Get the Status "undetectable"And staying there is often the primary goal for people living with HIV. People who maintain undetectable viral loads under 50 copies of the virus per milliliter of blood, not only improve their own health butDiminuiem the probability of transmission for sexual partners of HIV. But getting the right to access to medicines and get health care are a big part of the equation, is not all. Even people who are adhered to their medication regimens may experience occasionally algumuns "blipes" in their viral loads, and has the experience of high viral load or that remain in constant rebound, even if low, viral load above undetectable levels.
This can be a source of confusion and fear. David Fawcell, PhD, LCSW recentlyThey wrote down negative emotions the rebounds in viral load.He experienced after his viral load undetectable to unexpectedly rise from 400, and then returned to above detectable levels. "Not having medical and psychological support () in its" safety net "to be" undetectable "aroused the uncertainty of living with HIV, which torment the concern about the future that I had put out of my consciousness as undetectable is aggravated when I see others who cultivate thoughtlessly having their status achieved undetectable, "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 can not be detected by standard viral load measurements. Typically, "not detectable" refers to a viral load than under 40 copies / mL. But different tests can detect the amount of virus copies in blood in different thresholds. Our laboratory can actually detect the lowest levels for lower scores 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 a visit and 40 next, and we do not want patients (who can access their laboratory results via computer) make efforts and attempts to get changes viral load at that 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 her ARVs every day, but could be another reason for people not obtain or remain at the level of undetectable viral load. I know at least one patient who is incredibly sticky and he never misses doses. In each of his visits to the clinic he'll have a viral load that appears between 50 and 200 copies / mL. It's kind of a puzzle why this is happening.
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 sticka detectable viral load?
If compliance is not the problem, there are some different ideas on this low level of viremia. There may be some therapeutic regimens, usually composed of three drugs are not totally suppressing HIV replication. It may be that drugs are not sharp enough to fully enter and work within the body, as the bowels and lymphatic tissues, or areas of the central nervous system that are "tax havens" or reservoirs for HIV. Lymphoid tissue in HIV-infected patients are often very frightening, perhaps because they offer sanctuary for HIV with the deep tissues. Course or bursts of inflammation may also contribute to the activation of HIV in tissue that can shed 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 mutation resistant to medications, what to do? You change HAART scheme of the person?
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 laboratory made a switch to a new type of test that we used to run viral load tests. And suddenly a lot of our patients who were suppressed emerged with viral loads between 100 and 500 copies / mL. We genotype tests to determine if people have developed drug resistance, and found that many were resistant to emtricitabine with M184V mutation or efavirenz with K103N mutation. Before we begin to act on this new information and refer people to new regimens, we changed our test and viral load test procedure to one that had more confidence in and then most of these patients had remission of their charges viral and went back to being undetectable.
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's why, before this event, I automatically say that if you detect a resistance mutation at a low level of viremia, you need to change the treatment regimen. But because we find resistance mutations in people who turned out to be retested as undetectable, I would say that for me, which is perhaps not so black and white. I am not as dogmatic drug therapy change as soon as a mutation of resistance is detected. Fortunately, we have now these more powerful schemes, simpler schemes driven by dolutegravir protease inhibitors, and that have a high barrier resistance so that drug resistance we 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 originalUndetectable & Low-level HIV Viral Replicationand reviewed by Mara Macedo
5 January 2016,PorEmily Newman