HIV Flashcards
Main cellular targets for HIV
CD4 lymphocytes-in lymph nodes,gi tract and other tissues-99% or circulation-1%
macrophage-in all tissue and lymph system
role-phagocytosis and presentation of foreign antigens
CD4 levels
should be above 400 but ours usually start at 800
hiv CD4 level trends in blood
initial dip is sudden then latent and slowly continue to dip
his levels are high and then decrease again and remain latent and then spike again before death
most affections in 6 weeks
as cd4 counts decrease
recurrent infections
risk of aid related cancers
organ specific HIV related complications
less than 200 can transmits hiv sexually
why do we have grading
CD4 is too expensive
examples of grading
Angular cheilitis- grade 2
oral hairy leucoplakia – grade 3
Candidiasis- grade 4
Carposy sarcoma - 5
routes of his acquisition
Sexual intercourse (Sex work, MSM, Bisexual, any sexual encounter)
IV drug use
Mother to child transmission (MTCT)
Infected blood products
Occupational
risk reduction
Sexual transmission
Condoms, sero-sorting, sero-positioning, regular STI screening,
TasP ( treatment as prevention – is partner who ahs HIV has treatment and load is below 200 then that means they cannot pass on the virus,
PREP(pre exposure prophylaxis which is giving 2 drugs as a preventative measure taking it regularly and around time o exposure
IVDU
Needle exchange programmes
In Newcastle a lot lesshiv + iv in drug uses
MTCT
Ante-natal screening, TasP, birth plan, PEP for baby(1/3 of babies mothers without treatment will get it if they are treated and don’t breast feed then it is about 0.1%), avoid breast feeding
Blood products
BBV Screening,
what means you need hiv testing
Respiratory: Tuberculosis, Bacterial pneumonia, Pneumocystis, Aspergillosis
Neurology: Cerebral toxoplasmosis, Aseptic meningitis /encephalitis, Primary cerebral lymphoma, Cerebral abscess, PML, GBS, SOL, Cryptococcal meningitis, Peripheral neuropathy, Dementia
Dermatology: Kaposi’s sarcoma, Severe or recalcitrant seborrhoeic dermatitis, Severe or recalcitrant psoriasis, herpes zoster
Gastroenterology: Persistent cryptosporidiosis Oral candidiasis, Oral hairy leukoplakia, Chronic diarrhoea, Weight loss, Salmonella, shigella or campylobacter
Hepatitis B infection, Hepatitis C infection
Oncology: Non-Hodgkin’s lymphoma Anal cancer or anal intraepithelial dysplasia, Lung cancer, Seminoma, Head and neck cancer, Hodgkin’s lymphoma, Castleman’s disease, Gynaecology Cervical cancer Vaginal intraepithelial neoplasia, Cervical intraepithelial neoplasia
Haematology: thrombocytopenia, neutropenia, lymphopenia
Ophthalmology: Cytomegalovirus retinitis, Infective retinal diseases including herpesviruses and toxoplasma, unexplained retinopathy
ENT: Lymphadenopathy of unknown cause, Chronic parotitis, Lymphoepithelial parotid cysts, Mononucleosis-like syndrome
Pyrexia of unknown origin
GUM: sexually transmitted infection
what is HAART
Highly active anti retro viral treatment
HAART aims and targets
Aims: inhibit viral replication present high genetic barrier to resistance 3+drugs/2+classes allow CD4 count to recover
Target for HAART: Cell entry Co-receptor antagonism – CCR5 Fusion inhibition Enzyme inhibition Reverse transcriptase – NRTi/NNRTi Integrase Protease
hiv in pregnancy increased transmutation risk risk
High viral load Advanced immunodeficiency Sero-conversion during pregnancy-GET IT WITHIN EARLY STAGES STI infection IVDU/ Hepatitis C Malnutrition Complicated labour
best way to stop vertical transmission
ARV NO breast feeding and c-section
key issue in HIV care
Late diagnosis
Stigma
Adherence- take treatment regually ( drug users struggle)
Interactions- website on drugs
Partner notification and testing
Prevention of transmission
Management of co-morbidities
Conception and Pregnancy planning
plan for baby care for HIV
Plan Test baby at 3 months and 18 months (PCR/ serology) Test Partner Avoid breast feeding PEP for baby
HIV treatment
What to Start
2x NRTI + NNRTI/ boosted PI/ II (protease inhibitor/integrase inhibitor or non-nucleotide reverse transcriptase inhibitor)
You use at least 3 drug classes and as otherwise you will not have a strong enough barrier and the virus will replicate in the presence of low level drug causing resistance to that whole class- they cannot miss drugs
Also a lot of drugs can interfere e.g steroid inhaler
as soon as someone is diagnosed they get treatment straight away rather than waiting until more thana certain amount
hiv infection video explained
Step 1 – infect suitable host cell such as cv 4 + t-lymphocytes . There needs to be certain receptors on the cell which interact with protein complexes embed in the viral envelope with 2 glycoproteins. The cells then bind which is attachment which then causes co-reptor binding that then. Then the receptor folds out an inserts into the virus and folds in on itself so the virusu gets closer and then fuses
Cd4 count is down
2 rna cells and 3 proteins- integrase protease and reverse transcriptase. Rna double helix then polymerase then turns it into a double dna strand. Integrase then cleaves a di-nucleotide from the 3 prime side of the dna creating 2 sticky ends. Integrase then transfers the dna into the cell nucleus and facilitates its integration to the host cell genome. This induces p transcription of pro-viral dna into messenger Rna and this goes into the cytoplasm ot be turned into viral proteins and some have to be processed by the viral protease and this protease cleaves longer viral proteins into smaller core proteins this is crucial to create an infectious protein. Two viral rna strand and the viral protein come together and core proteins assemble around them creating a capsid which is an immature viral cell which requires a new envelope of host and viral proteins. The virus matures and comes ready to infect other cell. Can destroy immune system.
Drugs: can be blocked by fusion inhibitors to stop viral entry and fusion with host cell
Inhibition of reverse transcriptase by nucleoside inhibitors or by non-nucleoside reverse transcriptase inhibitors is. Part of standard anti-viral drugs.
Integrase can be blocked
Protease inhibitors
