DURBAN, S. Africa (Reuters) - Intermittent use of the cancer drug interleukin 2 (IL-2) can boost the immune system of HIV-infected patients already taking standard antiretroviral drugs, conclude researchers from the US National Institutes of Health (NIH), in Bethesda, Maryland.

"After a year there was a substantial increase in CD4 (immune cell) counts," in patients taking combination therapy, explained study co-author Dr. H. Clifford Lane. He presented the findings, which are to be published in the July 12th issue of The Journal of The American Medical Association, at a press briefing held here Saturday as part of the XIII International AIDS Conference.

Antiretroviral drug cocktails--powerful combinations of protease inhibitors and other HIV-suppressing medications--have helped many HIV-infected patients keep the symptoms of AIDS at bay over the long term.

The NIH researchers speculate that IL-2, which has long proven useful against certain cancers despite its sometimes toxic side effects, might also give 'added value,' to standard HIV therapy.

Although IL-2 has no direct effect in suppressing the proliferation of HIV, it does have a stimulating effect on the growth of immune system CD4 cells, which are white blood cells that are the prime targets of the virus that causes AIDS. In fact, low levels of CD4 cells in the blood are an ominous indicator of a weakened immune system, signaling that the patient may be vulnerable to the infections and illnesses that characterize AIDS.

In their study, Lane and his colleagues assigned 39 HIV-positive adults a combination of standard anti-retroviral therapy and 5-day courses of twice-daily injections of IL-2, given once every two months over the course of a year. Another group of 43 patients received anti-retroviral therapy alone.

"After one year there was a very substantial increase in the CD4 count in the IL-2 treated group" compared with those who went without the drug, Lane told reporters. Patients on IL-2/antiretroviral therapy saw their CD4 cell counts rise an average of 112% over the course of treatment, compared with a rise of just 18% in those receiving standard therapy.

The researchers note that improvements in immune function seemed to rise with increasing dosage of IL-2, with those receiving the highest dose charting a 207% rise in CD4 cell counts compared with the average 39% increase seen in patients on the lowest dose.

Finally, the NIH team was pleased to report that the viral load--a measure of the amount of virus found in a patient's blood--actually fell slightly in those taking IL-2 compared with those not taking the drug. In fact, two-thirds (67%) of patients taking IL-2 saw their viral load level decline to the very low level of fewer than 50 copies of HIV per milliliter of blood. In contrast, just 37% of those who did not take the drug achieved that goal.

There was a down side to the combo therapy, however. IL-2, while safe over the long term, does have side effects. "Toxic effects were common among patients," on the IL-2 therapy, the researchers report, and included flu-like complaints such as fever, fatigue, and muscle aches. However, most patients were able to minimize these effects by skipping or re-scheduling IL-2 dosages, or by using pain-relievers such as ibuprofen or acetaminophen.

Lane also pointed out that once IL-2 nudges CD4 to healthier levels, treatments can be stretched out over longer and longer intervals before the next booster treatment is required.

"You get the (CD4) pool large enough and it replicates and replenishes," he told Reuters Health. "We've had patients who haven't had a cycle of therapy for three, four years."

The next step, he said, will be to find out if IL-2-generated CD4 cells are as functional and effective as immune cells produced the natural way. Two international trials, involving thousands of patients are underway to assess whether the rise in CD4 prompted by IL-2 is of lasting clinical benefit.

Lane is betting the results will be positive. "As best we can tell in tests in the laboratory these cells are indistinguishable from other CD4 cells," he said.

SOURCE: The Journal of the American Medical Association (JAMA)