im the last 2 months om truvada and kaletra.but my last test showed resistance to meds.cd4 540 viralload 14000.
before i used truvada,norvir and reyataz.cd4 600 viralload 200.
is 200 in viralload to high?what is recommended viralload?how is high and low viralload defined?
i use poppers and viagra,can this interact with the meds,and be the reason why the viralload continue to be to high?i started treatment 1 year ago,and the viralload have been around 200 on treatment with reytaz,norvir and truvada.what medical complications can use of poppers and viagra lead to,in interaction with hivmeds?
what is the supervirus?how can you find out if you have a supervirus?do some people develop resistance to all hiv treatments?
if my viral load continue to be high(over 50) on new treatment(i will start a new regime in 1 month,after taking a new test in 2 weeks),what can do this mean for my possibilities to have a long life?(im 32 now)
do high viralload lead to reducement of cd4 counts over long time?
if you change treatment regime many times,can this lead to a higher risk of resistance?
my viralload is now 14.000.this is very high.how long time can i expect to get to 0 in viralload,if i start a new treatment now?
are there some meds that is better than other thinking og effect and risk of sideeffects.is reyataz ,norvir and truvada recommended?
Please take your many questions and the responses below to your doctor and discuss each one. It is very important that you understand what your situation is now, how you got here, and the options for treatment that are available to you now.
A viral load that is persistently above the level of detection, i.e. greater than 50 copies/ml, is associated with a greater risk of virologic failure and drug resistance than a viral load < 50 cp/ml. It sounds as though you were having ongoing viremia (i.e. viral load > 50 cp/ml) while on Reyataz, and that allowed drug resistance to occur, leading to resistance to your current regimen of Truvada and Kaletra.
There are no adverse interactions with poppers and ART that I am aware of. Poppers might be a problem if they lead to dis-inhibition and a lesser likelihood of your staying adherent to your medications. You should let your doctor know if your drug-taking has interefered with your adherence to your medications.
Viagra has no effect on the levels of ART; however, Kaletra, or rather the ritonavir in Kaletra, does effect Viagra by increasing the level in the blood. It is recommended that you use the lowest dose of Viagra when you take it with Kaletra. You should talk to your doctor about your dose of Viagra and its effects.
There is no such thing as a 'supervirus'. HIV is not super, whether it is 'wild type' (i.e. it has no resistance mutations) or it has one or many drug resistance mutations. In fact, HIV virus with mutations is usually less fit, i.e. less able to cause disease progression, than wild type. Still, it is reasonable to be wary of drug resistant viruses, as they can compromise the response to ART, as appears to be happening in your situation.
There is some good news for people with some ART resistance in this era. There are more and more potent new drugs, including new classes of drugs, that have been approved or are likely to be approved in the US in the near future that may be useful for such individuals. I suggest that you talk to your doctor about them.
The new drugs include members of existing classes that are FDA approved such as tipranavir and darunavir, new classes that are FDA approved such as miraviroc, and other drugs in existing or new classes that are under FDA review and/or available by expanded access such as the integrase reltegravir and the NNRTI etravirine. Your doctor may be planning to use one or more of these drugs in your next regimen.
The availability of these drugs led the HHS Guidelines Panel in October, 2006 to change the goals of therapy of treatment experienced patients. In the past, the goal had been to stabilize the viral load and either increase or stabilize the CD4 cell count, recognizing that complete viral suppression might not have been possible. Because of clinical trials with the new medicines showing that a majority of patients could be fully suppressed, the goal was changed to be full viral load suppression to < 50 copies/ml and continued immunologic improvement, i.e. rising CD4 cells.
In those trials, most patients who achieved a viral load below 50 copies/ml did so by 6 months after starting the new regime, though occasionally it may take longer than that.
I will end these observations with a strong note of caution. While there are reasons to be optimistic about the range of options for people with drug resistance, great care should be taken in trying to understand why ART has led to virologic failure in the past, and in trying to change factors that led to the development of drug resistnce. The most common reason, and the one that only you control, is adherence to your medicines. Please talk about this with your doctor and develop a plan to maximize your adherence to ART, so that you take optimal advantage of the next regimen.
A common reason for poor adherence is side effects, so I also urge you to talk to your doctor about side effects, if they are a potential problem, so that steps can be taken to either treat them and lessen their impact, or switch to an alterative regimen.