (CD8) lymphocytes [cell mediated]
  • Cell-mediated immune response copes with microbes located within cells.
  • HIV infects & destroys CD4 cells
  • Loss of cells leads to immune system collapse & HIV disease.
  • Decline in CD4 cells is used as a marker of the progression of HIV.
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5
Q

HIV and CD8 cells

A
  • Important in initial immune response to HIV & at latent stage
  • Kill infected cells that are producing virus
  • Secrete soluble factors that suppress HIV replication: block by occupying receptors necessary for the entry of certain strains of HIV into the target cell
  • New information shows two new strains of the HIV virus that target CD8 cells
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6
Q

HIV Immune function effects

A
  • CD4 cell: decreased lymphokine production loss of stimulus for t and b activation
  • CD8 cell: impaired cytotoxic activity; impaired feedback
  • Macrophages: decreased phagocytosis, less IL-1 production, impaired antigen presentation
  • B cells: diminished AB production

ALL THIS leads to increased susceptibility to opportunistic infection

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7
Q

HIV replication and mutation

A

Replication rate
Billions per day
99% of HIV in blood is from newly infected cells
30% of HIV in plasma replaced daily
Entire HIV population turnover Q14 days
High mutation rate
1 in 3 replication cycles: 3300 mutant viruses per day
½-life = 1-2 days
Extensive seeding occurs early in disease
“Sanctuary sites”
Dendritic cells of lymph nodes & glial cells of the CNS
HIV transported to CNS via macrophages: body doesn’t detect it

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8
Q

Transmissible body fluids

A 
Blood
Semen
Vaginal secretions
Breast milk                        
Cerebral spinal fluid          
Synovial fluid                     
Pleural & 
amniotic fluid
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9
Q

Transmission

A
  • Unprotected sex-oral, anal (more risky), vaginal
  • Blood to blood-sharing needles, occupational exposure, fighting, tattooing, body piercing, transfusions
  • Mother to newborn-in utero, childbirth, breast feeding
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10
Q

Risk factors

A

Sexual activity
Injection drug use
Recipients of blood products (1975-March 1985)
Hemophiliacs who received pooled plasma
Children of HIV-infected women
30% will be infected w/o Treatment
Breastfeeding is a possible route of transmission
Prenatal, intrapartum & postpartum AZT significantly decreases risk of HIV transmission from mother to child (29% to 2%)
Needlestick
Post-exposure treatment with zidovudine (Retrovir)

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11
Q

Transmission risk r/t activities

A

Receptive anal intercourse: 1/100 – 1/300
Insertive anal intercourse: 1/1000
Receptive vaginal intercourse: 1/1000
Insertive vaginal intercourse: 1/10,000
Receptive fellatio with ejaculation: 1/1000
Needlestick with infected blood: 1/300
Illicit drug use with needle sharing: 1/150
HIV infected blood donor: 95%
Screened blood (viral load testing): 1/1,000,000
HIV infected mother: 2%-40%

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12
Q

Factors that Increase risk

A
  • Acute infection, roughly the 12 weeks after contracting HIV, can increase transmission likelihood 26 times, raising a 1.43% risk to 37%—higher than 1 in 3. This is because viral load skyrockets during the acute phase.
  • Presence of other sexually transmitted infections (STIs) can amplify risk by as much as 8 times.
  • Exposure to gender inequality and intimate partner violence can raise a woman’s HIV risk 1.5 times.
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13
Q

Factors that decrease risk

A
  • Circumcision can lower heterosexual men’s risk by 60%.
  • Treatment as prevention, TasP, when HIV-positive people on meds maintain an undetectable viral load, can reduce transmission risk by 96%. Some research hints that the number may approach 100%.
  • Pre-exposure prophylaxis, PrEP, when HIV-negative people take daily med Truvada, can decrease risk by upwards of 92%, depending on adherence. Post-exposure prophylaxis, PEP, works similarly.
  • Condoms, according to the CDC, lower risk on average by 80%.
  • Forms of seroadaptation, such as having condomless sex only with people of your same sero status, can also lower risk, but the outcomes vary.
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14
Q

HIV testing

A

DNA HIV - Viral nucleic acid tests (12 days)

  • Polymerase Chain Reaction (PCR)
  • Nucleic acid sequence-based amplification
  • Branched chain DNA tests

