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Breakthrough in hiv research at the AMC

by Editorial Staff in Health & Body , 03 juni 2010

Dit artikel is ook in het Nederlands beschikbaar

Hiv, the virus that causes aids, uses an immune response of the first cells it encounters in the body to multiply itself. This immune response, which usually prevents infection in a person, helps hiv to spread out. Researchers of the Academic Medical Centre in Amsterdam published their discovery in the scientific magazine Nature Immunology today. The team, under management of professor Teuynis Geijtenbeek, labels the discovery as unexpected. It was a known fact that the aids virus first encounters so-called dendrite cells.

These defensive cells pick up the intact virus and pass it on to the T-cells. This is how the T-cells get infected and are destroyed so that the immune system collapses. When the dendrite cell sensors detect hiv they send signals into the cell crucial for an affective defense against the virus.

Hiv however, uses these signals for its own benefit. It creates a viral protein hiv needs to keep going. If these signals of the danger sensors could be blocked, the virus will not be able to multiply. The researchers think that could stop the infectious character of hiv.

New knowledge

These findings could be the start for new medications and it creates doubts for a number of treatments that are used at the moment. It is also important to hiv-positive people in whom the virus is almost undetectable because of the drugs they’re taking.

The virus is still present, but is asleep. As long as it is present in the dendrite cells, a co-infection – getting infected with another type of virus – can set off and deteriorate the process of signals and multiplication, say the scientists.

The current therapeutic vaccines that don’t prevent infection but curb its repercussions, need to be re-examined, think Geijtenbeek and his co-authors. “The vaccines in the laboratory today could in theory start off the multiplication of hiv, instead of blocking it.



published Jan 2016       

published Aug 2015       


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