Decoded hookworm DNA helps highlight drug targets

Scientists have sequenced the DNA of the hookworm, a parasite
that feeds on blood in the human digestive tract.

The study identified genes responsible for the worm invading the
body, as well as controlling its feeding and growth, and named certain proteins
as potential drug and vaccine targets.

'We now have a more complete picture of just how this worm invades the
body, begins feeding on the blood, and successfully evades the host immune
defences', said Dr Makedonka
Mitreva of the Washington University in St Louis, USA, who led
the study.

Hookworm infections affect ten percent of the world's population. Although
they have been kept in check with drugs, there are many areas where the
parasite has become resistant, and infections are spreading. They
rarely lead to death, but are very dangerous to pregnant women, causing
anaemia and malnutrition, and they delay the development of affected children.

The scientists identified the proteins that allow hookworm larvae to
enter the human body through skin, as well as those needed by the adult
hookworm to feed on blood in the gut.

The team also found which proteins help the hookworm evade the body's
defence mechanisms: SCP/TAP proteins. These are thought to be crucial to
hookworm survival and therefore make ideal drug targets. Because they are
involved in suppressing the host's immune system, they are also being
investigated as potential treatments for auto-immune and inflammatory diseases.

'It is our hope that the new research can be used as a springboard not
just to control hookworm infections but to identify anti-inflammatory molecules
that have the potential to advance new therapies for autoimmune and allergic
diseases', added Dr Mitreva.

The scientists also screened a class of drugs known as protein kinase
inhibitors to find out their effects on hookworms' cell function. They found
that more than 200 of these drugs could
be effective in fighting hookworms, with the most promising candidate currently
used in treating leukemia.

The study was published in Nature Genetics.