HIV and AIDS Flashcards
aids stands for
acquire immune deficiency syndrome
what causes aids
HIH
basic disease causing mechanism of HIV
destroys CD4T cells
originally caled
GRID
first recognised clinically in US in the
1980s in intravenous drug users and gay men who showed symptoms of Pneumocystis carinii pneumonia (PCP)
PCP
Pneumocystis carinii pneumonia
how many infected per yer in US
50,000
how many deaths globally since 1980
39 millionn
how many new cases in 2014
2 million
how many people receiving ART in 2015
15 million
2/4 infected
from sub-saharan africa
1/5
in asia
vast majority of AIDs is caused by
HIV 1
Pneumonocystis pneumoniia
is a form of pneumonia caused by yeast-like fungi Pneumocystis jirovecii
Pneumocystis is commonly found
in the lungs of healthy people
PCP is a
opportunistic pathogen
where is PCP especially seen
people with cancer, undergoing chemo
HIC/AIDS
Immunosuppressants
where did HIV-1 originate from
southern cameroon
what dud HIV-1 originate from
simian immunodeficiency virus
simian immunodeficiency virus
is a retrovirus
how was SIV introduced into humans
through bushmeat activities with
subsequent mutation into HIV
transmission of disease from one species to another requires
one or more high-risk transmission channels for human to human spread
what channel was created (absent prior to 20th century)
growth of colonial african cities- societal changes such as prostitution
advent of prostitution lead to
increased frequency of STDs (genital ulcers e..g syphilis) that allowed sexually transmitted infection
earliest document case of HIV
1959
though to have been in the US as early as
1966
origin of aids pandemic traced back to
1920s in Kinshasa (congo)
structure of HIV
- lipid membrane
- docking glycoproteins
- transmembrane glycoproteins
- HLAClass I, DR
- HLAClass II, DR
docking glycoprotein
gp120
transmembrane glycoprotein
gp41
HLA-DR
human leukocyte antigen- antigen D related
HLA-DR act as a
ligand for T cell receptors
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
HIV access through M cells
prevalent in tonsil and rectal epithelia
gain access via epithelia damaged
by ulcerative infections, or by trauma or injection (i.v. drug use or blood transfusion)
vaginal epithelia lack
M cells
Epithelial cells in small intestine express
CCR5, chemokine receptors
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
HIV transport to the lymph nodes
Once HIV has managed to cross epithelial barriers, HIV encounter sub-epithelial dendritic cells
which type of receptor on the dendrite cell binds to HIV
C-type lectin receptor- bind gp120 glycoprotein on viral envelope
interaction with c-type lectin receptor intiitaes
dendritic migration to regional lymph nodes
one in the lymph nodes
intax virus internalised with C-type lectin receipts is re-exposed at the surface and displayed to T cells
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
entry of HIV into cells is mediated by
viral envelope glycoprotein- gp120
HIV binds to
CD4 and chemokine receptors on host surfaces
what does gp41 on the envelope of HIV do
mediates fusion of
the virus envelope with the host cell membrane
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
a wave of viral proliferation in lymph nodes
peaks 4-7 days after infection
virmeia peaks at
14 day
all lymphoid tissues infected
by 3 weeks
HIV is quiescent in resting CD4 T cells but..
on T cell activation virus production is also activated and the host cell dies
> 99% of virus
is produced by newly infected CD4 t cells
what happens as a result of loss of helped activities
loss of cytotoxic T cell response
loss of antibody response of B cells
sympotms
flu-like illness from days to weeks after exposure
flu-like illness from days to weeks
after exposure
associated with a drop of CD4 T cells in the blood
what is responsible for a prolonged period of stable virmeia
CD4-dependent antiviral cytotoxic CD8 T cell response - viral set point
patients are normally asymptomatic until
CD4 T cell count declines further
opportunistic infections begin
when CD4 T cell counts reach levels of <200ul
death ensues about
2 year after
aids causes increased risk of
microbial infection
example of a brain infection
cryptococcal meningitis
eye infection
cytomegalovirus
mouth and throat
cadndidiasis
lung
pneumocystis carinii pneumonia and TB
gut
cytomegalovirus
skin
herpes
shingles
genitals
genital herpes
vaginal candidiasis
which fungus causes cryptococcal meningitis
cryptococcus neoformans and cryptococcus atti
cryptococcal meningitis
usually affect immune-compromised patients
how many cases of cryptococcal meningitis world wide
950,000
how many deaths by cryptococcal meningitis
600,000 (70% in sub-saharan)