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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