HIV/AIDS Flashcards
Describe how to ensure that someone is not going to tranmitt their HIV
once the viral load is undetectable it is untransmissable!
- condoms
- circumcision
- ART
WHat s PrEP
- pre-exposure prophylaxis
- daily oral antiretroviral with a fixed -dosecombination of tenofovir fumarate (TDF) and emtricitabine(FTC)
- safe and effective in reducing the risk of HIV acquisition in adults
- only works if you take it!
WHich test is the most likely to detec HIV infection the EARLIEST?
HIV RNA NAAT
After a person is infected with HIV how long might it take before they have antibodies in their system
30 days!
what test does the CDC reccommend for warly HIV testing and how soon after infection can it detect HIV?
- 4th/5th generation HIV Ag/Ab combination test which can detect both the p24 antigen and HIV antibody
- test can be positive as early as 14 days post infection
What is the HIV RNA NAAT tets
- a test that can detect HIV as early as 10 days post infection. The earliest test!
Dexcribe the transmission process of HIV
- MOst infections occur at the mucosal surface (vaginal or rectal)
- virus crosses the mucosal surface and infects target cell-activated CD4+ T Cells, Dendritic cells and macrophages
- small foci of infection are established locally and then expand and disseminate infection through the draining lymph node and into the blood
Who from team host immune system is involved in the counter attack?
- Innate
- Dendritic cells (DCs)
- Natural Killer (NK) cells
- Intrinsic
- antiviral restriction factors
- adaptive
- B cells
- T cells
- When HIV is recognized by the TCR is causes cytokine release which recruits mor CD4 T cells, but that is kind of bad bc T cells are what HIv infects
WHat is the main role of NK cells
- lyse malignant or infected cells
- NK cell activation is stimulated by innate cytokines including IFN-1, IL-15 and IL-18 and is regulated by receptor ligand interactions
- they combat HIV-1 replication by killing infected cells (perforin and granzyme, Fas ligand mediated apoptosis, ADDC)
- produce antiviral factors including IFNy, TNFa and B-chemokines
What is intrinsic immunity and what role does it play during HIV infection?
- Intrinsic, intracellular restriction factors inhibit viral replication directly
- main restriction factors in HIV: APOBEC3G, TRIM5a, tetherin (BST-2) and SAMHD1
- HIV-1 counteracts some of these restriction factors via acessory proteins
- Describe the role that B cells play in HIV and how HIV avoids this
- adaptive immunity, an initial Ab response to Env occurs but it is non-neutralizing
- neutralizing antibodies eventually develop but slowly, about 12 weeks after infection. this is too late
- Abs to conserved areas of Enc are rare so excape from Abs occurs
- HIV induces the lysis of follicular B cells and leads to the loss of germinal centers which results in defects in the ability to rapidly generate Abs
- How do CD8 T cells fight HIV
the first specific CD8 T cell responses are seen as viremia peaks, initially specific for ENv and Nef
virsu sequence chnages dramatically w rapid selection of escape mutant but T cell seventually become more targetd to conserved epitopes
Describe how an individuals genetics may relate to their clinical significane of infection
- Individuals with MHC class I alleles, KLA B57, HLA 27 are associated with control of viremia
- the combination of NK receptors KIR3DS1 and KIR3DL1 with HLA-B57 has been associated with delayed progression to AIDS
- alite controllers, a subset of HIV infected individuals who spontaneously control HIV may have more functional CD8 T cells (more perforin and granzyme)
WHy do we need a cure to HIV if we can suppress the viral load with ART?
- Even when the viral loads are supressed ART does not fully restore normal health and immune dysregulation
- cost and access to medications worldwide is an issue
Describe the pathogenesis of HIV if a person is being treated and what are the consequences of this?
- chronic HIV infection is characterized by persistent infammation and immune dysfunction even whe patients are supressed on ART
- consequences:
- ongoign HIV replication
- infection with co-pathogens such as CMV
- dysfunctional immunoregulatory factors
- mcrobial translocation
- lymphoid fibrosis