HIV and AIDS symposium Flashcards
HIV =
AIDS =
Human immunodeficiency virus
Acquired immunodeficiency syndrome
AIDS caused by
Manifests as
Originated
HIV
Retroviruses
Kaposi’s sarcoma - darkening of skin
In Africa
HIV transmission
Sexual contact Blood - blood contact Infected blood products In utero Breast milk
HIV types and strains
HIV 1 and 2
1 most common
2 less easily transmitted and less pathogenic
HIV is good at
Mutating rapidly because reverse transcriptase does not proofread sequences produced
Hard to produce vaccine
3 main groups of HIV1
Main (M-pandemic trains)
New (N)
Outlier (O) - confined to Cameroon
Infected individuals contain a heterogenous viral popn
Origins of infection
Chimp co-infection with two SIMEON INFECTIVE VIRUS strains
Viral crossover creates new strain
Transferred to human
Origin of HIV-1 in cameroon - spread to congo
Further spread /
Urbanisation, diamonds, rail travel, independence
Virus characteristics
Central capsule which protects single stranded RNA genome
Adhesins on exterior which bind to cell receptors
Lipid coat around virion - less resistant to survival outside host
ssRNA genomed virus which is pertinent for its replication
Infections
Mechanism
Promoted by
CD4 positive cells - T cells
Initial attachment via gp120 binding to CD4
Loss of cell mediated response
Humoral response
Virus binds to receptors
Heterozygous mutation
Homozygous mutation
CCR5/CXCR4 receptors
Co-receptor binding
People with CCR5 mutations are resistant as receptor will no longer bind to virus
Reduced susceptibility
Completely immune
Virus mechanism after attachment
When cells are activated
Membrane fusion and internalisation
Virus hides inside host genome
Decorating of virus releases viral mRNA and the reverse transcriptase and integrate enzymes
Converts RNA to DNA in nucleus and then integrates into the chromosome –> RETROVIRUS
Viral proteins produced and thousands of new virus progeny synthesised
Virus variation during HIV infection
Isolates from early on in infection - CCR5
- LOW CYTOPATHIC EFFECT
- MORE TRANSMISSABLE
Isolates from late infection - CXCR4
- HIGH CYTOPATHIC ABILITY - LESS TRANSMISSIBLE
INFECTION AND DISSEMINATION
Can cross blood-brain barrier
Disease progression
Start
End
Associated flu like symptoms, high plasma HIV levels, transient CD4 cell depletion
Ask about graph ??
Opportunistic infections are common
Post latency period
**Bacterial-
- Mycobacterium tuberculosis
Salmonella
Haemophilus, Streptococcus, Pneumococcus- Pyogenic infections (pus formers)- recurrent
**Protozoa-
Cryptosporidum (chronic diaarhoea)
Toxoplasma gondii (disseminated, including CNS- from Cats)
Fungal- Aspergillus - pneumonia **Candida- oral presentation **Cryptococcus neoformans- CNS **Pneumocystis jiroveci/ carinii- pneumonia
**Viruses-
**HSV- Herpes simplex virus- chronic oral infection
EBV- Hairy leukoplakia, and B- cell lymphomas
HHV-8 – Kaposis Sarcoma
Oral manifestations in HIV infection
Thrush
Erythematous candidosis
Gingival erythema
Hairy leukoplakia
Progression to AIDS often occurs if
Untreated
10% of HIV infected subjects progress within 2-3 years
5-10% clinically asymptomatic
Remaining subjects progress to AIDS within 10 years
Situation drastically improved by ARVT
Graph explained
Steady HIV diagnoses
By 2005 it peaks
Most new infections occur
Amongst homosexual communities
Asian and African epidemic more heterosexual
- high STD levels –> ulceration
HIV drug targets
Fusion inhibitors
NRTIs - nucleoside reverse transcriptase inhibitor
NNRTIs - non-nucleoside reverse transcriptase inhibitors
Integrase inhibitors
Protease inhibitors
CCR5 entry inhibitors
NRTI mechanism
Nucleotide analogues provided
Analogues cause chain termination when RT builds DNA from RNA
Treatment is called HAAT
HIGHLY ACTIVE ANTI-RETROVIRAL THERAPY
First line reg
2 NRTIs
1 NNRTI - for HIV 2
OR protease inhibitor
