HIV Flashcards

1
Q

3 enzymes HIV must have in packaging

A

reverse transcriptase, integrase and protease

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2
Q

HIV Type in USA

A

HIV-1B

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3
Q

Is incidence of disease going up or down?

A

the incidence is decreasing overall, but increasing in places like china and russia

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4
Q

GP41/120 proteins in HIV

A

outer transmembrane membrane proteins, important for attachment and entry of virus

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5
Q

P24 protein in HIV

A

important for capsid of HIV surrounding nucleus

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6
Q

P17 protein in HIV

A

matrix protein

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7
Q

two interactions for HIV entry into cell?

A

CD4 and chemokines (CCR5 and CXCR5)

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8
Q

CD4 interaction

A

primary interaction, with T cells, macrophages and microglial cells

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9
Q

CCR5 interaction and type of HIV

A

usually in macrophages, called M-tropic HIV (M5 virus)

associated with virus transmission

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10
Q

CXCR4 interaction and type of HIV

A

in T cells and called T-tropic HIV (X4 virus)

associated with disease progression…usually later in infection

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11
Q

binding of Dual mixed virus

A

CXCR4 and CCR5

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12
Q

Steps of reverse transcription

A

make ssDNA, destroy RNA, make dsDNA, integrate

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13
Q

classes of antiretroviral meds

A

reverse transcriptase inhibitors
protease inhibitors
fusion/entry inhibitors
integrase inhibitors

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14
Q

Zidovudine information

A

NRTI

drug for infants

IV

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15
Q

Abacavir information

A

NRTI

serious hypersensitivity…blood test prior

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16
Q

Lamivudine and Emtricitabine information

A

NRTI

treats hep B and HIV

combo with Zidovudine

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17
Q

Tenofovir information

A

NRTI, very common, Hep B and HIV

less toxic

given for HIV PREP

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18
Q

Lopinavir/ritonavir information

A

protease inhibitor

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19
Q

Raltegravir information

A

integrase inhibitor

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20
Q

Maraviroc information

A

unique class that inhibits co receptor…may not always work

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21
Q

two types of prophylaxis with HIV

A

pre (prep) and post exposure (PEP)

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22
Q

common classes in HAART treatment of HIV

A

NRTI, integrase and protease inhibitors

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23
Q

correlation between plasma viral load and CD4 levels?

