resistance to most drugs


I have been poz since 1982, hereunder the drugs i have been taking for 12 years Atripla (efavirenz + tenofovir + emtricitabine) Combivir (zidovudine + lamivudine, AZT + 3TC) Videx (didanosine, ddI) Crixivan (indinavir, IDV) Invirase (saquinavir, SQV) Norvir (ritonavir, RTV) Viracept (nelfinavir, NFV) Last CD4:180 copies Viralload: 9500 Nucleoside and Nucleotide RT Inhibitors zidovudine (AZT): Possible Resistance didanosine (ddl): Resistance lamivudine (3TC)/ emtricitabine (FTC): Resistance stavudine (d4T): Possible Resistance abacavir (ABC): Resistance tenofovir (TDF): Resistance Non Nucleoside RT Inhibitors nevirapine (NVP): Resistance efavirenz (EFV): Resistance etravirine (ETR): Possible Resistance Protease Inhibitors saquinavir + ritonavir (SQV/r): Resistance indinavir (IDV): Resistance IDV/r**: Possible Resistance nelfinavir (NFV): Resistance amprenavir (APV)/ fosamprenavir (FPV): Resistance APV/r or FPV/r**: Resistance lopinavir + ritonavir (LPV/r): No Evidence of Resistance atazanavir (ATV): Resistance atazanavir + ritonavir (ATV/r)**: Possible Resistance tipranavir +ritonavir (TPV/r): No Evidence of Resistance darunavir + ritonavir (DRV/r): No Evidence of Resistance

** Protease Inhibitors administered with low-dose ritonavir for pharmacological boosting. Summarizing interpretation: The following resistance-associated mutations of the viral Reverse Transcriptase gene were identified: M41L, L74V, L100I, K103N, M184V, L210W, T215Y. These mediate resistance to NRTIs and NNRTIs as indicated above. In the Protease gene the following resistance-associated Mutations were detected: L10I, L19I, K20I, M36I, A71I, L90M, I93L. These mediate resistance to PIs as indicated above. Genotype: The underlying strain has been identified as group M, subtype B Method: Identification of resistance-associated mutations within the HI-viral protease and reverse transcriptase genes by reverse transcription, polymerase chain reaction and direct bidirectional DNA-sequencing.


You didn't actually ask a question, so I will just respond to the information that you have provided, and urge you to talk to your doctor about these remarks. From the outset, you should understand that it is not possible to make specific treatment recommendations via the internet in highly complex, treatment experienced patients like yourself. In spite of all that you have offered in your history, there is a huge amount of important information that I would need to consider your next best treatment option.

You have near-complete resistance to the NRTI class and first line NNRTIs, and partial PI resistance.

If you and your doctor were to decide that a change is needed in order to achieve complete virologic suppression, which is achievable at present, you could choose to use several of the new drugs, including drugs in new classes, that have been approved in the United States. These drugs include new PIs (boosted darunavir (Prezista) and tipranavir) and the well-known older PI lopinavir (Kaletra), to which you are susceptible; the new integrase inhibitor raltegravir (Isentress); the new second generation NNRTI etravirine (Intellence); the new CCR5 blocker entry inhibitor miraviroc (Selzentry) or the fusion inhibitor enfurvitide (Fuzeon).

To date, several clinical trials of combinations of these drugs in patients with resistance profiles much like yours have shown high rates of full virologic suppression (65-85%) with rising CD4 cells after two years. These are remarkable outcomes in highly treatment experienced patients.

The other main comment that I will make is that you and your doctor will need to understand, as well as possible, why you have so much drug resistance. If poor adherence to medications played a role, it will be important to try to overcome the reasons for the poor adherence, or these new drugs will not work for you. It will be important to talk at some length with your doctor about past adherence, as well as the other information that I mentioned above.