Viral Culture

  • Highly specific but negative result meaningless
  • Not frequently used to diagnose HIV

Immunofluorescence Antibody Testing
- Alternative to Western Blot for confirmation of HIV infection

Urine & Saliva Serologic Testing

  • Urine EIA
  • Saliva EIA
  • Rapid Enzyme EIA

Home Testing: Fingerstick specimen sent to a laboratory

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15
Q

ELISA testing

A

Screener test
Enzyme Linked ImmunoSorbent assay (ELISA) determines response of antibodies to HIV virus
Used in children older than 18 months
High sensitivity but low specificity: many false positives

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16
Q

Western blot test

A

Confirms the presence of HIV antibodies
Useful in children older than 18 months of age
A positive HIV antibody test in children younger than 18 months of age indicates only that the mother is infected
More specific for HIV

17
Q

P24 antigen test

A

Indicates active replication

  • Used to detect HIV antigen in children younger than 18 months
  • Test can be useful at any age
  • Only a positive result is significant
  • Two or more positive results are diagnostic for HIV infection
18
Q

CD4+ test

A

Used to assess immune status, risk for disease progression, and need for PCP prophylaxis

+ Absolute CD4 count: Predictor of HIV progression - Monitor Immune Function
- incr. risk infection/malignancy if CD4<200 cells/mcL

+ CD4 Percentage count:

  • Predictor of HIV progression
  • Monitor Immune Function
  • Incr. risk infection/malignancy if CD4<200 cells/mcL
19
Q

Home HIV tests

A

Home Access HIV-1 Test system
Involves pricking one’s finger to collect blood and sending to lab. Anonymous. Manufacturer provides confidential counseling and referral for treatment.

OraQuick In-Home HIV Test
Involves swabbing mouth and using a kit in the home to test. Results in 20 min. If positive, need follow-up test. Counseling and referral included. Some false neg.

20
Q

Lab criteria for diagnosis

A

Positive result from an HIV antibody screening test (e.g., ELISA) confirmed by a positive result from a supplemental HIV antibody test (e.g., Western blot)
OR
Positive result or report of a detectable quantity from any of the following HIV virologic (i.e., non-antibody) tests:
- HIV nucleic acid (DNA or RNA) detection test (e.g., polymerase chain reaction [PCR])
- HIV p24 antigen test, including neutralization assay
- HIV isolation (viral culture)

21
Q

HIV S&S

A 
\+Acute Infection
-Mononucleosis-like syndrome
-Fever
-Rash
-Myalgia
-Malaise
Self-limited syndrome lasting ~6-8 weeks post-infection
Associated with development of HIV antibody

+ Asymptomatic Infection
Follows initial infection
Variable duration

+ Persistent Generalized Lymphadenopathy
Lymph node enlargement 1 cm or greater in two or more extra-inguinal sites
Adenopathy persists longer than 3 months

22
Q

HIV Staging

A

Stage 1

  • No AIDS-defining condition and either
  • CD4+ T-lymphocyte count of >500 cells/mcL or
  • CD4+ T-lymphocyte percentage of total lymphocytes of >29%

Stage 2

  • No AIDS-defining condition and either
  • CD4+ T-lymphocyte count of 200–499 cells/mcL or
  • CD4+ T-lymphocyte percentage of total lymphocytes of 14 - 28%

Stage 3 (AIDS)

  • CD4+ T-lymphocyte count of <200 cells/mcL or
  • CD4+ T-lymphocyte percentage of total lymphocytes of <14% or documentation of an AIDS-defining condition
  • Documentation of an AIDS-defining condition supersedes a CD4+ Tcell count of >200 cells/mcL and a CD4+ T-lymphocyte percentage of total lymphocytes of >14%
23
Q

HIV disease spectrum

A 
1-3 months; HIV infections w/ flu-like symptoms
1-10+ years: 
Asymptomatic: No symptoms
Symptomatic:
Fatigue
Diarrhea
Fever
Thrush
Skin rash
Weight loss
Swollen glands
24
Q

