Flashcards in HIV 2 - pathology, Tx Deck (15):
Subtypes of HIV
HIV-1 and HIV-2 (more in Africa, slower response)
Fast replication, high error prone, lack of proof reading. All leads
HIV attachment and fusion
Needs CD4 and CCR5 or CCXC4. Attaches to dendritic cells, and Th cells
How HIV makes you sick?
Destroys CD4 cells. Drops rapidly in the first few weeks, then rebounds a bit, but slowly drops down. Treatment zone is best before 200. CD4 loss results in low immune memory
CD4s in gut lining
HIV depletes these as well. This results in other infections etc diffusing from the gut.
Train analogy for HIV
Speed is the viral load, CD4 count is the distance from the cliff; treatment can slow down, stop or back up the train
CD4(+) cell depletion with stimulation of remaining cells (Chronic B cell activation leading to elevated gammaglobulin levels. Chronic cytokine release, resulting in fever, wasting). Opportunistic infections (OI) – low virulence pathogens usually controlled by CTL. Malignancy – specific tumors resulting from chronic viral co-infection
Complications with HIV treatment
If you already had some opportunistic infections as a result of low CD4, when you start treatment and CD4 start recovering, it can have an intense inflammatory response and cause problems
Common infections (from high CD4 to low)
HSV and pneumonia; shingles; 200: PCP; 100: cryptococcal meningitis; Candida esophagitis; 50: Toxoplasmosis; CMV (retinitis, many other things); PML (white matter disease); mycobacterium avian complex
Groups to treat for coexisting conditions
Pregnancy (AI); History of an AIDS-defining illness (AI); HIV-associated nephropathy (AII); HIV/hepatitis B virus coinfection (AII)
So many! Specifics: Candida (recurrent thrush, esophygeal, vaginitis); pneumocystis (persists in many, but reactive with weak immune syst.); TB (most important, all HIV+ should be tested for TB and vice versa); cancers (Kaposi’s sarcoma (lesions in mouth, GI, skin), EBV (lymphona), HPV (cervical, anal))
Goal is to suppress viral replication, use multiple agents, must be dedicated to Tx.
RT inhibitors (nucleotide and non), protease inhibitors, fusion inhibitors, integrase inhibitors, CCR5 antagonists
Failure of therapy
Nonadherence, resistance (use genetic sequencing early and follow up), inadequate potency