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New antibody therapy “profoundly” successful at reducing inflammation from HIV

, by Emily Newman

In a very small study of people living with HIV, a one-time antibody treatment significantly reduced the type of inflammation that can lead to heart attacks and other cardiovascular problems—a leading health concern for people living, and aging, with HIV. Priscilla Hsue, MD, FACC, a physician at the University of California San Francisco, presented these findings at CROI 2017 last month.

This study, and other studies that investigate therapies to reduce HIV-associated inflammation, will be increasingly important as people living with HIV are able to live longer. Even people with well-controlled HIV are at greater risk of developing cardiovascular disease—and increased inflammation is likely to blame. Antiretroviral therapy can decrease inflammation, but does not eliminate it completely.

Want to learn more about inflammation? Read this excellent article by Dr. Joanna Eveland on BETA.

Priscilla Hsue, MD, FACC

Priscilla Hsue, MD, FACC (Photo: BETA)

“I think it’s remarkable that in a small number of patients after just getting a single dose of canakinumab, were able to demonstrate a very significant and profound reduction in inflammation as well as a reduction in arterial inflammation,” said Hsue.

The treatment used in the study was an monoclonal antibody, named canakinumab, that binds and blocks an IL-1β receptor on cytokines (which is part of a cell signaling pathway upstream in a pathway that leads to inflammation). The ten participants in the study received one single dose of canakinumab (150 mg) under the skin. Safety labs were done at weeks 1, 2, 3, 4, 8 and 12; inflammation was measured at the beginning of the study and at week 8.

Canakinumab significantly reduced a marker of inflammation, interleuken-6 (IL-6), by 24% after four weeks. The therapy reduced IL-6 by 30% after eight weeks.

The antibody treatment also significantly reduced two additional markers of inflammation. High sensitivity C-reactive protein (hsCRP) was reduced by 41% after eight weeks and soluble CD163 was reduced by 9% after eight weeks.

Hsue’s team also assessed inflammation by taking scans of the bone marrow and artery walls before and after the antibody therapy.

“IL-1 β inhibition with canakinumab had a significant impact on arterial inflammation and bone marrow activity,” said Hsue. “There was a significant reduction in both of these indices. Quantitatively, there was a 10% reduction in arterial inflammation among people treated with canakinumab from baseline to week eight, and an 11% reduction in bone marrow metabolic activity from baseline to week eight.”

This study is one of the first to show that an immune-based therapy can profoundly reduce markers of inflammation in people with HIV—and importantly, in people with already well-controlled HIV. (Everyone in the study had been living with HIV for over 20 years and had good viral control, i.e., were on antiretrovirals with an undetectable viral load.) The antibody therapy did not have any negative effects on viral control of CD4 count, and was well-tolerated by people in the study.

Canakinumab is already approved by the FDA as a treatment for other conditions, but further research is needed to demonstrate if it is safe and effective at reducing inflammation for people living with HIV. A study is currently underway, said Hsue, of 100 people randomized to a placebo-controlled study. People receiving the investigational drug will get two doses, and will be followed for a total of 36 weeks.

Read more HIV research news from the 2017 Conference on Retroviruses and Opportunistic Infections.

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