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43 Cards in this Set
- Front
- Back
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HIV1 or HIV2 is a retroviridae in what sub-family?
a. Lentivirinae b. Spumavirinae c. Oncovirinae d. Herpesimplex |
Lentivirinae
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What key enzyme allows HIV to convert it ss+RNA strand into a dsDNA, with what gene?
a. integrase, env b. protease, gag c. reverse trancriptase, pol d. viral envelope, env |
RT, pol gene
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How is mature virus released from host cells?
a. cell lysis b. virus makes holes on plasma membrane c. budding of host cell |
budding of host cell
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What 3 genes are contained in the enveloped ss+RNA HIV virus required for replication?
a. gag, pol, vif b. vpr, gag, pol c. gag, pol, env d. vpri, vif, gag |
gag (viral core p24), pol (protease, RT, integrase), env (gp120, gp41 envelope proteins)
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What component of HIV allows human infection as it binds to CD4+ receptors and macrophages?
a. p24 and p17 b. p24 and g 120 c. g120 and g41 d. g41 and p17 |
both glycoproteins on envelope so g41 and g 120 = g160
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As the HIV virus binds to CD4+ receptors, what addition components are required?
a. p24 attachment b. CCR5 or XCR4 c. g 41 d. p 17 |
coreceptors CCR5 or XCR4
remember p41 and p17 are proteins surrounding the capsid (nucleus) |
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What components are targets of HIV medications, except?
a. RT b. protease c. integrase d. CD4+Receptor blocker |
all except CD4+ RECEPTOR BLOCKER
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Although RT is a vital player in the conversion of ss+RNA to dsDNA, what is its other function?
a. binding of strands b. initiating stop codons c. also functions as an elongation factor d. ribonuclease H enzyme as it cleaves the strands |
scissors (ribonuclease H enzyme) cleaves the strands
note: this can also be a good target for medications |
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which one is the correct order of HIV viral process?
a. attachment, uncoating, integration, RT,proviral transcription, translation, cleavage, assembly, maturation, and release b. attachment, uncoating, RT, integration, proviral transcription, translation, cleavage, assembly, maturation, and release c. attachment, uncoating, RT, integration, assembly, cleavage, maturation, and release d. uncoating, attachment, RT, integration, assembly, cleavage, maturation, and release |
b. attachment, uncoating, RT, integration, proviral transcription, translation, cleavage, assembly, maturation, and release
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After the HIV virus is released via budding is it mature.
a. true b. false |
false, no it still has to get post-budding maturation (not known mechanisms)
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After the HIV converts into a provirus with its dsDNA, how is it transcribed into mRNA?
a. virus has RNA pol b. uses host RNA pol II c. uses host DNA pol II d. virus has DNA pol Ii |
uses host RNA pol II
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Which viral proteins are embedded into the membrane?
a. gag b. env c. pol d. tat |
env (embedded in the membrane), whiel gag proteins are assembled inside the membrane
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HIV must complete 3 steps during attachment in order to successfully enter CD4+. What are they?
a. CD4+ and g120 + g41 b. gp41 detachment c. coreceptor binding (CCR5 or CXCR4) due to confirmational change in g120 d. fusion of virus and cell membrane |
a. CD4+ and g120 + g41
c. coreceptor binding (CCR5 or CXCR4) due to confirmational change in g120 d. fusion of virus and cell membrane NOT gp41 detachment |
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HIV is an enveloped ss+RNA composed of how many base pairs (requires all proteins)
a. 5, 000 bp b. 10, 000 bp c. 15,000 bp d. 20, 000 bp |
10, 000 bps
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Which gene protein is located in nucleocapsid of virus, composed of icosahedryl capsid surrounding nucleic acids?
a. gag b. pol c. env d. tat |
gag (group specific antigen)
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Which gene codes for envelope proteins responsible for attachment and fusion?
a. gag b. pol c. env d. tat |
env gp120 and gp41 important in fusion and attachment
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Which gene codes for enzyme that allows integration of DNA into host cell DNA and cleavage of protein precursors?
a. gag b. pol c. env d. tat |
pol (RT)
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What allow the virus to undergo hypermutation?
a. APOBEC3 b. Cul5 c. EloC d. A3G |
APOBEC3 results in non-infectious vif (viral inactivity factor) virion --> RT --> deamination (dC-->cU) --> hypermutation
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What factor inhibits APOBEC3 packaging by inducing proteasome mediated degradation?
a. vif b. vpr c. vpu d. uridine |
vif (viral inactivity factor)
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What particle stimulates the release of budded virions HIV1 from the cell surface?
