Get the Status "undetectable"And staying there is often the primary goal for people living with HIV. People who maintain undetectable viral loads with less than 50 copies of the virus per milliliter of blood not only improve their own health but Diminuiem the probability of transmission from HIV to sexual partners. But getting the right access to medicines and getting health care are a big part of the equation, that's not all. Even people who are adhering to their therapeutic regimen medication may occasionally experience some blipes on their viral loads, and experience viral load elevation, or keep rebounding, even if low, with viral load above undetectable levels.
This can be a source of confusion and fear. David Fawcell, PhD, LCSW recently They wrote down negative emotions the rebounds in viral load. He experimented after having his viral load undetectable until he unexpectedly climbed up from 400, and then returned to the above detectable levels. "Not having medical and psychological support () in their" safety net "of being" undetectable "has aroused the uncertainty of those living with HIV, who are plagued by concern about the future that I had put out of my consciousness while undetectable is aggravated when I see others who cultivate recklessly having their undetectable status attained, "he said.
For some tips on how to get and stay undetectable and the reason why some people struggle to achieve or remain undetectable, we talked to Keith Henry, MD, an expert in HIV Hennepin Medical Center which has over 25 years of experience caring for people with HIV.
BETA: let's review first, what is "undetectable"?
Dr. Keith Henry: Undetectable refers to a level of virus that is so low that it can not be detected by standard viral load measurements. Usually, "undetectable" refers to a viral load than under 40 copies / mL. But different trials can detect the amount of copies of the virus in the blood at different thresholds. Our lab can actually detect lower levels for counts smaller than 20 copies / mL, but intentionally the report indicates low levels as simply "less than 40". At this point, there is no clinical relevance if the person's viral load is 20 on one visit and 40 the next, and we do not want patients (who can access their lab result through the computer) to make efforts and attempts to get changes viral load at this level.
Let's talk about instances of low-level viremia (low viral replication) between 40 and 500 copies / mL. You see people at his clinic with viral load in this range, which have previously been undetectable or never reached undetectable shortly after the start of treatment?
Yes. And let me explain some nuances here.
If a person was undetectable, then your viral load rises again to a low level and will quickly return to being detectable, which is called "blip". This can happen for a variety of reasons, such as, poe example, if there is a lapse in drug adherence. Sometimes it can happen without blips without any explanation, and generally are not something to worry about if the person will again have undetectable viral load levels.
Viral loads that remain in the range between 50 and 200 copies / mL are a little more difficult to interpret. It may be that the person is not taking their ART daily, but it could be another reason for the person not getting or staying at the undetectable viral load level. I know at least one patient who is incredibly adherent and he never misses doses. In each of his visits to the clinic he will have a viral load that appears between 50 and 200 copies / mL. It's kind of a puzzle why that happens.
People living the experience of more sustained viral loads above 200 copies / mL are a bit more troubling. It is more likely that they will experience treatment failure and that their medications will stop working to control their viral loads at all levels and that they will develop a resistant mutation to such drugs.
You can speculate about why a person who is 100% would stick detectable viral load?
If adherence is not the problem, there are some different ideas about this low level of viremia. It may be that some therapeutic regimens, usually composed of three drugs, are not totally suppressing HIV replication. It may be that the drugs are not penetrating enough to fully enter and work inside the body, such as viscera and lymphatic tissues, or areas of the central nervous system that are "tax havens" or reservoirs for HIV. Lymphoid tissues in HIV-infected patients are often very frightening, perhaps because they offer a sanctuary for HIV with deep tissue. Stroke or gusts of inflammation may also contribute to the activation of HIV in tissues that can spill the virus into the bloodstream where it is detected.
Drug resistance is another matter. We know that some drugs, such as Atripla, are more likely to produce resistant strains of HIV. Some therapeutic regimens, as driven by the protease inhibitors and dolutegravir are less likely to cause drug resistance. So when we get to a rebound in viral levels high enough for concern about drug resistance, we genotyping.
If you find a drug resistant mutation, what do you do? Do you change the person's ART scheme?
If a person has a viral load that remains over 500 copies / mL, and tested positive for the resistance mutation, that would be therapeutic failure-proof. I would like at this point to alter the therapeutic regimen.
But this is a difficult question to answer if someone is constant in viral load that the 200 500 copies / mL. Here's one reason why I think that:
A few years ago, our lab made a switch with a new type of assay that we have used to run the viral load tests. And suddenly a lot of our patients who were suppressed came up with viral loads between 100 and 500 copies / mL. We performed genotype tests to determine whether people had developed resistance to drugs, and found that many had resistance to emtricitabine with the MUUMXV mutation, or to efavirenz with the K184N mutation. Before we started to act on this new information and subject people to new therapeutic schemes, we changed our trial and viral load test procedure to one that we had more confidence in and then most of those patients had remission of their charges viral and became undetectable again.
This really surprised us. It is possible that the test was used to test the resistance was able to detect HIV strains that are minority, but were resistant, but that somehow in general, they were not able to fill the entire system so that people still have capable of maintaining low levels of virus in their blood.
But that is why, before this event, I would automatically say that if you detect a resistance mutation at a low level of viremia, you need to change the therapeutic scheme. But because we find mutations of resistance in people who ended up being retested as undetectable, I would say that for me, that maybe not so black and white. I do not have dogmatic drug therapy change as soon as a mutation of resistance is detected. Fortunately now we have these even more potent schemes, simpler schemes driven by protease inhibitors and dolutegravir that have a high resistance barrier so we see drug resistance very rarely.
There are other reasons why people can get the low-level viremia?
I always holistically evaluate all patients and how their bodies react. This includes food, over the counter medicines and alternative medicines. I had a patient for a while suffered a viremic crisis could not figure out what was going on. He revealed that he started to drink a lot of grapefruit juice, and it was causing a decrease in the levels of its protease inhibitor. Nanaimo wine, proton pump inhibitors and histamine blockers-2 receivers as cimetidine can also affect the metabolism of some HIV drugs
Translated by Claudio Souza's original Undetectable & Low-level HIV Viral Replication and reviewed by Mara Macedo
January 5 of 2016, By Emily Newman