HIV 1 Flashcards
What can HIV lead and two and what are the two things that causes
AIDS - acquired immunodeficiency syndrome
opportunistic infections
AIDS related cancers
AIDS related conditions are the single highest predictor for what
of mortality in HIV
1/4 of deaths caused by late diagnosis - too late for effected treatment
when can AIDS be prevented
early HIV dx
What happens to LE of a person with HIV
is HIC preventable
near normal LE
yes
Is HIV the same as AIDs
No
HIV can lead to AIDS
but HIV does not equal AIDS
how is HIV transcribed
retrovirus
what is the difference between HIV2 and HIV 1
HIV 2- less virulent - less likely to get AIDS
what is CD4
why is it important in HIV
where is found
glycoprotein on the surface of cells
CD4 receptors are the target site for HIV
T helper cells (aka CD4 cells),
dendritic cells, macrophages, microglial cells
What do CD4 T lymphocytes do
essential for induction of adaptive immune response
recognise MHC2 APC
activation of B cells
activation of CD8 cells
cytokine release
what effect does HIV response have on immune response (5)
sequestration of cells in lymphoid tissue - reduce circulating CD4 cells
reduced prolif of CD$ cells
reduced CD8 cell activation - increased susceptibility of viral infections
reduction in antibody switching class
chronic immune activation - loss of lymphoid tissue in the gut - bacteria gets into blood - other systems are activated
what does the effect of HIV infection on the immune system lead to
susceptibility to viral/fungal/mycobacterial infections, infection-induced cancer
normal range of CD4 cells
risk of opportunistic infections
500-1600cells/mm3
<200cells/mm3
however 200-500 may still get opportunistic infections
HIV viral replication - when
new generation when
rapid replication in very early and late infection
new gen every 6-12 hours
average time to eat without treatment is what
9-11 years
process of infection from first intro to the spread
infection of mucosal CD4 cells (langerhans and dendritic)
transport to regional Los
infection established within 3 days of entry [can intervene with prophylaxis at this point)
replication and dissemination of virus
primary HIV infection
how many present with symptoms
how long after infection
symptoms
transmission risk
diagnosis rate
up to 80% present with symptoms
2-4 weeks after
fever, rash (maculopapular), myalgia, pharyngitis, headache/aseptic meningitis
high risk of transmission
often go undx
after the primary infection of HIV what stage does the infection enter
what is happening during this phase
risk of transmission
asymp HIV infection
ongoing viral replication, ongoing CD4 count depletion, ongoing immune activation
risk of onward transmission if remains undx
definiton of opportunistic infections
an infection caused by a pathogen that does not normally produce disease in a healthy individual - uses the opportunity of a weakened immune system to cause disease
pneumocystis pneumonia caused by what
CD4 count
symptoms
signs
CXR
dx
treatment
prophylaxis
pneumocysic jiroveci (fungal)
<200
insidious onset, SOB, dry cough
exercise desaturation - sats go down
may be normal. interstitial infiltrates, reticulonodular markings
BAL and immunflouresence +/- PCR
high dose co-trimoxazole (+/- steroid)
low dose co trimoxazole if just CD4 count low
what is commoner in HIV + patients connected to TB
what should you be aware of in someone who has both
symptomatic primary infection reactivation of latent TB lymphadenopathies military TB extra pulmonary TB multi drug resistant TB immune reconstitution syndrome - immune system is activated but is very very aggressive
drug - drug interactions
cerebral toxoplasmosis organism CD4 what does HIV cause symptoms/signs on MRI/XR
toxoplasma gondii
<150
reactivation of latent infection, multiple cerebral abscesses, choriorentitis
headache, fever, focal neurology, seizures, reduced consciousness, raised inter cranial pressure
ring enhancing lesions
cytomegalovirus organism CD4 what does HIV do and what does it lead to presentation screening
CMV
<50
reactivation of latent infection which can cause retinitis, colitis, oesophagitis
reduced visual acuity, floaters, abode pain, diarrhoea, PR bleeding
ophthalmic screening for all indivduals with CD <50
HIV and skin infections
herpes zoster - multi dermal and recurrent
herpes simplex - extensive, hypertrophic (warty/tumour like), acyclovir resistant
HPV - extensive, recalcitrant, dysplastic
pencilliosis, histoplasmosis
HIV assoc neurocognitive impairment organism
CD4
presentation
why?
