Five new malaria vaccine targets identified

US scientists have identified five malaria vaccine targets that have the potential to reduce the parasite's ability to invade blood cells.

Malaria is a disease caused by a plasmodium parasite, transmitted by the bite of infected mosquitoes.

In 2015, malaria was responsible for the death of nearly half a million people globally and it infects more than 200 million people each year.

The results showed that the vaccines may be most effective if they target multiple parasite factors at its most vulnerable stage -- when invading human red blood cells.

Red blood cell invasion is an essential step in the parasite's lifecycle and is a stage when the parasite is at its most vulnerable and exposed to the immune system.

Further, the malaria parasite should be targeted in combination.

Alone, no single antibody gave protection against malaria in people. However, combinations of the new antibodies did protect against the parasite, the researchers suggested.

"Producing a successful vaccine against parasites is challenging because they are very complex organisms with many components, making it difficult to know which ones to target," said Gavin Wright, from the Wellcome Trust Sanger Institute in the US.

For the study, published in the journal PNAS, the team raised rabbit antibodies against 29 potential targets, then tested the antibodies against two different strains of the deadly Plasmodium falciparum malaria, one from Africa and one from Asia.

Of the 29 antibodies, the researchers discovered five that reduced the parasite's ability to invade red blood cells in both malaria strains.

Moreover, the researchers also used video microscopy to watch the parasite attempt to invade red blood cells with and without the presence of antibodies.

They discovered that the different antibodies were attacking the parasite at different steps as it invaded the red blood cell.

Thus pairing antibodies that each acted at different steps led to a more effective combination, the researchers said.

--IANS

rt/him/mr