HIV Infection Flashcards
Discuss the structure of HIV
So you have this VIRAL ENVELOPE and on it are these markers shaped like flowers. The stems are gp41 and the flowers are called gp120.
Inside the envelope is another layer made of p17. Inside that layer is another layer made of p24.
Inside p24 is where the fun is, we have:
- proteases
- reverse transcriptase
- integrase
- ss+ RNA
HIV 1 vs. HIV 2
HIV 1 is everywhere. The only place we find HIV 2 is northwestern half of Africa.
What is a retrovirus?
Uses reverse transcriptase to go backwards (so instead of going from DNA to RNA to protein, it goes from RNA to DNA to RNA
Discuss HIV binding
Binds to a CD4+ T cell, gp120 attaches to CD4 and gp41 attaches to CCR5 usually, or, in the case of those infected, CXCR4, which causes rapid disease progression since it is always expressed, whereas CCR5 is not.
Why is HIV an infection for life?
Integrates into the human genome. Now a part of you.
When is the risk of HIV infection the highest?
When plasma viral loads are highest.
Stage 1 of acute infection in the first year, peaking at 6 months and later on in stage 3, 5.5 to 7 years, rising after that.
Interestingly, the end of stage 1 through all of stage 2 (1 year to 5 years) is a very low risk stage of transmission, only 1 transmission in 1000 coital interactions.
Can HIV cross the placenta?
NOPE! But breaking fluid compartments like during birth will cause HIV transmission
If you do show symptoms at first, what will they be?
Flu like symptoms
How do we diagnose HIV?
HIV antibody ELISA or p24 ELISA
When testing for HIB, what markers will come up and when?
- viral RNA in 2 weeks
- p24 antigen by day 20
- positive ELISA day 22
- Western blot positive day 25
- Western blot positive for p31 - at day 30
- Western blot positive for p31 + at day 70.
Basically, a high risk person who comes in less than two weeks after the incident and is HIV negative is not out of the woods yet. Wait 3 months or 6 months to reassess.
Discuss when certain ARV (antiretroviral) drugs hit the HIV viral replication cycle.
So HIV enters the cell. ENTRY INHIBITORS work here.
If it gets beyond that, and the RNA genome is released inside the target, NON NUCLEOSIDE REVERSE TRANSCRIPTASE INHIBITORS stop it from progressing.
NUCLEOSIDE/NUCLEOTIDE REVERSE TRANSCRIPTASE stop the reverse transcription process of RNA to DNA.
If the DNA gets made, traverses the nucleus envelope and tries to integrate into the host DNA, INTEGRASE INHIBITORS stop it.
Should this fail, and a protease is generated, PROTEASE INHIBITORS stop it from causing the maturation and release of the cell.
AIDS defining illness occurs when:
CD4 counts drop below 200 cells per ul.
