Malaria paradoxically blocks further malaria infection

[Saddle Bronc 124]

http://www.bbc.co.uk/news/health-13387983

Malaria blocks 'super-infection'

2011/05/15 13:04 ET

People can be bitten by 700 malaria-infected mosquitoes a year in some countries

The malaria parasite can ensure it keeps a host body all to itself by preventing further malarial infections, according to international researchers.

The parasite initially reproduces in the liver and moves into the blood.

A study on mice, published in Nature Medicine, showed the parasite can trigger iron deficiency in the liver and therefore prevent more infections.

An expert said the research was "very cool and very interesting", and improved understanding of infection.

The researchers were looking at super-infections, when a patient already infected with malaria is infected with another batch of malaria parasites.

People in high-risk areas can be bitten by up to 700 different malaria-infected mosquitoes each year.

Protecting turf

In experiments on mice, researchers showed that parasites in the blood were able to stimulate the production of the hormone hepcidin, which regulates iron levels.

This reduced the level of iron in the liver, preventing other malaria parasites from reproducing in the organ.

Dr Hal Drakesmith, from the Weatherall Institute at Oxford University, who was part of the Medical Research Council team, said: "Now that we understand how malaria parasites protect their territory in the body from competitor parasites, we may be able to enhance this natural defence mechanism to combat the risk of malaria infections."

Malaria is often accompanied by anaemia, which is treated with iron supplements.

In this study, mice given iron supplements were more susceptible to additional infections.

Dr Drakesmith said: "We may need to look again at the advisability of iron supplementation programmes in malaria-endemic regions, as possible increased risk of infection may need to be weighed against benefits."

Dr Rita Tewari, a malaria researcher at the University of Nottingham, said: "It's very cool and very interesting.

"It tells us a bit more about the mechanism of malaria infection and gives us some sort of tool, this molecule hepcidin, that you can manipulate which can affect infection."

[IR5FORMUMSIE 850]

http://www.bbc.co.uk...health-13387983

I don't think that it is that surprising but the upshot of regulation of iron levels to help combat the spread of Plasmodium is very interesting. The article didn't go on to discuss the concept of infecting someone with, for example, a relatively benign for of malaria such as P. ovale in an effort to fend off one of the nastier types of malaria such as P. falciparum. I wonder if this might be an idea worth pursuing?

[justashooter 430]

I don't think that it is that surprising but the upshot of regulation of iron levels to help combat the spread of Plasmodium is very interesting. The article didn't go on to discuss the concept of infecting someone with, for example, a relatively benign for of malaria such as P. ovale in an effort to fend off one of the nastier types of malaria such as P. falciparum. I wonder if this might be an idea worth pursuing?

i wouldn't put much faith in that, or in the findings of this report. my own experience with vivax and subsequent research into the life cycle indicates that the subtypes have significant differences in reproduction cycle. iron deficiency may be co-related, but is likely not the inhibiting factor.

cystic reproduction within the liver is common, but the liver is a very complex organ, many of the functions of which we do not understand even today.

[IR5FORMUMSIE 850]

i wouldn't put much faith in that, or in the findings of this report. my own experience with vivax and subsequent research into the life cycle indicates that the subtypes have significant differences in reproduction cycle. iron deficiency may be co-related, but is likely not the inhibiting factor.

cystic reproduction within the liver is common, but the liver is a very complex organ, many of the functions of which we do not understand even today.

If we're talking about something like vivax or ovale which can have dormant hypnozoites (cysts) that can reinfect after days, months or even years, then I would agree. However, since falciparum is the monster, any technique that can stop it or limit it, is worth pursuing.

The liver is a very complex organ, with many functions, we haven't figured out how to emulate all its functions.

[justashooter 430]

"stimulate the production of hepcidin", and do what else? the liver makes hundreds of "hormones" for dozens of purposes. some are endo-exocrines, and some are exo-endocrines. who is to say that the inhibition isn't an incidental interdiction of the plasmodium repro process. all the article gives us in one of many potential correlations.

that being said, penecillin was first noted as a territorial inhibitor of competing bacterium...logic leads me to believe that any inhibiting factor is a product of the parasite, itself (that happens to create anemia), rather than an induced product of the host. always look for the simplest answer.

[IR5FORMUMSIE 850]

"stimulate the production of hepcidin", and do what else? the liver makes hundreds of "hormones" for dozens of purposes. some are endo-exocrines, and some are exo-endocrines. who is to say that the inhibition isn't an incidental interdiction of the plasmodium repro process. all the article gives us in one of many potential correlations.

that being said, penecillin was first noted as a territorial inhibitor of competing bacterium...logic leads me to believe that any inhibiting factor is a product of the parasite, itself (that happens to create anemia), rather than an induced product of the host. always look for the simplest answer.

