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Path Infectious Diseases Test #1 > HIV/AIDS > Flashcards

HIV/AIDS Flashcards

(55 cards)

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1
Q

single largest group who contracts HIV

A

men who have sex with men

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2
Q

how do you transmit HIV

A

exchange of infected bodily fluids that allows for entry of virus across a mucosal membrane or injected parenterally
blood, semen, vaginal fluid, breast milk

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3
Q

three routes of pediatric/perinatal HIV infections

A

transplacental
infected birth canal
ingestion of breast milk

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4
Q

how to decrease risk of infection from infected untreated mother?

A

treatment of both mother and infant with AZT or HAART (better)

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5
Q

structure of HIV

A

retrovirus related to lentiviruses

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6
Q

molecular structure of HIV

A 
gag = core proteins
pol = reverse transcriptase
p24 = core protein; screening antibodies made to this
gp120 = coat protein that binds CD4
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7
Q

HIV envelope expresses

A

the protein envelope that is capped by gp41 and 3 copies of gp120

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8
Q

lipids within the viral envelope are derived from

A

host cells on budding

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9
Q

HIV core includes

A

major capsid protein p24
nucleocapsid proteins
viral enzymes necessary for reproduction (protease, integrase, and reverse transcriptase)
two copies of genomic RNA

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10
Q

therapeutic protease inhibitors inhibit

A

cleavage of three large protein precursors that are coded for by the genome

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11
Q

What’s responsible for avoiding antibodies made against the virus?

A

genetic variability among the envelope glycoproteins

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12
Q

what does HIV have a tropism for

A

hematopoietic, nervous tissue

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13
Q

gp120 binds

A

CD4 molecule on lymphocytes, macrophages, dendritic and glial cells

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14
Q

fusion and entry into cells results from

A

interaction of gp120 with CCR5 or CXCR4 receptors

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15
Q

Describe what happens when the virus enters cell

A

virus uncoats
viral RNA and reverse transcriptase released
viral DNA synthesized
viral DNA integrated into host DNA (via integrase)
viral assembly and budding occurs on inner wall of host cell membrane

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16
Q

SEVI stands for

A

semen-derived enhancers of viral infection

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17
Q

Where is the HIV virus found in the body

A

within lymphocytes and monocytes, and in a cell-free state (in blood, fluids)

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18
Q

the increased presence of dendritic cells in the foreskin may in part explain

A

the increased transmission associated with uncircumcised males

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19
Q

what does virus require for entry into host cells

A

co-receptor CCR5 or CXCR4

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20
Q

virus infects cells that display

A

both CCR5 and CD4

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21
Q

some individuals who are apparently resistant to HIV infection have proven to be

A

homozygous for CCR5 mutations

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22
Q

how does a genetic change late in the infection alter the co-receptor

A

alter its co-recentpr requifrement from CCR5 to CXCR4

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23
Q

CCR5 is expressed on

Study These Flashcards
A

monocytes and lymphocytes

monocytotropic (M-tropic)

24
Q

CXCR4 (also known as fusin) is expressed on

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A

only on T-lymphocytes

lymphotropic (L-tropic)

25
CXCR4 dependent virus causes
syncytia formation in lymphoid tissues | referred to as a syncytium-inducing strain of HIV
26
Switch to the CXCR4 phenotype is associated with
rapid loss of T lymphocytes and clinical deterioration extremely poor prognostic sign CXCR4 viruses bind to a wider range of T cell types, including naive T cell and thymocytes switch allows viral destruction of more lymphocytes
27
CXCR4 switch is due to
hypervariable regions on the gp120 gene | inhibitions of viral replication may alter or delay this switch
28
activated CD8 cells produce
RANTES, MIP-1-a, MIP-1-b | bind to the CCR5 receptor and partially block virus uptake (inhibited once switched to CXCR4)
29
describe uptake of the virus
gp120 binds CD4 molecules - exposes new recognition sites for CCR5 or CXCR4 on binding of gp120 to co-receptor, gp41 binds gp41 undergoes conformational change that results in the insertion of a fusion peptide that permits fusion of the virus membrane to the host cell membrane
30
plays an important role in establishment of the infection
infection of macrophages
31
macrophages provide
transportation of the virus throughout the body, including CNS
32
severe disease is associated with an
increase in virus proliferation and cytotoxicity in activated lymphocytes
33
primarily an infection of
lymphoid tissues | little presence of virus in peripheral lymphocytes
34
first phase decay due to
virus-specific CD8 T cell response | CD8 antiviral response destroys virally-infected cells and terminates early infection
35
second slower decay is thought to be due to
loss of longer lived viral reservoirs
36
progression of infection occurs because of three main factors:
1. continued loss of CD4 cells 2. inflammatory cytokine-mediated disruption of lymph node-associated immune processing, lymph node architecture, and CD8 effector functions 3. evolutionary changes in the virus that result in increased T cell syncytia formation and cell death
37
continued loss of CD4 cells due to
1. viral replication in CD4+ cells 2. induction of memory CD4 cell apoptosis 3. CTL destruction of virally-infected cells
38
results in progressive systemic inflammatory activation by pathogens
loss of CD4 mediated protective mechanisms in the gut
39
many of the CD4 T cells are initially lost from
Peyer's patches in the gut
40
apoptosis of uninfected memory CD4 lymphocytes in lymph nodes results from
TLR-induced entry into S-phase (mediated by TLR-7 and TLR-8)
41
treatment with HAART results in
an increase in CD4 cells
42
which cells are never recovered even after HAART
HIV-specific CD4 cells
43
progression of disease is reflected in
absolute peripheral CD4 count
44
progressive defects in immune function result from
loss of memory T cells (CD4) and disruption of effector T cell (CD8) mediated processes
45
chronic immune and inflammatory activation of both CD4 and CD8 cell populations results in
1. increased viral replication and cell death by cytolysis 2. enhanced apoptosis of non-infected cells 3. disruption of CD8 effector mechanisms
46
what does a sticky effector CD8 T cell mean
expression of CD69 | CD8 T cells retained within lymph nodes instead of migrating to the periphery to provide protective functions
47
Two current treatment maxims resulted from evolution of drug-resistant strains
1. maximal inhibition of virus replication should result in a decrease in the frequency of drug resistance 2. treatment should also include multiple agents
48
HIV RNA levels are currently used to
diagnose acute infection follow effectiveness of therapy indicated breakthrough of virus predict prognosis in combination with CD4 levels
49
full blown AIDS is diagnosed when
CD4 count drops below 200/ml
50
HIV/AIDS infection of the CNS is associated with
subacute meningoencephalitis with a chronic inflammatory infiltrate with microglial nodules and multinucleated giant cells
51
Associated neoplastic conditions
Kaposi's sarcoma, Hodgkin's disease, and lymphoma
52
Opportunistic infections
1. Candidiasis 2. Pneumocystis pneumonia 3. Cryptococcus 4. CMV/Herpes/Zoster 5. GI infections (Giardia, amebiasis, cryptosporidiosis) 6. reactivation of latents - TB, toxo, herpes zoster 7. fungal infections
53
Kaposi's sarcoma
masses of proliferative spindle-shaped cells that form blood-filled channels involves skin, mucous membranes, GI tract angiogenic and inflammatory cytokines synthesized by virally infected cells appear to drive the vascular proliferation
54
Non-Hodgkin's lymphoma
highly aggressive B cell lymphomas
55
inhibits viral repliation
HAART

Path Infectious Diseases Test #1 (10 decks)

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