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
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
ritonavir (SQV/r): Resistance
indinavir (IDV): Resistance
IDV/r**: Possible Resistance
nelfinavir (NFV): Resistance
fosamprenavir (FPV): Resistance
APV/r or FPV/r**: Resistance
ritonavir (LPV/r): No Evidence of Resistance
atazanavir (ATV): Resistance
ritonavir (ATV/r)**: Possible Resistance
tipranavir +ritonavir (TPV/r): No Evidence of Resistance
ritonavir (DRV/r): No Evidence of Resistance
** Protease Inhibitors administered with low-dose
ritonavir for pharmacological boosting.
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.
The underlying strain has been identified as group M, subtype B
Identification of resistance-associated mutations within the
HI-viral protease and reverse transcriptase genes by
reverse transcription, polymerase chain reaction and direct
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.