HIV & AIDS - Information Technology Services
HIV & AIDS
Chapter 19
HISTORY of HIV/AIDS
1981: CDC - large number of cases of PCP (Pneumocystis carinii pneumonia)
Kaposi’s sarcoma & other opportunistic infections as well
Decreased T cell numbers
Young homosexual men
1983: Causative agent = virus
Discovered by Luc Montagnier at the Pasteur Institute
Called HIV-1: Human immunodeficiency virus type 1
HIV-2 was discovered in 1985
Causes severe immune deficiency leading to susceptibility to opportunistic infections and neoplasms
Transmitted by three major pathways:
Perinatal
Parenteral
Sexually (70% of all transmissions)
Global summary of the HIV and AIDS epidemic, December 2005
Global estimates for adults and children
end 2005
People living with HIV ------------ 40.3million (36.7 – 45.3)
New HIV infections in 2005 ----- 4.9 million (4.3 - 6.6)
Deaths due to AIDS in 2005 ---- 3.1 million ( 2.8 – 3.6)
End-2005 global HIV and AIDS estimates
Children ( CMV, Mycobacterium infections, PCP, toxoplasmosis of the brain, Kaposi’s sarcoma, others
Death
HIV EVASION of the IMMUNE SYSTEM
Virus becomes latent
Virus infects non-proliferating memory cells
Antigenic changes due to rapid mutation rate
Syncytia = fusion of several T cells
Syncytia forming forms are rapidly more fatal
Destruction of CD4+ T cells = “CENTER” of the immune system ---> susceptible in infections & cancer
No help to activate B cells or CD8+ T-cells
ANTI-RETROVIRAL TREATMENTS #1
Nucleoside base analogs
Competitively bind to RT and inhibit the activity of RT
Require phosphorylation to become activated
AZT: azidothymine
ddI: dideoxyinosine
ddC: dideoxycytosine
3TC: lamivudine (Epivir)
Non-nucleoside RT Inhibitors
Bind non-competitively to the HIV RT causing a disruption in the catalytic site of the RT
Do not require activation by phosphorylation
Nevirapine (Viramune)
ANTI-RETROVIRAL TREATMENTS #2
PROTEASE INHIBITORS
Acts late in late replicative stage of HIV infection
Prevents cleavage of capsid & other polyproteins
1995: Saquinavir
1996: Ritonvir & Indinavir
1997: Nelinavir
COMBINATION THERAPY
CHEMOKINE RECEPTOR BLOCKERS
FUSION INHIBITORS
VACCINE???
What epitope(s) important?
Viral mutation rate is high
What type of immunity required?
Becomes “latent”
Systemic vs mucosal immunity
Whole Inactivated HIV-1
Deadly virus ∴ inactivated or attenuated = RISKY
Subunit vaccine: WHAT PART IS IMPORTANT?
Recombinant subunit vaccines
Live recombinant vaccines
Peptide based vaccines
DNA-based vaccines
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