HIV Flashcards
methods of transmission for HIV
blood, semen, vaginal fluid, breast milk
80-85% of men and women contract HIV via this
unprotected sex
what is more infective in accidental needle stick: hepatitis B or HIV?
Hep B
3 routes of infection in pediatric/perinatal HIV infection
transplacental, infected birth canal, ingestion breast milk
this HIV variant appears to be less aggressive
HIV-2
glycoprotein that mediates binding of CD4 (located on viral envelope of HIV)
gp 120
glycoprotein that mediates fusion to cell membranes (located on viral envelopes of HIV)
gp 41
major capsid protein that is diagnostic for antibodies (what we measure in screening tests…Ab to this)
p24
viral enzymes necessary for HIV reproduction
protease, integrase, reverse transcriptase
HIV binds to this molecule on lymphocytes, MP, and glial cells
CD4
cells that have CD4 molecule for HIV to bind
lymphocytes, MP, glial
where are HIV viruses latent?
unactivated lymphocytes
what causes proliferation of HIV after latent phase?
lymphocyte activation (cytotoxic to host cell)
ratio of CD4:CD8 in AIDS; what is normal?
.5:1; 2:1
CD4 count less than this = AIDS
200
co-receptor for CD4-GP 120 binding in *early* HIV infection
CCR5
co-receptor for CD4-GP 120 binding in *late* HIV infection
CXCR4
these destroy virally-infected cells and terminates early infection of HIV
CD8 (virus-specific)
3 factors responsible for progressive development of immune deficiency
loss CD4 and CD8, evolutionary change in virus
neoplastic conditions associated with AIDS
Kaposi’s sarcoma, Hodgkins disease, lymphoma
GI opportunistic infections in AIDS patients
Giardia, entamoeba, cryptosporidiosis (parasites more common, crypto more deadly)
may see these reactivated latent infections in AIDS patients
toxoplasmosis, TB, herpes zoster
Kaposi’s sarcoma is associated with this infection
HHV8
opportunistic infection in AIDS that is more common in homosexual/bi males; 15% AIDS patients get it
Kaposi’s
cells that proliferate in Kaposi’s
endothelial cells, SMC, pericytes
factors that are related to high efficacy of sexual transmission of HIV
abundant lymphoid tissue, secretions, concurrent infections (or mucosal breaks), local reservoir (as in uncircumcised pts)
HIV may adhere to these cells in mucosa (instead of going directly into blood vessels)
dendritic cells
these express high amounts of CCR5
genital dendritic cells and GI lymphoid
CCR5 receptors are located on these cells
monocytes and lymphocytes (monocytotropic)
CXCR4 receptors are located on these cells
T-lymphocytes (lymphotropic)
mutation in this switches co-receptor from CCR5 to CXCR4
gp 120
CXCR4 dependent virus causes this in lymphoid tissue –> bind to wide range of T cells (naive and thymocytes) –> rapid loss of lymphoid tissue
syncytia formation
early in HIV infection, these block co-receptor binding –> therapeutic strategy
inflammatory chemokines
early in infection…HIV is primarily an infection of this tissue (in establishing viral reservoir)
lymphoid tissues
these provide transport of virus throughout body –> including CNS
MP
viral reservoir for HIV located in these cells
follicular dendritic cells
entry and transport of HIV occurs in these cells
mucosal dendritic cells
even with appropriate HAART treatment these cells continue to decline
mononuclear cells and lymphocytes
early CD4 cell loss in these locations in gut allows gut pathogen products to be released into blood stream –> inflammatory reaction and increase in proliferation –> apoptosis/cytolysis (in HIV)
Peyer’s patches
upon activation, CD8 cells become sticky due to these molecules being expressed; what happens to the CD8 cells then?
CD69; retained in lymph node
this is responsible for apoptosis of unaffected lymphocytes in HIV
soluble gp 120 (binds to CD4 in absence of virus)
2 other mechanisms for decreased immune function in HIV (besides cytolysis)
apoptosis (due to soluble gp120) and blocking of immune function (gp120 binds CD4 and interferes with antigen presentation), toxic lymphokines
evolution of virus from CCR5 to CXCR4 co-receptor is associated with this (poor prognosis)
syncytia formation
two treatment protocols that help decrease amount of drug-resistant HIV strains
maximal inhibition of viral replication and multiple agents
this occurs as a result of initial activation of immune cells by specific and innate (TLR) mechanisms
lymphadenopathy (germinal center hyperplasia) and hypergammaglobulinemia
4 things to remember in immune system dysfunction due to HIV
lymphadenopathy (initially), lymph node burn out, good PMN response, atypical infection presentation
time it takes for seroversion of HIV to occur
6-12 weeks
these HIV tests have specificity and sensitivity >99%
HIV serology and western blot
RNA at this level in blood is undetectable
50/mL
strongest indicator of HIV disease progression
CD4 count
this is expanded in lymph node –> signaling polyclonal activation
B cell area
occurs when viral particles are found in follicular mantle cells early in HIV infection
marked follicular hyperplasia
CNS infection of HIV seen with this chronic inflammatory infiltrate –> seen in subacute meningoencephalitis
microglial nodules and multinucleated giant cells
this occurs as result of proliferating mesenchymal spindle cells that form blood vessels (in HIV)
Kaposi’s sarcoma
high levels of viral replication, viremia, and widespread seeding of lymphoid tissue are seen in this; when does this develop after infection?
acute retroviral syndrome; 3-6 weeks (lasts 2-4)
this is responsible for initial drop in viral titers
anti-HIV CMI
CNS dementia caused when HIV infects these cells; what carries the virus to the brain?
microglial cells; infected MP
hallmark of original epidemic of AIDS –> nearly universal opportunistic infection
Pneumocystis pneumonia
cause of Non-hodgkins lymphoma (in 3% AIDS) in 30-50% of cases
EBV
appearance of this signals deterioration of immune function (in candidiasis)
thrush
this is probably cause of invasive carcinoma of uterine cervix in AIDS patients
HPV
stain used for Cryptococcus neoformans
india ink
has very thick capsule….stained with india ink in CSF
Cryptococcus neoformans