ATLANTA – Putting HIV controllers — who ordinarily don’t need therapy — on highly active antiretroviral treatment (HAART) appeared to reduce markers of chronic inflammation, a researcher said here.
In a small cohort study, the therapy yielded declines in markers of T cell activation both in blood and gut-associated lymphoid tissue (GALT), with significance values from P<0.05 to P=0.005 depending on the test, according to Hiroyu Hatano, MD, of the University of California San Francisco, and colleagues. The researchers also found significant reductions in what were already low levels of HIV RNA in plasma.
But there was no change in the numbers of important immune cells, the CD4-positive T cells, Hatano told reporters in a press conference here at the Conference on Retroviruses and Opportunistic Infections.
The study was prompted, Hatano said, by the observation that – although controllers have stable and low levels of HIV virus in their bodies and ordinarily are not treated – they show signs of both immune system activation and increased atherosclerosis.
The 16 patients in the study had a median plasma HIV RNA level of 77 copies per milliliter, despite a median duration of infection of 10 years. They also had relatively robust immune systems, with a median CD4 count of 615 cells per cubic millimeter of blood.
They were given three drugs for 24 weeks, Hatano said – raltegravir (Isentress) and the single-pill combination of tenofovir and emtricitabine (Truvada). The researchers measured both plasma and cell-associated HIV RNA, proviral DNA both in blood and in GALT, and markers of immune activation.
After the 24 weeks of therapy, they found:
Despite low starting levels, a significant decrease in plasma HIV RNA (P<0.001).
Trends toward decreases in cell-associated RNA and GALT proviral DNA.
No change in CD4 cell counts.
Hatano told MedPage Today that the therapy was well tolerated without any adverse events but, she added, “we fully recognize that the follow-up was short.”
The application of the finding to clinical practice is likely to be limited, largely because – by definition – controllers do not need antiretroviral therapy, commented Scott Hammer, MD, of Columbia University in New York City, the conference’s co-chair.
In any case, it’s not clear that treatment would have a clinical benefit, Hammer told MedPage Today, and “in order to prove there’s a clinical benefit, you would need a big study over many years – and we have other means of preventing atherosclerosis.”
Hammer noted that it is reasonable to put HIV controllers on powerful anti-HIV drugs in the context of a clinical trial, “where the risk and benefits are known.” But other than that, he said, the only circumstance in which he would do so would be if a controller got pregnant.
And even in that case, he said, it’s a concern that the drugs might “disturb the delicate balance between the immune system and the viral load.”
The majority of the patients have opted to continue therapy, so longer follow-up will be available, Hatano told MedPage Today.
Source: MedPage Today.
