Tokyo, July 3 (IANS) Researchers have developed a new approach to study liver cell infection by a malaria parasite which could lead to better diagnosis and treatment of the disease in India.
A new approach could illuminate a critical stage in the life cycle of one of the most common malaria parasites, the Plasmodium vivax, said the study published in the Malaria Journal.
“The Plasmodium vivax malaria parasite can stay dormant in a person’s liver cells up to years following infection, leading to clinical relapses once the parasite is reactivated,” said study co-author Kouichi Hasegawa, a stem cell biologist at Kyoto University’s Institute for Integrated Cell-Material Sciences (iCeMS) in Japan.
P. vivax is responsible for around 7.5 million malaria cases worldwide, about half of which are in India.
Currently, there is only one licensed drug to treat the liver stage of the parasite’s life cycle, but it has many side effects and cannot be used in pregnant women and infants.
The liver stage is also difficult to study in the lab.
For example, scientists have struggled to recreate high infection rates in cultured liver cells.
Hasegawa and his colleagues in Japan, India and Switzerland developed a successful system for breeding mature malaria parasites, culturing human liver cells, and infecting the cells with P. vivax.
While it does not solve the high infection rate problem, the system is providing new, localised insight into the parasite’s liver stage.
“Our study provides a proof-of-concept for detecting P. vivax infection in liver cells and provides the first characterisation of this infectious stage that we know of in an endemic region in India, home to the highest burden of vivax malaria worldwide,” said Hasegawa.
The researchers took blood cells from malaria-infected patients, coaxed them into pluripotent stem cells, and then guided those to become liver cells.
The scientists were able to study one of the many aspects of parasite liver infection.
They observed that the malaria protein UIS4 interacted with the human protein LC3 which protected the parasite from destruction.