HIV 1
any increased incidence with increased immunosuppression
reduced short term memory +/- motor dysfunction
CD4 present of microglial cells
progressive multifocal leukoencephalopathy organism
what does HIV do
CD4
presentation
JC virus
reactivation of latent infection
<100
rapidly progressing
lesions - focal neurology
confusion
personality change
neurological presentations with HIV
why
distal sensory polyneuropathy mononeuritis multiplex vacuolar myelopathy aseptic meningitis GBS viral meningitis (CMV, HSV) cryptococcal meningitis neurosyphilis
related to the viral replication rather than the immunosuppression
HIV associated wasting
causes
slims disease
metabolic (chronic immune activation)
anorexia - multifactorial
malabsorption/diarrhoea
hypogonadism
AIDS released kaposi;s sarcoma organism pathology CD4 presentation rx
human herpes virus 8
more common in MSM
vascular tumour
any increased incidence with increased immunosuppression
cutaneous, mucosal, visceral (pulmonary, GI)
HAART, local therapies, systemic chemo ofr visceral
non hodgkins lymphoma organism CD4 presentation dx rx prognosis
EBV
increase incidence with increase immunosuppression
more advanced, B symptoms, bone marrow involvement, extranodal disease, increase CNS involvement
as for HIV
as for HIV add HAART
approaching HIV -
cervical cancer organism
testing
screening
HPV
persistence of HPV infection
rapid progression to severe dysplasia and invasive disease
HIV testing should be offered to all complicated HPV disease
women with HIV are screened every year instead of every 3 years
Non symptomatic HIV symptoms
mucosal candidiasis secorrhoeic derm diarrhoea fatigue worsening psoriasis lymphadenopathy parotitis STIs, Hep B, Hep C
haematological manifestations caused by what
CD4
(2)
HIV, opportunistic infections, AIDS malignancies, HIV drugs
any increased incidence with increased immunosuppression
anaemia (affect up to 90%)
thrombocytopenia (CD4 300-600)
modes of HIV transmission sexual
what increases risk
94% of all infections
between 51%
man to woman 45%
anoreceptive sex
trauma
genital ulceration
concurrent STI
tranmission parenteral
injection drug use
infected blood products
iatrogenic
transmission mother to child
how
how many will become infected
mortality
risk
in utero/placental
delivery
breast feeding
1/4 babies at risk
1/3 HIV + babies will die before their 1st birthday if untreated
risk 1.2% but <0.1% if viral load undetectable at delivery
epidemiology of HIV
MSM larges risk group
hetero men most likely to be undx and present late
HIV in people who inject drugs is uncommon
who is tested
universal testing in high prevalence areas
opt out in certain clinical settings - TOP, GUM, drug dependency, antenatal, assisted conception
screening of high risk groups - MSM, female partners of bisexual men, people who inject drugs, partners of HIV+, adults from endemic areas, children from endemic areas, sexual partners form endemic areas, history of iatrogenic exposure in an endemic area
testing in the presence of clinical indicators
endemic areas
sub saharan africa
thailand
carribbean
testing on clinical grounds
when HIV falls into differential disgnosis list - test regardless of risk factors
how to take a HIV test
if incapacitated
consent, obtain venous sample for serology
only test if in patients best interest, consent form relative not required, if safe wait till patient regains capacity, obtain support from HIV team if required
what markers of HIV are used in the lab to detect infection
Viral RNA
capsule protein - p24
antibody
3rd gen test
HIV 1 and 2
detect IgM, IgG
very sensitive/specific in established infection
window period - 20-25 days
4th gen test
combined antigen (p24) and antibody shortens window period by 5 days the one which is used in tayside
rapid HIV tests
POCT
finger prick specimen of saliva
results within 20-30 mins
3rd gen (Ab) 4th (Ab/Ag)
advantages of using POCT
disadvantages
simple, no lab, no wait up, good sensitivity
expensive, quality control, poor positive predictive value, can’t be relied on in early infection
RITA is what
incidence testing
used to identify if an infection occurred within the preceding 4-6 months
large margin of error
home sampling which is available online
finger prick/saliva
