4 Matching Annotations
  1. Jul 2018
    1. On 2013 Jul 16, Matthew Child commented:

      A fascinating story, complemented by elegant proof-of-principal experiments presented by Regev-Rudzki, N (PMID:23683579). Like rats from a sinking ship, the parasite seeks to escape the hostile environment induced by the drug. It neatly addresses phenomenological observations noted during P. falciparum culture and transfection; the process of electroporation and subsequent drug selection for a transgenic population can often result in the production of large numbers of gametocytes.

      One question and point of epidemiological relevance that arises in light of these data is as follows; is the rate of parasite transmission greater in areas where drug-treatment regimes are instigated? Could it be that we have in fact been inadvertently increasing the likelihood of parasite transmission through drug treatment programs that induce gametocytogensis of the parasite population in an infected individual? The data may already be available to answer this, and I’d be fascinated to hear if anyone out there knows of any published studies that have sought to address this point.


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    2. On 2013 Jun 25, Dave Richard commented:

      In this paper, Mantel et al provide an in-depth characterization of P. falciparum infected red blood cell derived microvesicles (RMVs) and provide evidence for their role in stimulating the human immune system and interestingly, as a means of cell-to-cell communication leading to increase parasite gametocytogenesis, a phenomenon also described in a recent paper published in Cell by Regev-Rudzki and Wilson et al.

      Intriguingly, the authors demonstrate that RMVs are exempt of knob components such as KAHRP and PfEMP1. The latter's role in modulating host responses is well documented so it will be of great interest to identify what components of the RMVs interact with the host immune system. Moreover, to gain insight into the mechanisms behind RMV secretion, it would be interesting to look whether RMVs produced by knobless parasite strains like D10, where PfEMP1 is distributed more uniformly on the erythrocyte surface, would still be devoid of PfEMP1.


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.

  2. Feb 2018
    1. On 2013 Jun 25, Dave Richard commented:

      In this paper, Mantel et al provide an in-depth characterization of P. falciparum infected red blood cell derived microvesicles (RMVs) and provide evidence for their role in stimulating the human immune system and interestingly, as a means of cell-to-cell communication leading to increase parasite gametocytogenesis, a phenomenon also described in a recent paper published in Cell by Regev-Rudzki and Wilson et al.

      Intriguingly, the authors demonstrate that RMVs are exempt of knob components such as KAHRP and PfEMP1. The latter's role in modulating host responses is well documented so it will be of great interest to identify what components of the RMVs interact with the host immune system. Moreover, to gain insight into the mechanisms behind RMV secretion, it would be interesting to look whether RMVs produced by knobless parasite strains like D10, where PfEMP1 is distributed more uniformly on the erythrocyte surface, would still be devoid of PfEMP1.


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.

    2. On 2013 Jul 16, Matthew Child commented:

      A fascinating story, complemented by elegant proof-of-principal experiments presented by Regev-Rudzki, N (PMID:23683579). Like rats from a sinking ship, the parasite seeks to escape the hostile environment induced by the drug. It neatly addresses phenomenological observations noted during P. falciparum culture and transfection; the process of electroporation and subsequent drug selection for a transgenic population can often result in the production of large numbers of gametocytes.

      One question and point of epidemiological relevance that arises in light of these data is as follows; is the rate of parasite transmission greater in areas where drug-treatment regimes are instigated? Could it be that we have in fact been inadvertently increasing the likelihood of parasite transmission through drug treatment programs that induce gametocytogensis of the parasite population in an infected individual? The data may already be available to answer this, and I’d be fascinated to hear if anyone out there knows of any published studies that have sought to address this point.


      This comment, imported by Hypothesis from PubMed Commons, is licensed under CC BY.