Hi Doc, my question is the following: how come there are patients that are undetectable and never taken any meds? if there is a chance that someone get rid of his virus, what test will tell this person if he is virus free?

A small percentage of patients who are infected with HIV, e.g. who have a positive HIV antibody test and a positive confirmatory Western Blot blood test, are able to control the level of the virus in their blood for a period of time, and so have plasma RNA levels, i.e. 'viral loads', that are below the level of detection.

When these individuals maintain this status for 10 years or more, during which time they have no signficant decrease in their CD4 cell count and no HIV/AIDS opportunistic infection, we refer to them as 'long term non-progressors'.

In general, 1 in 4 people infected with HIV have higher viral load set points and a more rapid clinical course, and often will progress to AIDS in a time period that is shorter than the normal 10 years (in the United States and Europe). (In other countries of the world, there are shorter time periods for HIV to develop into AIDS with serious opportunistic infections, e.g. 5-7 years in Kenya, Thailand, and Ukraine; this phenomenon is more likely related to other health issues in those countries, including other infections and nutritional status.) For the other 3/4 of patients in the US and Europe, a slower course of disease progress occurs, and this has been associated with a lower average viral load 'set point'.

Finally, 1-2% of patients may have the undetectable viral load and extremely slow disease progression, and these are the 'long term non-progressors.' Unfortunately, it appears that these individuals do eventually develop a detectable viral load, falling CD4 cells, and clinical signs of AIDS eventually.

It is likely that an individual's genetic make up contributes to these differences. In a dramatic recent example that was presented at the recent CROI meeting in Boston in February, a person with HIV who was on HAART with a viral load below detection, developed a leukemia for which a bone marrow transplant was required. His physicians found a bone marrow donor who was homozygous for the CCR5 entry protein delta 32 insertion mutation that has been associated with protection from HIV infection. His HAART was stopped, and the bone marrow transplant was successful. Since then, he has had no more HAART after 7 months, and he remains with a viral load below detection.

This will not provide a practical solution for most patients, but it does show an example of the potential impact of genetic control of HIV.

The importance, then, of people with HIV who have an undetectable viral load with HAART is that they probably are among those patients with a slower natural history; however, they eventually will need ART like all patients with HIV.

Importantly, these individuals have NOT 'gotten rid of the virus;' they are still HIV infected and able to transmit the virus to others, and they should still follow safer sex recommendations to ensure that they do not infect others.

In the meantime, we may learn important and useful information from the long term non-progressors that can add to our understanding of the pathophysiology of AIDS and lead to new options for HIV treatments.