29 - HIV Flashcards
whats the difference between HIV and AIDS?
HIV - the virus
AIDS - the disease
when was HIV first recognised?
in 1981 in San Francisco in the male homosexual population
increase in unusual infections and tumours
• pneumocystis - fungal infection of the lungs
• Kaposi’s sarcoma - tumour that lead to dark red patches on the skin
transmission of HIV
sexual
mechanical
• needles, piercing
• surgery, blood transfusions
veritcal
• prenatal - placental
• perinatal - during birth
• postnatal - through breast milk
types of HIV
HIV-1 is the strain that causes AIDS
HIV-2 is a milder form of the disease
have 40% homology
what is SIV?
simian immunodeficiency virus
similar virus to HIV that infects monkeys
milder disease and less virulent
chimpanzee SIV has homology with HIV-1
sooty mangabev SIV has homology with HIV-2
why was Kinashasa in the 1920’s the ‘perfect storm’?
Kinashasa is in the republic of Congo
in 1920 there was lots of industrialisation
• increased industry - transport network hub
• increase in male population
• increase in sex workers
• increase in STIs
• increase in needles for treatment
transport meant it spread
Kinshasa to Haiti to USA
structure of HIV-1 virion
- double envelope
- P17 capsid
- P24 capside - vase structure
- ssRNA diploid
- reverse transcriptase
- integrase
- gp41
- gp120
lifecycle of HIV-1 virion
recap
cellular response to HIV-1
recap
opportunistic infections associated with HIV-1 infection
- Pneumocystis sp.
- TB (Mycobacterium tuberculosis)
- Malaria (Plasmodium falciparum)
- Candida sp. (thrush) – fungal infection
- Toxoplasma sp. – usually passed on from cats – infects brain in AIDS patients
- Human papilloma Virus (HPV)
reactivation of latent infections
herpes virus
Varicella zoster virus to chicken pox when younger to shingles when older
Epstein Barr virus to glandular fever to B-cell lymphomas
Cytomegalovirus to lymphomas
HSV-8 to Kaposi’s sarcoma
prevention of HIV-1 infection
education
why are vaccines a challenge for HIV?
very high mutation rate
poor protection of mucosal surfaces
no good animal model
anti-HIV therapies
triple therapy – highly active anti-retroviral therapy (HAART)
nucleoside analogues e.g. abacavir – competitive inhibitor of RT
peptide analogues – e.g. saquinavir – competitive inhibitor of HIV protease
anti-CCR5 therapy – individuals with mutation in CCR5 gene are highly resistant to HIV. Blocking CCR5 or bone marrow transplant from CCR5 defective individuals are possible therapeutic interventions