a. vif b. vpr c. vpu d. uridine |
vpu + virus buds
vpu - HIV1 accumulates at cell surface and w/in intracellular vesicles (cells tethered to surface of cell) |
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vpu interferes with tetherin useful for virus to attach to cell membrane as it buds off, what is it made of ?
a. single transmembrane domain, an extracellular coiled coil domain and putative C-terminal GPI b. single transmembrane domain c. phospholipid d. extracellular coiled coil domain |
a. single transmembrane domain, an extracellular coiled coil domain and putative C-terminal GPI
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Which intrinsic resistance factors that inhibit HIV-1 are in correct relationship?
a. vif -- APOBEC b. vpr -- tetherin c. vpu -- TRIM5 alpha d. vif-- tetherin |
vif -- APOBEC ( hypermutation)
vpu --tetherin (budding release) vpr - TRIM5 alpha (interfere w/nucleic capsid of virus) |
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Primary infection of HIV results in replication and viermia, what is the duration?
a. 2 weeks b. 8-12 wks c. 3 months d. 8-10yrs |
8-12 wks acute seroconversion may not test HIV positive send viral RNA test
while clinical latency last 8-10yrs |
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As the virus disseminates throughout the lymphoid organs when can you expect an immune response?
a. 1-2 days b. 1-3 weeks c. 1 month d. 2-4 months |
1-3 weeks (cell mediated immunity kick in)
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When will you often start to see constitutional symptoms in HIV positive patients?
a. early in clinical latency b. < 300 CD4+ count c. at the onset of primary infection d. at the same time of opportunistic infections |
a. early in clinical latency NO
b. < 300 CD4+ count ** YES c. at the onset of primary infection NO d. at the same time of opportunistic infections NO, these occur later as the CD4+ level tanks right before death b/c these are often what causes death |
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Lymphoid organs are the sites of HIV replication, HIV actually alters the architecture of these nodes
a. true b. false |
true HIV alters lymph node architecture
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HIV multiplies inside glial cells
a. true b. false |
true cytokines released via MO damage brain cells
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What cells are used as reservoir of the HIV virus?
a. endothelial b. CD8+ c. macrophages d. neurological cells |
macrophages (non cytopathic replication and dissemination)
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The immune system responds to the attack via HIV, but because of HIV's high level of this function, it can't keep up.
a. dissemination b. depletion of CD4+ cells c. damage to neurological cells d. replication |
Yes, HIV's high level of replication leads to slow progressive decline of CD4+ cell count resulting in a limited response later to the virus due to limited amount of CD4+ cell effective (or left)
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With HIV infection you often see the clinical disease in what three forms?
a. opportunistic infections b. disseminations c. neoplasms d. neurological diseases |
opportunistic infections (>> morbidity and mortality), neoplasms, and neurological diseases
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What in HIV treatment has revolutionized outcomes and pt longevity with the disease?
a. HAART triple drug therapy b. isolation of the virus c. treatment of opportunistic infections |
HAART triple drug therapy management with compliance and decreased resistance as was often seen with monotherapy
Pt must be ready to COMPLY with therapy in order for improved outcomes!! |
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32 y/o female presents to the clinic for a f/u, you notice she is sob and coughing. She adds she has notice a fever in the past few days and admits to a non-productive cough. After reviewing her records you notice that she gave birth to an HIV baby about 6 months ago. After reviewing her CXR you note diffuse/patchy infiltrates. Pt denies any chest pain at this point. What is a MAJOR diagnostic tool at this point?
a. silver stain b. bronchoscopy c. Gallium stain d. elevated serum LDH |
bronchoscopy since you have so much hx; although all the other methods are also appropriate
treat w/high dose of Trimethoprim/Sulfa IV and steroids (clearly beneficial, although they do result in immuno-suppression) She can also be started on a prophylaxis of daily TMP/SMZ for prevention |
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All of these infections are responsible for >95% of all deaths in AIDS, as "usual" pathogens, EXCEPT:
a. Pneumococci b. Mycobacterium tuberculosis c. Salmonella, Shigella d. Pneumocytstic carinii e. Histoplasmosis, coccidiodomycosis f. syphillis |
a. Pneumococci
b. Mycobacterium tuberculosis c. Salmonella, Shigella d. Pneumocytstic carinii --> opportunistic infection e. Histoplasmosis, coccidiodomycosis f. syphillis |
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What are the opportunistic organisms responsible for taking advantage of the immunocompormised AIDS pt?
