Largest HIV clinic in the Netherlands
A combination of strengthening and weakening – that is how immunologists and infectiologists hope to bring HIV under control: by giving the immune system a boost whilst hitting the virus hard.

HIV (the human immunodeficiency virus) is a major topic of research at AMC. This is hardly surprising, given that the hospital runs the largest HIV clinic in the Netherlands. The clinic’s multidisciplinary team treats about 1800 patients a year. AMC is working closely with the National AIDS Therapy Evaluation Centre (NATEC) on the development of medicines and an evaluation of combination therapies.

AMC and the city’s public health service (GGD) collect epidemiological data through the Amsterdam Cohort Studies, which is a project to track over a long period a group of people who are infected with HIV. Work in the laboratory includes studies into how the virus is evolving, the influence of the host’s genetic make-up, and potential new vaccines. Meanwhile, the Emma Children’s Hospital at AMC has become a centre of expertise on the treatment of youngsters with AIDS. The institution is thus heavily engaged in a wide range of research activities, all of which share the ultimate goal of finding HIV’s Achilles’ heel.

Delivering anti-inflammatory molecules with pinpoint accuracy
Recent decades have seen a substantial rise in the number of autoimmune diseases and allergies in the Western world. However, opportunities for treatment have been improved by the development of anti-inflammatory molecules. In the case of rheumatoid arthritis, the target is TNF, a protein that occurs in large quantities in patients’ joints. To minimize side effects, the TNF blocker should ideally be active only in the inflamed joints. The solution may be gene therapy with an adeno-associated virus (AAV) that's been rendered incapable of replication. Major advantages: its impact is strictly local and it has long-term clinical effects. The researchers have also built in an ‘on-off switch’ that responds to inflammatory factor; therefore, the introduced gene produces TNF-blocking proteins only during an active inflammation.