HIV 1 Flashcards by Aisha Mujahid

What can HIV lead and two and what are the two things that causes

AIDS - acquired immunodeficiency syndrome

opportunistic infections
AIDS related cancers

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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

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when can AIDS be prevented

early HIV dx

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What happens to LE of a person with HIV

is HIC preventable

near normal LE

yes

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Is HIV the same as AIDs

No
HIV can lead to AIDS
but HIV does not equal AIDS

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how is HIV transcribed

retrovirus

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what is the difference between HIV2 and HIV 1

HIV 2- less virulent - less likely to get AIDS

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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

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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

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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

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what does the effect of HIV infection on the immune system lead to

susceptibility to viral/fungal/mycobacterial infections, infection-induced cancer

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normal range of CD4 cells

risk of opportunistic infections

500-1600cells/mm3
<200cells/mm3

however 200-500 may still get opportunistic infections

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HIV viral replication - when

new generation when

rapid replication in very early and late infection

new gen every 6-12 hours

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average time to eat without treatment is what

9-11 years

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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

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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

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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

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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

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pneumocystis pneumonia caused by what

CD4 count

symptoms

signs

CXR

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