Resistance of HIV to antiretroviral drugs was studied in 210 samples taken in the last two years from patients at the Molecular Biology Unit of the Microbiology Department of the Hospital La Fe in Valencia, Spain. Once the viral load in plasma was determined, resistance was detected using complete gene sequencing for protease until position 3464 of the HIV-1 inverse transcriptase gene. The results were analyzed using the programs Omiga 1.2 (Oxford Molecular Group) and HR-ASAP 1.0 (Stanford University). The protease inhibitors the least affected by the presence of mutations leading to resistance were amprenavir (68.96% activity), and lopinavir (70.69% activity), and of the inverse transcriptase inhibitors, tenofovir (94.02% activity), D4T (74.62% activity) and 3TC (76.12% activity). The treatment combination with the greatest activity, based on the different mutations, was D4T + 3TC + NNRTI. To justify the persistence of viremia with relatively low genotypic resistance to antiretroviral drugs other variables must be considered, such as treatment compliance and the pharmacokinetics of the drugs.