A

if high plasma HIV load…typically lowering CD4 count

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24
Q

Cells that encounter HIV first

A

langerhans in vagina and foreskin

macrophages, dendritic and NKs in subepithelium

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25
Components of adaptive response to HIV
antibodies develop against core antigens CD8 t cells become activated CD4 cells activated, but lose these
26
what happens when HIV virus has tons of mutations?
fitness of the host and virus actually decreases so it decreases the likelihood of transmission
27
What cells have the CCR5 receptors?
mainly dendritic, macros, and T cells in GALT, other T cells only about 20-30% have the CCR5
28
DC sign
on dendritic cells...can recognize HIV too
29
What do APCs do once they have the HIV virus?
present to CD4 cells around it and travel to nodes to present
30
acute HIV infection has what effect on mucosal CD4 cells?
knocks these out!!!
31
acute HIV infection effect on CD4 cells?
causes a large decrease in CD4 cells
32
AIDs effect on CD4 cells?
causes large decrease in CD4 cells
33
asymptomatic HIV phase effect on CD4 cells?
CD4 cells are actually increasing during this time
34
how do CD4 cells increase during asymptomatic HIV?
CD8 cells are activated and killing of virus
35
Viral load changes in acute, asymptomatic phase of HIV and AIDs
high in acute, decline and steady in asymptomatic, then increases again in AIDs
36
Acute HIV presentation and onset
usually symptomatic with fever sore throat lymphadenopathy and rash couple weeks after infection
37
What is the best test for early acute phase HIV diagnosis?
P24 antigen testing
38
What is the HIV viral set point? and what does it mean for progression of AIDs?
it is the viral load of a patient the higher it is, the more likely for the progression to AIDs
39
Two main adaptive T cells for HIV immune response
CD4 HIV specific, need for presentation with APCs and CD8 activation CD8 HIV specific,
40
3 ways CD8 HIV specific cells can fight HIV
1. lead to lysis of infected cells before virus released 2. inhibit viral reproduction with IFN-gamma 3. inhibit viral entry into surrounding cells by blocking CCR5
41
Two main steps in CD4 cell loss in HIV?
virus leads to lysis of the CD4 cells....virus prevents replacement of CD4 cells by inhibiting thymus, bone marrow
42
Which leads to AIDS faster, CXCR4 or CCR5 or Dual?
dual and CXCR4 lead to AIDs faster because all T cells have the CXCR4 receptor whereas not all T cells have the CCR5 receptor
43
Chronic latency or asymptomatic period of HIV characteristics
clinical latency, but no viral latency...the virus is still replicating inside cells and killing some CD4 cells
44
up to date HIV test name
4th generation HIV 1/2 immunoassay tests for HIV Antigen and antibody comobination
45
HIV tests for HIV antibody
ELISA and western blot
46
best test for acute inflammation? When to test?
avoid latent period of about a week, but after that test for p24 antigen
47
is there an oral rapid HIV test?
yea, and actually not a bad test but has concerns
48
what is HIV DNA PCR important for and why?
diagnosing infant, and because you cant do the antibody testing in an infant because will have Moms
49
characteristics of Initial T cell response to HAART?
rapid increase in T cells, mainly memory cells, so will have forgotten pathogens
50
characteristics of later T cell response to HAART?
more naive T cell growth, can develop new T cell repertoires and specificities, unlike initial response
51
IRIS name
immune reconstitution inflammatory syndrome
52
IRIS disease progression
usually right after HAART treatment was started and as immune system is recovering you have an increased inflammatory response to a pathogen
53
Most common way of perinatal transmission of HIV, a big risk for it, and how to prevent?
during delivery if mother contracts disease during pregnancy HAART is best way to prevent transmission
54
common clinical signs and symptoms of HIV/AIDS
recurrent bacterial and viral infections, thrush, hepatomegaly and splenomegaly, lack of growth, developmental delay, lymphadenopathy, opportunistic infections autoimmune disease and malignancy
55
Why are herpes simplex virus and Zoster rashes more recurrent in HIV?
because the T cells are diminished and they can come back easily
56
infections in individuals with CD4 count over 200?
have more true pathogen infections than usual...
57
common true pathogen infections in HIV
strep pneumo, M tuberculosis, Herpes simplex, shingles, syphilis, salmonella, staph aureus
58
TB and HIV presentation
often an abnormal presentation...nothing in chest X ray, PPD test may be negative because diminished immune response
59
Pneumocystis Jirovecu pneumonia in HIV
most common opportunistic AIDS pathogen shortness of breath and low Oxygen saturation CD4 count less than 200
60
fungal infections in AIDS patients
PJP, candida, and cryptococcus
61
common viral infections with AIDS patients
cytomegalovirus, herpes simplex 1/2, human herpes 8, JC virus
62
CMV and AIDS presentation
very low CD4 count less than 50, leads to retinitis!!
63
Kaposis Sarcoma and HIV
these are vascular nodules in skin in immune suppressed individuals with CD4 counts less than 200
64
Causative agent of Kaposis Sarcoma
Human Herpes Virus 8...sex spread
65
Other common infections with AIDS
toxoplasma, cryptosproidia, mycobacterium avium complex
66
Mycobacterium Avium complex presentation in AIDS
low CD4 count, fevers and night sweats with diarrhea and weight loss also anemia!
67
3 AIDS infections with CNS effects
toxoplasmosis, primary CNS lymphoma, and JC virus
68
drug to prevent pneumocystis pneumonia?
bactrim and septra
69
drug to prevent mycobacterium avium?
azithromycin
70
NABC clinical diagnosis of HIV
N is asymptomatic A is mild B is moderate C is severe
71
123 clinical diagnosis of CD4 cell count
1 is no suppression (greater than 25) 2 is mild (15-25) 3 is extreme (less than 15)
72
Should you give HIV kids vaccines?
they do have lower CD4 cell counts, and likely less antiibodies and CD8 cells but still thought to be effective