Clinical features of AIDS Flashcards
what causes the immune dysfunction in HIV infection?
-loss of functional CD4 lymphocytes-> loss of memory CD4 cells, and inability to modulate new cell-mediated and antibody-mediated immune response
what happens with CD8 cells in HIV infection?
eventual loss of CD8 cytotoxic cells and ability to mount T cell mediated responses against opportunistic infections
what happens with B cells in HIV infection?
polyclonal activation (non-antibody specific) of B cells with inability to mount new antibody responses
diagnosis of infection
based on demonstrating antibody to multiple HIV antigens: gp120/160 + gp41 or P24
- must have BOTH, one + one
- shown on western blot
what is the sensitivity and specificity of HIV testing?
HIV serology + WB-> >99%
why can’t test for seroconversion in HIV?
may not take place for 6-12 weeks
what is the “gold standard” for diagnose and monitor HIV infection?
HIV RNA level
- follow effectiveness of therapy
- indicated breakthrough of virus
- predicts diagnosis in combination with CD4 levels
what is a full blown AIDS CD4 count level?
below 200/ml
-long lasting fever, fatigue, weight loss, diarrhea
what is the strongest indicator or disease progression?
CD4 count
in HIV infection, what do the lymphoid tissue show?
loss of T-cells (particularly peyer’s patches) and expansion of B cell area (b/c of polyclonal acitvation) and generalized lymphadenopathy
what is found in the follicular mantle cells in early infection?
marked follicular hyperplasia, viral particles
in later stages, what to the lymph nodes show signs of?
“burn out” pattern: loss of most lymphoid elements
- chronic inflammation leads to cell loss, fibrosis
- infected tissue may show formation of lymphocyte syncytial (giant cells) with the X4 type of virus
what is infection of the CNS associated with?
subacute meningoencephalitis with chronic inflammatory infiltrate with microglial nodules and multinucleated giant cells
what are some complications to HIV?
Kaposi’s sacroma (proliferating mesenchymal spindle cells that form blood vessels) and AIDS associated B cell lymphomas
what are two IMPORTANT facts with the pathology of those with AIDS?
- ) infections in patients with AIDS don’t present in typical manner, present in atypical manner with fewer symptoms
- )serology not helpful in diagnosing-> unable to mount an antibody response
what can present at time of transmission?
constitutional symptoms-> fever, malaise, rash
what is acute retroviral syndrome?
high levels of viral replication, viremia, widespread seeding of lymphoid tissue (controlled by host antiviral immune response)
when are antibodies not yet detectable?
seroconversion may not take place for 6-12 weeks, “window
when antibodies not detectable
what do initial drop in viral titers correspond with?
development of specific anti-HIV cell mediated immunity
a patient can remain well during what period?
period in which his/her immune function undergoes slow deterioration with gradual loss of CD4 cells and immune dysregulation
(can last several years)
what is a predictor of progression of the disease?
level of steady state viremia
what do concurrent infection appear to do with this disease?
accelerate the disease process by activating the immune system and causing increased proliferation of virus
what do patients suffer from with HIV infection of microglial cells?
CNS dementia
-virus carried to brain by infected macrophages
associated neoplastic conditions?
Kaposi’s sarcoma, Hodgkin’s disease and lymphoma
Opportunistic infections with HIV?
Candidiasis Pneumocytis Cryptococcus GI infection: Giardia, entamoeba, cryptosporidiosis Mycobacterium avium, Pneumocystis j. CVM
what can give overwhelming viral infections?
CMV, herpes zoster
reactivation of latent infections?
toxoplasmosis, TB, herpes zoster
AIDS associated cancers
Kaposi’s sarcoma
non-Hodgkin’s lymphoma
invasive carcinoma of uterine cervix (assoc. HPV)
Kaposi’s sarcoma
- more common in homosexual/bisexual males
- associated with HHV8 infection
- more aggressive than other cancers
- involves skin, mucous membranes, GI tract
- proliferation of endothelial cells, smooth muscle cells, pericytes
- inefficient vascular formation with blood-filled channels
non-Hodgkin’s lymphoma
highly aggressive
B cell origin, polyclonal B cell activation
extra nodal sites, brain
EBV in 30%
what causes the lack of immune response in this disease?
- immune exhaustion
- lack of T helper cells
- immune escape by virus
- host genetic factors
what is the problem with virus specific antibodies
how to promote anti-viral response in people without the destruction of HIV-specific CD4 cells in the process
what is the major focus of HIV eradication and therapy?
prevention
HAART minimizes viral load but does not eliminate the virus
what kind of vaccine might be helpful more than antibody mediated responses?
vaccines that stimulate cell-mediated responses
complications to HAART therapy?
lipoatrophy, lipoaccumulation, elevated lipids insulin resistance peripheral neuropathy premature cardiovascular disease renal, hepatic dysfunction
