2. Highly Active Antiretroviral Therapy (HAART) Cocktail Therapy

3. Examples of anti-retroviral drugs
Cocktail Drug Mixtures
Protease inhibitors
Non-nucleoside RT Inhibitors (NNRTIs)
Nuleoside/nucleotide RT inhibitors (NRTIs)
* Fusion Inhibitors *Fuzeon
Integrase Inhibitors

4. Fusion Inhibitors block
Co-receptors on host cell
Gp120/gp 41 on viral particle or

5. Acquired Immunodeficiency Disease

6. Symptoms of AIDS Decrease T cell count Rapid weight loss
Recurring fever and dry cough
Profound fatigue
Swollen lymph glands

7. Symptoms of AIDS Persistent diarrhea
Unusual blemishes on the tongue, mouth, or throat
pneumonia
memory loss, depression

8. Acquired Immunodeficiency Syndrome Opportunistic Diseases and cancer
pneumonia
Kaposi’s Sarcoma
Kaposi’s Sarcoma

9. Transmission of HIV

10. Transmission of HIV Biological fluids Blood
Sexual transmission (Semen)
Breast milk
Transplant tissues

11. Non-transmitting sources of HIV
Tears
Saliva
Mosquito or insects
Swimming pool
Food handling

12. Prevention Condoms Clean needles
Treatment of pregnant mother with anti-viral drugs
Blood screening
Abstinence

13. For Your Information and Files

14. Acquired Immunodeficiency Syndrome
Normal CD4+ count
Normal CD4+ (%)
AIDS
/mm3
20-40%
<350/mm3 begin anti-viral treatment
<14% serious immune damage

15. Antiretroviral Agents
Table 1. For Your personal Information: not for lecture.
Antiretroviral Agents   
Agent
Type
Dose
Major Toxicities
AZT
NRTI
300 mg bid
nausea, headache,  low blood counts
ddI
mg bid or mg qd (tablet form)
diarrhea, pancreatitis,  peripheral neuropathy
ddC
0.750 mg tid
diarrhea,  peripheral neuropathy
d4T
30-40 mg bid
abnormal liver function tests, peripheral neuropathy
3TC
150 mg bid
minor
abacavir
hypersensitivity reaction
tenofovir
NRTI (nucleotide)
300 mg qd
nausea, diarrhea, vomiting, flatulence

16. AZT/3TC (Combivir)
NRTI
one pill bid (300 mg AZT/150 mg 3TC)
see above
AZT/3TC/abacavir (Trizivir)
one pill bid (300 mg AZT/150 mg 3TC/ 300 mg abacavir)
nevirapine
NNRTI
200 mg bid
rash
delavirdine
400 mg tid
efavirenz
600 mg qhs
rash, dizziness, impaired concentration, insomnia, abnormal dreams
saquinavir (Fortovase) PI
1200 mg tid
diarrhea
ritonavir
600 mg bid
nausea/vomiting, drug interactions
indinavir
800 mg tid
kidney stones
nelfinavir
750 mg tid or 1250 mg bid
amprenavir
1200 mg bid
nausea/vomiting,  diarrhea, rash
lopinavir/ritonavir
three capsules bid (133.3 mg lopinavir/33.3 mg ritonavir)
diarrhea, nausea, weakness, headache

17. Experimental drugs are italicized, and approved drugs are in regular, non-italicized type)
Brand Name
Generic Name
Abbreviation
Experimental Code
Pharmaceutical Company
Fuzeon™
enfuvirtide
ENF
T-20
Trimeris and Hoffmann-La Roche
BMS
Bristol-Myers Squibb
GSK-873,140
GlaxoSmithKline
PRO-542
Progenics Pharmaceuticals
SCH-D
Schering-Plough Corporation
TNX-355
Tanox and Biogen Idec
UK-427,857
Pfizer

18. Interesting links on HIV
Links to global and US HIV/AIDS statistics
Links to HIV and pregnancy as well as numerous other links including statistics on global epidemic; HIV/AIDS quizzes and treatment.
Links to CDC and a comprehensive fact sheet on HIV transmission

19. Experimental drugs are italicized, and approved drugs are in regular, non-italicized type) Brand NameGeneric NameAbbreviationExperimental Code Pharmaceutical Company Fuzeon™enfuvirtideENFT-20Trimeris and Hoffmann-La Roche    BMS Bristol-Myers Squibb   GSK-873,140GlaxoSmithKline   PRO-542Progenics Pharmaceuticals   SCH-DSchering-Plough Corporation   TNX-355Tanox and Biogen Idec   UK-427,857Pfizer What are Entry Inhibitors (including Fusion Inhibitors)? Entry inhibitors work by preventing HIV from entering healthy T-cells in the body. They work differently than many of the approved anti-HIV drugs – the protease inhibitors (PIs), the nucleoside reverse transcriptase inhibitors (NRTIs), and the non-nucleoside reverse transcriptase inhibitors (NNRTIs) – which are active against HIV after it has infected a T-cell. Entry inhibitors work by attaching themselves to proteins on the surface of T-cells or proteins on the surface of HIV. In order for HIV to bind to T-cells, the proteins on HIV's outer coat must bind to the proteins on the surface of T-cells. Entry inhibitors prevent this from happening. Some entry inhibitors target the gp120 or gp41 proteins on HIV's surface. Some entry inhibitors target the CD4 protein or the CCR5 or CXCR4 receptors on a T-cell's surface. If entry inhibitors are successful in blocking these proteins, HIV is unable to bind to the surface of T-cells and gain entry into the cells. Only one entry inhibitor has been approved by the U.S. Food and Drug Administration (FDA): Fuzeon™ (T-20). This drug targets the gp41 protein on HIV's surface. Some experimental drugs target proteins on T-cells: BMS targets the gp120 protein, PRO-542 and TNX-355 target the CD4 protein, and SCH-D, GSK-873,140 and UK-427,857 target the CCR5 protein. HIV-positive people who have become resistant to PIs, NRTIs, and NNRTIs will likely benefit from the entry inhibitors because they are a different class of drugs. This is good news for HIV-positive people who have tried and failed many of the currently approved anti-HIV medications. To learn more on how HIV infects a T-cell and begins to create more viruses, and where each class of anti-HIV drugs blocks this process, click on the following lesson link: The HIV Life Cycle (and the targets of each class of anti-HIV drugs)