快猫短视频

VISITORS welcome shelter, transport and an influential friend to open doors
for them. And all three services may be ready and waiting for HIV when it enters
the body, courtesy of a little-studied type of immune cell. This cell could be
the key to finding ways to prevent or slow the disease.

Yvette van Kooyk of the University Hospital Nijmegen St Radboud in the
Netherlands and her colleagues were interested in dendritic cells, members of
the immune system that wait patiently under the skin or mucous membranes for any
sign of intruders. When they detect a virus or bacterium, they digest it and
hurry to present pieces of the invader to T cells. Once primed, the T cells
begin to multiply and mount an attack on the invader.

Dendritic cells have attracted little scientific attention. But when van
Kooyk鈥檚 group decided to investigate how they managed to find and interact with
the more aggressive T cells, they found that a protein on the dendritic cell鈥檚
surface, which they called DC-SIGN, played a key role in binding the two types
of cells together.

The researchers then compared the DC-SIGN sequence with a protein database
and found, to their surprise, that it matched a protein discovered in 1992 that
binds to HIV. 鈥淏ack then, nobody knew where the protein came from or what it
did, so no one followed up on it,鈥� says van Kooyk.

Next, they looked at how HIV interacted with the protein in test-tube assays.
HIV is known to use a variety of surface proteins on T cells as handholds to
invade and transform them into viral factories. But to their surprise, the
researchers found that DC-SIGN did not help the virus replicate. Instead, it
seems to provide the virus with at least three other services.

First, it stabilises the virus. Free virus degrades rapidly, loosing its
ability to infect cells in less than a day. In contrast, the researchers found
that viruses bound by DC-SIGN remain infective for four days. Secondly, the
protein boosts infectivity, allowing even small amounts of HIV to invade T
cells. The researchers think that the virus also uses its affinity for DC-SIGN
to hitch a ride from the site of infection right to the front door of the T
cells it attacks.

鈥淭his is a new, exciting glimpse at tricks the virus uses to stay afloat,鈥�
says Beatrice Hahn of the University of Alabama at Birmingham, who studies HIV
evolution and advises the US National Institutes of Health on vaccine
development. 鈥淎nd it could offer a new angle of attack.鈥� In fact, the
researchers suggest that naturally occurring mutations in DC-SIGN might already
protect some people, accounting for some of the unexplained instances of
individuals who are highly resistant to HIV. If that is true, then a vaccine
that blocked DC-SIGN, for instance, might slow or stop the spread of HIV
throughout the body.

To test this idea, van Kooyk and her colleagues plan to test the ability of
molecules that block DC-SIGN to forestall disease in primates.