Drug resistance testing

A

Genotypic Assays (done first, inform treatment decisions): Detect drug resistance mutations present in relevant viral genes
Phenotypic Assays (if genotypic treatment fails): Measure the ability of a virus to grow in different concentrations of antiretroviral drugs
____________________________
- Recommended for persons with HIV infection when they enter into care regardless of whether therapy will be initiated immediately
- If therapy is deferred, repeat testing at the time of antiretroviral therapy initiation should be considered
- A genotypic assay is generally preferred for antiretroviral-naïve persons
- HIV drug resistance testing should be performed to assist in the selection of active drugs when changing antiretroviral regimens
- Genotypic resistance testing is recommended for all pregnant women prior to initiation of therapy and for those entering pregnancy with detectable HIV RNA levels while on therapy

25
Q

Treatment goals

A

Reduce HIV-related morbidity and prolong survival

Improve quality of life

Restore and preserve immunologic function

Maximally and durably suppress viral load

Prevent vertical (parent to fetus) HIV transmission

26
Q

HAART

A

Highly Active Antiretroviral Treatment (HAART) - get it early, aggressively
Keep viral load to undetectable levels & minimize seeding of the lymphatic system with HIV
Multi-drug approach thought to strike at various points of the viral life cycle
Decrease development of resistance to medications
Minimize medication toxicities

27
Q

Reverse transcriptase inhibitors

A

Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
Non-nucleoside Reverse Transcriptase Inhibitors
Nucleotide Reverse Transcriptase Inhibitors (NrRTIs)

  • Act early in the life cycle of the HIV
  • Prevent the HIV enzyme from creating HIV proviral DNA from viral RNA which prevents new viruses from being produced
  • Nucleoside: work by chain termination & competitive inhibition of nucleoside triphosphates
  • Non-nucleoside: Do NOT require intracellular phosphorylation for activation; directly bind to & disrupt catalytic site of reverse transcriptase => chain termination
28
Q

Protease inhibitors

A 
(NNRTIs)
Cleave particles of viral proteins
Act late in the life cycle of the HIV
Block HIV enzyme protease
-  prevent creation or cleavage of HIV polyproteins necessary for production of new virions
29
Q

Fusion Inhibitor

A

Prevents Seeding
Attach to proteins on surface of T-cells or HIV
Prevent binding of proteins on HIV’s outer coat (GP 120, GP41) with surface receptors on T-cells (CCR5, CXCR4)
At present Enfurvirtide binds to GP 41

30
Q

Integrase inhibitor

A
  • Prevent viral DNA integration into the CD4+ cell chromosome (block the action of integrase, a viral enzyme)
  • Because they target a distinct step in the HIV life cycle, they can be used in combination with other HIV drugs
  • raltegravir (Isentress) and elvitegravir (part of the combination drug Stribild)
31
Q

PrEP - prevention

A

Pre-Exposure Prophylaxis (Truvada)

  • For HIV(-) folks who engage in risk-taking behaviors
  • Blocks HIV reverse transcriptase
  • no protection against other STDs
  • Must take daily and ideal to combine with other preventive measures
  • Requires quarterly testing for HIV, STDs, and side effects
32
Q

Side effects for HIV drugs

A 
Numerous:
Diarrhea
Pancytopenia
Dyslipidemias
Lipodystrophy
Lactic acidemia
Hypertriglyceridemia
Nephrolithiasis
Insulin resistance

Adherence is a KEY issue

  • Optimum therapeutic response
  • Treatment failure – increased seeding of lymphoid reservoirs
  • Prevention of drug resistance
33
Q

Prognosis

A 
Untreated HIV=>AIDS
	Life expectancy = 2-3 years
AIDS 
	Does not usually develop until CD4<200
HIV untreated infection
	CD4 counts decline at a rate of 50-80/yr and are more rapid as counts drop below 200

Potent antiretroviral regimens may delay or even reverse immune dysfunction

34
Q

Pediatric HIV and AIDS

A
  • Most are newborns who contracted it from gestating parent
  • Placenta (transplacental infection rate <30%)
  • Blood exchange during vaginal delivery
  • Milk during breastfeeding
  • Symptoms develop within 6 months
  • Life expectancy < 3 years
  • *Treatment of mother can reduce perinatal transmission by 66% (as low as 2%)
35
Q

PEP (Post-exposure Prophylaxis)

A
  • CDC (2005) recommends a 28-day HIV drug regimen for those who have been exposed to HIV
  • PEP nearly 100% effective in preventing the virus in those who received treatment within initial 24 hours of exposure
  • Effectiveness falls to 52% in those treated within 72 hours
  • Those not treated within the first 72 hours are not candidates for the regimen

Patho II (12 decks)

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