Without getting into a long discussion of falciparum adhesive factors and RBCs, this is not a case where this is a panacea. The major issue is whether altering the homeostasis of the liver, and thus the body will so alter the ability of the parasites to function. What the article did state is that the researchers came to the same conclusion that you did, albeit you disagree, to a certain extent, with respect to the source. This is a simple article, reading the actual research material might be more useful to deal with your questions.

As for penicillin, the beta-lactam ring of penicillin is a competitive inhibitor in as much as it prevents the bacterial cell walls from forming by the competitively binding to the enzyme and thus prevent formation of the cell wall. It is not a territorial inhibitor as you put it since it does not allosterically affect the binding site, if I read what you post correctly, but that is beside the point.

[justashooter 430]

Without getting into a long discussion of falciparum adhesive factors and RBCs, this is not a case where this is a panacea. The major issue is whether altering the homeostasis of the liver, and thus the body will so alter the ability of the parasites to function. What the article did state is that the researchers came to the same conclusion that you did, albeit you disagree, to a certain extent, with respect to the source. This is a simple article, reading the actual research material might be more useful to deal with your questions.

As for penicillin, the beta-lactam ring of penicillin is a competitive inhibitor in as much as it prevents the bacterial cell walls from forming by the competitively binding to the enzyme and thus prevent formation of the cell wall. It is not a territorial inhibitor as you put it since it does not allosterically affect the binding site, if I read what you post correctly, but that is beside the point.

the beta lactam ring inhibits the formation of peptidoglycan cross links in competing cell walls, thereby destroying the competing cells. it seems that the purpose or function of the ring is to prevent competing cells from absorbing resources immediately adjacent the cell emitting the exo-enzyme.

[웃 910]

I don't think that it is that surprising but the upshot of regulation of iron levels to help combat the spread of Plasmodium is very interesting. The article didn't go on to discuss the concept of infecting someone with, for example, a relatively benign for of malaria such as P. ovale in an effort to fend off one of the nastier types of malaria such as P. falciparum. I wonder if this might be an idea worth pursuing?

i wouldn't put much faith in that, or in the findings of this report. my own experience with vivax and subsequent research into the life cycle indicates that the subtypes have significant differences in reproduction cycle. iron deficiency may be co-related, but is likely not the inhibiting factor.

cystic reproduction within the liver is common, but the liver is a very complex organ, many of the functions of which we do not understand even today.

If we're talking about something like vivax or ovale which can have dormant hypnozoites (cysts) that can reinfect after days, months or even years, then I would agree. However, since falciparum is the monster, any technique that can stop it or limit it, is worth pursuing.

The liver is a very complex organ, with many functions, we haven't figured out how to emulate all its functions.

"stimulate the production of hepcidin", and do what else? the liver makes hundreds of "hormones" for dozens of purposes. some are endo-exocrines, and some are exo-endocrines. who is to say that the inhibition isn't an incidental interdiction of the plasmodium repro process. all the article gives us in one of many potential correlations.

that being said, penecillin was first noted as a territorial inhibitor of competing bacterium...logic leads me to believe that any inhibiting factor is a product of the parasite, itself (that happens to create anemia), rather than an induced product of the host. always look for the simplest answer.

Without getting into a long discussion of falciparum adhesive factors and RBCs, this is not a case where this is a panacea. The major issue is whether altering the homeostasis of the liver, and thus the body will so alter the ability of the parasites to function. What the article did state is that the researchers came to the same conclusion that you did, albeit you disagree, to a certain extent, with respect to the source. This is a simple article, reading the actual research material might be more useful to deal with your questions.

As for penicillin, the beta-lactam ring of penicillin is a competitive inhibitor in as much as it prevents the bacterial cell walls from forming by the competitively binding to the enzyme and thus prevent formation of the cell wall. It is not a territorial inhibitor as you put it since it does not allosterically affect the binding site, if I read what you post correctly, but that is beside the point.

the beta lactam ring inhibits the formation of peptidoglycan cross links in competing cell walls, thereby destroying the competing cells. it seems that the purpose or function of the ring is to prevent competing cells from absorbing resources immediately adjacent the cell emitting the exo-enzyme.

[IR5FORMUMSIE 850]

the beta lactam ring inhibits the formation of peptidoglycan cross links in competing cell walls, thereby destroying the competing cells. it seems that the purpose or function of the ring is to prevent competing cells from absorbing resources immediately adjacent the cell emitting the exo-enzyme.

That is one way of looking at it, at least from a survival point of view. It wouldn't make sense for the penicillin to act on itself, that's what various bacteria do by inactivating the beta-lactam ring. If the bacterial cell wall is not properly constructed then, yes, it will lyze and that will be a survival advantage to the penicillin fungi., thus by secreting it into the interstitial space, so to speak, it would indeed as an external enzyme or exoenzyme. It is quite fascinating the way in which bacteria deal with measures and counter-measures but we only seem to be providing fodder for some VJers.