Our knowledge of the biology of the malaria parasite Plasmodium spp. has increased dramatically since the early 1970s through improvements in molecular and cellular biology technology. However, translating this knowledge into an understanding of malaria pathology has been more of a challenge, not least because of the need to include the context of the host-parasite relationship in these studies. This Research Topic will look at the models representing malaria parasite – host cell interactions across a range of platforms based on in vitro, animal and human systems.
In 1976 George Box, a British statistician, wrote “All models are wrong, some are useful” and malaria models are no exception. At times passions have run high over the rightfulness or otherwise of these models, but our ability to translate basic knowledge into mechanistic insights into malaria pathology depends to a large extent on them. The pathologies of malaria disease, in particular severe, life-threatening clinical syndromes are defined by the nature of the combination of the invading pathogen and the host environment that the pathogen encounters and subsequently modifies. Key areas that have been identified that influence disease processes include immunity, inflammation and cytoadherence, all of which can be represented to varying extents using existing models. The goal of this Research Topic is to open a discussion on the models we have, where they have been used effectively and what the latest models can offer, as well as what is still needed. Our ability to develop adjunct therapies for severe malaria is impeded by the lack of representative models – this needs to change.
We welcome Original Research, Brief Research Report, Review and Minireview articles covering in vitro, animal and clinical models of malaria pathogenesis (including immunity). The term ‘clinical model’ may seem unusual, but malaria researchers have used controlled human malaria infection (CHMI) to investigate host responses to infection, and ‘surrogate’ samples of inflammation (e.g., plasma) are frequently used to help understand changes at cellular interfaces. The brief is to take an inclusive view of the models available to researchers and:
• Provide a description of the model(s).
• Show how they have been used and what they told us.
• Discuss their utility and limitations.
• Suggest how the model(s) might be improved.
We know so much about the Plasmodium parasite – models can help us turn this into an understanding of malaria.
Our knowledge of the biology of the malaria parasite Plasmodium spp. has increased dramatically since the early 1970s through improvements in molecular and cellular biology technology. However, translating this knowledge into an understanding of malaria pathology has been more of a challenge, not least because of the need to include the context of the host-parasite relationship in these studies. This Research Topic will look at the models representing malaria parasite – host cell interactions across a range of platforms based on in vitro, animal and human systems.
In 1976 George Box, a British statistician, wrote “All models are wrong, some are useful” and malaria models are no exception. At times passions have run high over the rightfulness or otherwise of these models, but our ability to translate basic knowledge into mechanistic insights into malaria pathology depends to a large extent on them. The pathologies of malaria disease, in particular severe, life-threatening clinical syndromes are defined by the nature of the combination of the invading pathogen and the host environment that the pathogen encounters and subsequently modifies. Key areas that have been identified that influence disease processes include immunity, inflammation and cytoadherence, all of which can be represented to varying extents using existing models. The goal of this Research Topic is to open a discussion on the models we have, where they have been used effectively and what the latest models can offer, as well as what is still needed. Our ability to develop adjunct therapies for severe malaria is impeded by the lack of representative models – this needs to change.
We welcome Original Research, Brief Research Report, Review and Minireview articles covering in vitro, animal and clinical models of malaria pathogenesis (including immunity). The term ‘clinical model’ may seem unusual, but malaria researchers have used controlled human malaria infection (CHMI) to investigate host responses to infection, and ‘surrogate’ samples of inflammation (e.g., plasma) are frequently used to help understand changes at cellular interfaces. The brief is to take an inclusive view of the models available to researchers and:
• Provide a description of the model(s).
• Show how they have been used and what they told us.
• Discuss their utility and limitations.
• Suggest how the model(s) might be improved.
We know so much about the Plasmodium parasite – models can help us turn this into an understanding of malaria.
