Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

It is estimated that over 200 million people each year suffer debilitating attacks of malarial fever, and roughly 2 million of these episodes are fatal. The fever is caused by tumour necrosis factor (TNF) and other pyrogenic cytokines that are released by the host immune system response to products of schizont rupture. TNF has anti-parasitic properties but excessive TNF production is thought to play an important role in the pathogenesis of cerebral malaria. This review summarizes recent attempts to achieve molecular characterization of the parasite components that stimulate the host TNF response, and to define the host and parasite factors that affect the level of TNF production. Of particular interest are host polymorphisms that may regulate TNF gene expression, and naturally acquired antibodies that prevent the parasite from inducing TNF, both of which correlate with the clinical severity of infection. Our understanding of these processes, which are potentially of considerable therapeutic relevance, remains very limited at both the molecular and the epidemiological level.

Original publication




Journal article


Ann Trop Med Parasitol

Publication Date





533 - 542


Child, Cytokines, Fever, Humans, Malaria, Cerebral, Polymorphism, Genetic, Tumor Necrosis Factor-alpha