|
| |
|
|
| Entry
Inhibitors (including
Fusion Inhibitors) |  | Fuzeon
(enfuvirtide) |  | Selzentry
( maraviroc) |
|
| Fixed-dose
Combinations | | Atripla
(efavirenz
+ emtricitabine + tenofovir) | | Combivir
(retrovir
+ lamivudine) | | Epzicom
(abacavir
+ lamivudine) | | Trizivir
(abacavir
+ zidovudine + lamivudine) | | Truvada
(tenofovir + emtricitabine) | |
 | 1.
HIV binds to CD4 cell surface molecules, entry into the cell also requires binding
to co-receptorsCXCR4 and CCR5). This step can be inhibited by fusion/entry inhibitors.
2. HIV is uncoated inside the cell
and reverse transcriptase copies genomic RNA into DNA, making errors at a frequence
of about one per replication cycle. Reverse transcriptase inhibitors were the
first class of HIV inhibitors to be used as drugs.
3.
Viral DNA can integrate into DNA and become a part of the cellular genome. This
step makes the infection irreversible, and may mean that eliminating the virus
from an infected individual is not possible. Integrase inhibitors are designed
to block this step of infection.
4.
The virus uses cellular machinery to synthesize viral proteins. Several of these
are long amino acid chains which must be cleaved by a specific viral protease
before new viral particles can become active. Protease inhibitors block viral
maturation at this step. |
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