News
Key Processes in Malaria Pathogenesis: Keeping on Top Down Under

https://doi.org/10.1016/S0169-4758(99)01437-4Get rights and content

Section snippets

Melbourne, Australia October 1998

Australia may well have been declared free of endemic malaria in 1981, but cutting-edge research towards a better understanding of the pathogenesis of this devastating disease continues to flourish. The breadth and quality of the Australian research effort was highlighted recently when more than 80 researchers from different groups throughout the country gathered together in Melbourne with researchers from overseas for a one-day malaria meeting.

Malaria and the Red Blood Cell

Chris Newbold (John Radcliffe Hospital, Oxford, UK) outlined recent advances in the identification and functional analysis of parasite-encoded proteins involved in the fundamentally important processes of parasite invasion, cytoadhesion and rosetting. Recent work by numerous groups has focused largely on the role of a family of variant surface proteins (known as Plasmodium falciparum erythrocyte membrane protein-1, PfEMP-1) in mediating adhesion of parasitized cells to a variety of receptors

Parasite Transfection

The recently developed transfection system for P. falciparum provides an immensely powerful approach to determine the precise function of a plethora of proteins. David Kemp (Menzies School of Health Research, Darwin) reported on their recent identification of a novel gene present on chromosome 9, appropriately dubbed CLAG (cytoadherence-linked asexual gene) that also appears to be necessary for cytoadhesion. Using transfection specifically to knockout this gene, and a more unusual approach

Malaria during Pregnancy

Malaria during pregnancy is a significant cause of maternal and infant morbidity and mortality. Pregnant women are more susceptible to malaria than their non-pregnant counterparts, experiencing more frequent infections with higher parasite densities. An important factor in infection during pregnancy is thought to be the adhesion of parasitized red blood cells to the glycosaminoglycan chondroitin sulphate A (CSA), which may enable parasites to accumulate in the placenta. James Beeson (WEHI,

Pathogenesis and Drug Development

Nick Hunt (University of Sydney, Australia) presented work describing the biochemistry of murine cerebral malaria. He showed that IFN-γ and TNF-α gene knockout mice were protected against cerebral malaria. However, gp91phox gene knockout mice (which cannot produce superoxide anion radicals and otehr reactive oxygen species), were not protected. Thus, IFN-γ and TNF-α seem to be essential for the pathogenesis of murine cerebral malaria, but phagocyte-derived reactive oxygen species do not appear

Acknowledgements

The meeting, held at La Trobe University, Bundoora, Victoria, Australia, 2 October 1998, as an adjunct to the Annual Meeting of the Australian Society for Parasitology (see L. Kumaratilake, this issue), brought together malariologists from different backgrounds and areas of expertise from throughout Australia and from overseas. It became clear that there are as many questions as answers in almost every aspect of malaria research. A range of viewpoints on the molecular basis of invasion,

First page preview

First page preview
Click to open first page preview

References (4)

  • B. Crabb

    Cell

    (1997)
  • R.L. Coppel

    Curr. Opin. Hematol.

    (1998)
There are more references available in the full text version of this article.

Cited by (0)

View full text