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CBI - UOE > HIV and AIDS > Flashcards

HIV and AIDS Flashcards

1
Q

aids stands for

A

acquire immune deficiency syndrome

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2
Q

what causes aids

A

HIH

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3
Q

basic disease causing mechanism of HIV

A

destroys CD4T cells

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4
Q

originally caled

A

GRID

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5
Q

first recognised clinically in US in the

A

1980s in intravenous drug users and gay men who showed symptoms of Pneumocystis carinii pneumonia (PCP)

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6
Q

PCP

A

Pneumocystis carinii pneumonia

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7
Q

how many infected per yer in US

A

50,000

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8
Q

how many deaths globally since 1980

A

39 millionn

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9
Q

how many new cases in 2014

A

2 million

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10
Q

how many people receiving ART in 2015

A

15 million

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11
Q

2/4 infected

A

from sub-saharan africa

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12
Q

1/5

A

in asia

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13
Q

vast majority of AIDs is caused by

A

HIV 1

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14
Q

Pneumonocystis pneumoniia

A

is a form of pneumonia caused by yeast-like fungi Pneumocystis jirovecii

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15
Q

Pneumocystis is commonly found

A

in the lungs of healthy people

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16
Q

PCP is a

A

opportunistic pathogen

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17
Q

where is PCP especially seen

A

people with cancer, undergoing chemo

HIC/AIDS

Immunosuppressants

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18
Q

where did HIV-1 originate from

A

southern cameroon

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19
Q

what dud HIV-1 originate from

A

simian immunodeficiency virus

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20
Q

simian immunodeficiency virus

A

is a retrovirus

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21
Q

how was SIV introduced into humans

A

through bushmeat activities with

subsequent mutation into HIV

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22
Q

transmission of disease from one species to another requires

A

one or more high-risk transmission channels for human to human spread

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23
Q

what channel was created (absent prior to 20th century)

A

growth of colonial african cities- societal changes such as prostitution

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24
Q

advent of prostitution lead to

A

increased frequency of STDs (genital ulcers e..g syphilis) that allowed sexually transmitted infection

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25
earliest document case of HIV
1959
26
though to have been in the US as early as
1966
27
origin of aids pandemic traced back to
1920s in Kinshasa (congo)
28
structure of HIV
- lipid membrane - docking glycoproteins - transmembrane glycoproteins - HLAClass I, DR - HLAClass II, DR
29
docking glycoprotein
gp120
30
transmembrane glycoprotein
gp41
31
HLA-DR
human leukocyte antigen- antigen D related
32
HLA-DR act as a
ligand for T cell receptors
33
name three ways in which HIV can enter via epithelial cells
1) through M cells 2) can gain access via epithelia damaged by ulcerative infection or by trauma 3) Chemokine receptors
34
HIV access through M cells
prevalent in tonsil and rectal epithelia
35
gain access via epithelia damaged
by ulcerative infections, or by trauma or injection (i.v. drug use or blood transfusion)
36
vaginal epithelia lack
M cells
37
Epithelial cells in small intestine express
CCR5, chemokine receptors
38
how does HIV gain access by binding to CCR5
binds to CCR5 (once tethered by galactosylceramide) via the viral envelope glycoprotein gp120 and the virus is transcytosed
39
HIV transport to the lymph nodes
Once HIV has managed to cross epithelial barriers, HIV encounter sub-epithelial dendritic cells
40
which type of receptor on the dendrite cell binds to HIV
C-type lectin receptor- bind gp120 glycoprotein on viral envelope
41
interaction with c-type lectin receptor intiitaes
dendritic migration to regional lymph nodes
42
one in the lymph nodes
intax virus internalised with C-type lectin receipts is re-exposed at the surface and displayed to T cells
43
where is the predominant site of virus replication early in the disease
small intestine- this reflects the large number of activated T cells that express CCR5 in that organ
44
entry of HIV into cells is mediated by
viral envelope glycoprotein- gp120
45
HIV binds to
CD4 and chemokine receptors on host surfaces
46
what does gp41 on the envelope of HIV do
mediates fusion of | the virus envelope with the host cell membrane
47
HIV infection cycle
1) gp120 on viral envelope binds to CD4 receptor on host membrane 2) gp41 mediates fusion of HIV with host cell membrane 3) contents of virus empties into cell 4) reverse transcription of viral genome 5) viral cDNA integrated into genome 6) transcribed and translated into a new HIV vision 7) forms at cel membrane and buds 8) matures
48
a wave of viral proliferation in lymph nodes
peaks 4-7 days after infection
49
virmeia peaks at
14 day
50
all lymphoid tissues infected
by 3 weeks
51
HIV is quiescent in resting CD4 T cells but..
on T cell activation virus production is also activated and the host cell dies
52
>99% of virus
is produced by newly infected CD4 t cells
53
what happens as a result of loss of helped activities
loss of cytotoxic T cell response loss of antibody response of B cells
54
sympotms
flu-like illness from days to weeks after exposure
55
flu-like illness from days to weeks | after exposure
associated with a drop of CD4 T cells in the blood
56
what is responsible for a prolonged period of stable virmeia
CD4-dependent antiviral cytotoxic CD8 T cell response - viral set point
57
patients are normally asymptomatic until
CD4 T cell count declines further
58
opportunistic infections begin
when CD4 T cell counts reach levels of <200ul
59
death ensues about
2 year after
60
aids causes increased risk of
microbial infection
61
example of a brain infection
cryptococcal meningitis
62
eye infection
cytomegalovirus
63
mouth and throat
cadndidiasis
64
lung
pneumocystis carinii pneumonia and TB
65
gut
cytomegalovirus
66
skin
herpes | shingles
67
genitals
genital herpes | vaginal candidiasis
68
which fungus causes cryptococcal meningitis
cryptococcus neoformans and cryptococcus atti
69
cryptococcal meningitis
usually affect immune-compromised patients
70
how many cases of cryptococcal meningitis world wide
950,000
71
how many deaths by cryptococcal meningitis
600,000 (70% in sub-saharan)

CBI - UOE (61 decks)

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