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Pathology (Guide) > Immunology - HIV > Flashcards

Immunology - HIV Flashcards

1
Q

What is the epidemiology of HIV?

A
  • > 37m people living with HIV-1/AIDs worldwide (2018)
  • 21m ppl receiving ART
  • 101,200 affected UK individuals
  • ~70% those on ART have undetectable viral load (UK)
  • Transmission: sexual, infected blood, mother to child (vertical - breastfeeding, in utero, intrapartum)
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2
Q

What is the HIV replication cycle?

A
  • RNA retrovirus
  • Binds CD4 via gp120 (initial binding) + gp41 (conformational change) on T helper cells, also CD4+ monocytes, DCs
  • Binds CCR5 or CXCR4 chemokine co-receptor
  • Replicates inside cells using reverse transcriptase enzyme to convert RNA into DNA which can be integrated into host genome
  • Hijacks host cell machinery to transcribe DNA + translate mRNA to viral proteins
  • Viral proteins packaged + released as mature virions
  • Gag protein: intra-structural support for HIV
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3
Q

What is the innate immune response to HIV?

A
  • Non-specific activation of macrophages, NK cells + complement
  • Stimulation of dendritic cells via TLR
  • Release of cytokines + chemokines
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4
Q

What is the adaptive immune response to HIV?

A
  • Neutralising Abs: Anti-gp41 IgM (first wks), anti-gp120 (later)
  • Non-neutralising Abs: anti-p24 gag IgG
  • CD8+ T cells can prevent HIV entry by producing chemokines MIP-1a, MIP-1b + RANTES which block co-receptors
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5
Q

What are some key features of HIV-1 infection?

A
  • CD4+ T cell depletino
  • Chronic immune activation
  • CD4 + CD8 T cell exhaustion
  • Disruption of lymph node architecture
  • Loss of Ag-specific humoral response
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6
Q

How does HIV damage the immune system?

A
  • Remains infectious even when Ab coated
  • Activated infected CD4+ helper T cells killed by CD8+ T cells
  • Activated infected CD4+ helper T cells anergised (disabled)
  • CD4 T cell memory lost + failure to activate memory CTL
  • Monocytes + dendritic cells are therefore not activated by CD4+ T cells + can’t prime naiive CD8+ CTL (due to impaired antigen presenting functions)
  • Infected monocytes + dendritic cells killed by virus or CTL
  • Quasispecies are produced due to error-prone reverse transcriptase = these escape from immune response
  • Effective immunity requires auto-antibodies to prevent infection + neutralise virus + sufficient CTL to eliminate latently infected cells
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7
Q

What are the 3 stages of HIV disease progression?

A
  • Acute
  • Asymptomatic (but progressive)
  • AIDS
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8
Q

What is the overall process of HIV disease progression?

A
  • Transmission high during first 6 mths
  • Flu-like Sx in 70%
  • Median time from infection to development of AIDS = 8-10yrs (typical progressors)
  • Median time from infection to development of AIDS = 2-3yrs (rapid progressors = 10%)
  • Long term non-progressors = <5% (show stable CD4 counts + no Sx after 10yrs
  • Initial viral burden (set point) predicts disease progression
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9
Q

What are some important CD4 counts in a patient with HIV?

A
  • 75: Mycobacterium Avium Complex (MAC) disease
  • 75: Pneumocystis jiroveci
  • 300-350: Pulmonary TB
  • 400: Kaposi’s sarcoma
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10
Q

What is the screening test for HIV + what does it test for?

A
  • ELISA
  • Detects anti-HIV Ab
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11
Q

What is the confirmation test for HIV + what does it look for?

A
  • Western Blot
  • Detects Abs
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12
Q

What are some requirements for a positive screening/confirmation test for HIV?

A
  • Requires pt to have Seroconverted
  • Happens >~10wks incubation period
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13
Q

When are HIV-1 RNA tests used?

A
  • Negative serology
  • High clinical suspicion
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14
Q

What testing is used for children <18mths

A

HIV-1 RNA +/or DNA
- Serology not useful due to passive transfer of Abs from Mum

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15
Q

What tests are required post-HIV diagnosis and why?

A
  • Viral load (PCR): Detects viral RNA (v. Sens)
  • CD4 count (FACS/flow cytometry): Assesses course of disease, onset of AIDS correlated with diminution in number of CD4+ T cells
  • Resistance testing: Resistance to ARVs
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16
Q

What CD4+ T cell count is seen in a patient with AIDs?

A

<200 cells/uL blood

17
Q

What are the two types of resistance testing and how are they done?

A

Phenotypic:
- Viral replication is measured in cell cultures under selective pressure of increasing concentrations of ARV drugs - compared to wild-type

Genotypic:
- Mutations determined by direct sequencing of amplified HIV genome

18
Q

What guidelines are used for HIV treatment?

19
Q

When should HIV patients receive treatment?

A

Immediately once diagnosis confirmed

20
Q

What is the mainstay of treatment for a patient with HIV?

A

HAART (Highly Active Anti-Retroviral Therapy)
- 2NRTIs (Nucleotide Reverse Transcriptase Inhibitors) + PI (Protease Inhibitor) (or NNRTI (Non-nucleoside reverse transcriptase inhibitor))

21
Q

What are the aims of HIV treatment?

A
  • Substantial control of viral replication
  • Increase in CD4 T cell counts
  • Improvement in their host defences: dramatic decline in opportunistic infections + deaths
22
Q

What are the implications/prognosis of HIV treatment?

A

Px: Similar life expectancy to age + sex-matched controls (if started before too much immune damage)

IF STOPPED: HIV detectable in blood 2-3wks later

23
Q

What is an example HIV regimen?

A
  • Emitricitabine
  • Tenofovir
  • Efavirenz
24
Q

What is the treatment of HIV in a pregnant patient?

A
  • Zidovudine (PO: antepartum, IV: delivery)
  • PO zidovudine to newborn for 6/52 (reduces transmission from 26% to 8%)
25
Q

What are some limitations to HAART?

A
  • Doesn’t eradicate latent HIV-1
  • Fails to restore HIV-specific T cell responses
  • Toxicities
  • High pill burden
  • Adherence
  • Threat of drug resistance
  • QoL
  • Cost
  • Doesn’t usually reverse chronic immune inflammation
  • RF for: CVS, liver, bone, CNS disease
26
Q

What are the monitoring requirements for HIV treatment (HAART)?

A
  • Regular HIV-1 viral load
  • CD4 monitoring not needed if >350 cells/uL
  • Assess CVS, osteoporosis risk, monitor liver/renal/bone/lipid toxicity
27
Q

What are the different phases of the HIV life cycle?

A
  1. Attachment + entry
  2. Reverse transcription + DNA synthesis
  3. Integration to host DNA
  4. Viral transcription
  5. Viral protein synthesis
  6. Assembly + budding
28
Q

How does the treatment regime work on the different stages of the HIV life cycle?

A

Attachment/Entry:
- Attachment inhibitors (e.g. CCR5i = Maravivoc)
- Fusion inhibitors (e.g. Enfuviritide)

Reverse transcriptase + DNA synthesis
- Reverse transcriptase inhibitors
- NRTI (tenofovir)
- NNRTI (Efavirenz)
- NtRTI

Integration to host DNA
- Integraase inhibitors (Raltegravir)

Viral transcription

Viral protein synthesis

Assembly + Budding
- Protease inhibitors (Ritonavir)

Pathology (Guide) (84 decks)

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