a. pneumocystic carinii b. mycobacterium avium c. toxoplasmosis d. CMV e. pneumococci f. candida g. cryptococcosis |
a. pneumocystic carinii
b. mycobacterium avium c. toxoplasmosis d. CMV e. pneumococci -- usual suspect f. candida g. cryptococcosis |
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What are common malignancies seen in immunocompromised pt infected with AIDS?
a. Kaposi's sarcoma b. multiple myeloma c. primary intracranial lymphoma (Bcell) d. non-hodgkins lymphoma |
EXCEPT --> multiple myeloma
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What is the new problems surfacing with the common extrapulmonary disease present in AIDS pts?
a. colonization and spread b. very contagious c. multi-drug resistance d. debilitating symptoms |
MULTI-DRUG RESISTANCE!! (MDRTB) of mycobacterium tuberculosis
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59y/o male presents to clinic complaining of build up at the back of his throat. Upon careful examination thrush, suspecting a Candia albicans infection, so you use KOH for confirmation. What are you concerned about at this point, as a complication?
a. meningitis b. pneumonia c. esophageal disease d. retinopathy |
esophageal disease!!
treat Candida with nystatin (swish and swallow) a. meningitis (Cryptococcosis) b. pneumonia (mycobacterium) d. retinopathy (CMV) |
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63y/o pt presents with a long hx of HIV infection. Today, he is complaining of HA, fever, and his wife adds he has been acting "weird" states his "brain is off". In addition, she adds that 2 of their CAT's recently died. You are suspecting some brain abnormalities. You order a CAT scan, examine the RETINA, and order serology.
What is the recommended therapy? a. nystatin b. sulfa/pyramehtamine c. ampho B/ fluconazole d. trimethoprim/Sulfa |
ok he has Toxoplasma gondii (CAT's) often common in AIDs, preggers, resulting in brain MASS this is why you would want a CT scan, it also damages the retina, so do a thorough eye exam reveal retinal inflammation. With serology you will notice elevated IgG titers. A biopsy would be ideal, but it is NOT practical so CT will do
a. nystatin (Candida) b. sulfa/pyramehtamine YES!! c. ampho B/ fluconazole (cryptococcosis LT) d. trimethoprim/Sulfa (pneumocystic carnii) |
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46y/o male present to clinic complaining of a subacute HA for the past 3 weeks. Because this is the ONLY presentation, you remember an opportunistic infectious organ, what is a diagnostic tool?
a. KOH b. CT scan c. lumbar puncture w/Indian ink d. silver stain and bronchoscopy |
you are dealing with Cryptococcosis with complications of meningitis so you must do a lumbar puncture w/Indian ink stain
a. KOH (candida) b. CT scan (toxoplasmosis) c. lumbar puncture w/Indian ink (YES) d. silver stain and bronchoscopy (pneumocystic carnii) |
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The HAART regime, more specifically DHPG (ganciclovir and Foscarnet) has revolutionized the treatment for this complication of AIDS, as it is the most common cause of blindness (retinopathy).
a. Candida albicans b. Toxoplasmosis c. CMV d. pneumocystic carnii |
HAART is targets VIRUSES remember so CMV is you option here
a. Candida albicans (esophageal disease) b. Toxoplasmosis (brain abscess or encephalitis) c. CMV (retinopathy) YES d. pneumocystic carnii (dyspnea on exertion) |
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a. Candida albicans (esophageal disease)
Which is incorrectly matched: b. Toxoplasmosis (pneumonia) c. CMV (retinopathy) d. pneumocystic carnii (dyspnea on exertion) e. cryptococcosis (meningitis) |
toxoplasmosis (encephalitis or multiple brain mass)
CMV (retinopathy) pneumocystic carnii (dyspnea on exertion) cryptococcosis (meningitis) |
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This is often a system disease in AIDS pts resulting in fevers, sweats, fatigue and WEIGHT LOSS. Common in pts with low CD4+ count. The treatment includes 3 drugs that are poorly tolerated. What is the opportunistic organism?
a. mycobacterium tuberculosis b. pneumocystic carinii c. toxoplasmosis d. mycobacterium avium |
mycobacterium avium complex (atypical mycobacterium) MAC
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This malignancy is common in pts with AIDS specifically in MSM or IVDA, often infects oropharynx, GI, lung, or even brain. Although, not very effective therapy can be used (radiation, alpha interferon, surgery and chemo).
a. Non-hodgkins lymphoma b. Kaposi's Sarcoma c. primary CNS lymphoma |
b. Kaposi's Sarcoma
a. Non-hodgkins lymphoma (AGGRESSIVE found with a CT of abdomen) c. primary CNS lymphoma (limited response to tx, difficult to dx, LP not of help) |
