As discussed in "What is Drug Resistance?", HIV drug resistance means a reduction in the ability of a drug -- or combination of drugs -- to block HIV reproduction in the body.
Drug resistance occurs as a result of mutations in HIV's genetic structure. HIV's genetic structure is in the form of RNA, a tight strand of proteins needed by the virus to infect cells and produce new virus.
Mutations are very common in HIV. HIV reproduces at an extremely rapid rate and does not contain the proteins needed to correct mistakes made during the copying of genetic material.
Nucleoside analogues [Retrovir (AZT), Videx (ddI), Hivid (ddC), Zerit (d4T), Epivir (3TC), and Ziagen (abacavir)] and non-nucleoside reverse transcriptase inhibitors [Viramune (nevirapine), Rescriptor (delavirdine), and Sustiva (efavirenz)] target the reverse transcriptase enzyme.
Protease inhibitors [Fortovase (invirase), Crixivan (indinavir), Norvir (ritonavir), Viracept (nelfinavir), Agenerase (amprenavir), and Kaletra (lopinavir)] target the protease enzyme.
In order for these antiretroviral drugs to be effective, they must attach themselves to the necessary enzyme. Certain mutations can prevent a drug from binding with the enzyme and, as a result, make the drug less effective against the virus.
HIV drug-resistance mutations can occur both before and during therapy.
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