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Flashcards in IDMM Week 5 PBL Deck (39):

replicative cycle of HIV

1. free virus
2. entry: virus binds to a CD4 molecule and one type of "co-receptor" (either CCR5 or CXCR4)--receptor molecules are common on the cell surface. The virus fuses with the cell
3. Penetration: virus empties contents into cell
4. Reverse transcription: single strands of viral RNA are used by the reverse transcriptase enzyme to create double stranded DNA
5. integration: viral DNA is inserted into the cell's own DNA by the integrase enzyme
6. transcription: when the infected cell divides, the viral DNA is read and long chains of proteins are made
7. assembly: sets of viral protein chains come together
8. Budding: immature virus pushes out of the cells, taking some cell membrane with it. The protease enzyme starts processing the proteins in the newly formed virus
9. immature virus breaks free of the cell
10. maturation: the protease enzyme finishes cutting HIV protein chains into individual proteins that combine to make a new working virus


what enzyme incorporates HIV viral DNA into host cells DNA



How is lifelong infection maintained in HIV

by infection of monocytes and macrophages--HIV replicates and is protected within these cells from the immune system


List the modes of HIV transmission

1. sexual activity
2. blood products
3. IV drug use with needle sharing
4. vertical transmission
5. needle stick


How is the HIV virus NOT spread

mosquito bites
casual contact--kissing, sharing food
not transmitted in saliva, urine, tears or sweat


What is the most common method of HIV transmission



Why are women more likely than men to get HIV with vaginal intercourse?

20X more likely

due to prolonged exposure to seminal fluids


Highest sexual risk for HIV transmission

receptive anal > insertive anal > vaginal


List some blood products through which HIV may be spread

whole blood
concentrated RBCs
concentrated clotting factors and plasma
(not assoc. with gamma globulins)


What screens are performed on donor blood products?

EIA for HIV1 and HIV2, and for p24 antigen


3 ways of HIV vertical transmission

during delivery
breast milk


Risk of contraction (%) with needle stick

approx. 0.3%


Why do HIV + patients experience immunosuppression?

-immunosuppression is the result of HIV induced CD4 T cell death
-CD4 cells are the mediators of the acquired immune response (humoral and cell mediated)--therefore, destruction of CD4 cells leads to immunosuppression

***infection of CD4 cells by HIV virions leads to the expression and integration of viral protein gp160 n CD4 cell cytoplasmic membrane


What protein is expressed in HIV infected CD4 T cell cytoplasmic membranes?



Describe the three mechanisms of HIV induced CD4 T cell death in HIV infection

1. binding of the gp160 to adjacent CD4 receptors on the same T helper cell membrane during budding results in tearing of the T cell membrane

2. binding of the gp160 to other CD4 cells, resulting in cell fusion and the formation of a multinucleated giant cell

3. expression of gp160 on CD4 cell cytoplasmic membrane marks it as nonself, resulting in autoimmune destruction by CD8 cytotoxic T-killer cells

(likely kills CD4s by directly inhibiting host cell protein synthesis as well)


HIV train analogy: what is the speed of the train? what is the length of track left?

1. speed of train = viral load...the higher the viral load, the faster the patient will die without treatment

2. the length of track left = CD4 cell count... the higher the CD4 count, the more time the patient has before they succumb to opportunistic infections due to decreased immune system


Describe the natural history of HIV

1. initial decline in CD4 cells and spike in viral load
2. Viral load then becomes low (due to overcompensation of CD4 cell production) and eventually will start to rise while CD4 cell count slowly descends
**the higher the viral load at which is stabilizes can be an indicator for how long before progresses to AIDS


Name the methods used to diagnose HIV

ELISA and Western Blot confirmation


How long after infection do antibodies begin to appear in circulation

2-12 weeks


What is the standard blood screening test for HIV? How sensitive it is?



What is the most commonly used confirmatory test for HIV after ELISA?

Western Blot

assay takes advantage of the fact that multiple HIV antigens of different, well characterized molecular weights elicit the production of specific antibodies

these antigens can be separated on the basis of molecular weight, and antibodies to each component can be detected as discrete bands on the Western blot


What are the factors associated with false positive EIA tests?

antibodies to class II antigens
auto antibodies
hepatic disease
recent influenza vaccination
acute viral infections

this is why you do a confirmatory western blot


What does it mean when an HIV+ person undergoing early treatment subsequently shows a negative EIA?

NOT clearing of infection--level of ongoing exposure just isnt high enough to maintain a detectable antibody response


If a new patient has a positive or indeterminate EIA and a negative Western blot... do they have HIV?

No--definitely not. EIA was false positive.


What is conclusive evidence of HIV infection?

A Western blot demonstrating antibodies to products of all three of the major genes of HIV (gag, pol and env) is conclusive evidence of infection with HIV


Why are HIV+ patients more likely to contract diseases like Hep B/C and other STIs?

1. are immunocompromised, especially if not treated
2. they are typically more likely to be participating in sexual acts with other individuals that are more likely already in possession of an STI (although under no circumstances should this assumption be made for an HIV+ person--simply statistical correlation)


HIV: bacterial opportunistic infections

staph aureus
staph epidermidis
haemophilus influenzae
strep pneumo
m. tuberculosis
m. avium complex


HIV: fungal opportunistic infections

candida albicans
cryptococcus neoformans
histoplasma capsulatum
coccidioides immitis


HIV: viral opportunistic infections

herpes zoster
epstein-barr virus
herpes simplex virus


HIV: protozoal opportunistic infections

pneumocystis carinii pneumonia
toxoplasma gondii


What is the most common opportunistic infection in HIV+ patients

pneumocystis carinii pneumonia (PCP/PJP)


Tx/prevent pneumocystis carinii pneumonia

TMP/SMP given prophylactically when CD4 drops below 200-250


Tx/prevention for toxoplasmosis

treat with pyrimethamine/sulfdiazine

prophylaxis with TMP/SMX (same as PCP!!)


Tx/prevention for M. TB

treatment same as with non-HIV patient


Tx/prevention for MAC

azithromycin or clarithromycin DAILY


Tx/prevention for HSV, VZV



Tx/prevention for candida albicans

oral clotrimazole, nystatin or fluconazole


When might HIV patients be able to come off prophylaxis?

once they have a CD4 count of 200 or above for more than 6 months after ART has been initiated


HIV treatment guidelines

act earlier and more aggressively than old guidelines

start ART if ONE of following is tru:
1. CD4 count is