Immunology - AIDS Flashcards
Test for autoimmune diseases
ANA - antinuclear Rheumatoid factor IgM anti IgG (beads) Immune complex in cold immunofluorescence DAT/IAT Immunohistochemical: Enzyme to final Ab
Describe disease progression initally {virus] and [Ab]
Virus peaks at 6 weeks
Ab peaks at 9 weeks and virus falls
HIV enters mucous membrane and attaches to _____ on _____ cells
lectin
Dendritic
DC cells acts as a _____ and takes HIV to ______
trojan horse
lymph nodes
gp120 binds to ____
CD4
gp120-CD4 causes a conformation change which then binds to ______
CCR5
Once gp120 binds to CD4 and CCR5, conformation allows for _______ to __________
gp41
pierce membrane + viral/cell fusion
Once cell and virus fuse, ___________
virus enter cell, reverse transcriptase convert RNA to DNA
DNA enters nucleus with the help of _____
Integrase (part of RT)
Gag/pol/env separated by _____
proteases
ART = ? includes?
Standarized antiviral therapy: 2 NRTI + 3rd drug of diff class 25,000$/yr
Infected cell fate:
- die rapidly - bud en masses - holes/die
- Persistent virus production
- Latency
Syncytium = ?
Virus puts gp120/41 on cell surface –> fuse with another cell. Spread without extracellular phase - antibody useless
Seropositive HIV
antibody to HIV detected in serum
AIDS
T< 200
Major opportunistic infections, late AIDS demential (Toxic cytokine release)
Common Opportunistic infections for AIDS pts
viral (cytomegalovirus, hept, herpes, zoster
Fungi (candida albincan)
Protozoan - toxoplasma, cryptosporalinum
NOT bacterial - Tfh independent Ab response is ok
Bacterial infection not opportunisitic factor because _____ still intact
Tfh independent Ab response
LTS (long term survivors) have ____
mutation 32 bp deletion: CCR5
Elite controllers are infected but do not progress to AIDS because they have ______
HLAB57, effective CTL to HIV
HIV origination
SIV simian - 1920/congo
jumped about 4x
Symptoms of HIV/AIDS
fatigue, weight loss, malignancy, opportunisitc infections, lower T cell count, fever, night sweats
HIV vaccine challenges
- global genetic diversit
- mutation capacity - evade T and B cells
- Latent - antiretroviral no use
- No spontaneous clearence in history
- bnAb rare and cannot be induced
NRTI - nucleoside reverse transcriptase inhibitor works by
competitive inhibition, chain terminators
NNRTI - non-nucleoside reverse transcriptase inhibitors works by
bind hydrophobic pocket - conformation change - stop catalytic site activity
Protease inhibitor targets
protease - stuck as single gag/pol/env polyprotein
Enfuviritide/fuzeon works by
small peptide fusion inhibitor - bind to gp41 - cannot change conformation to fuse
Raltegravir is an ____ and works by
integrase inhibitor - prevents DNA from making to nucleus