The parasite that causes malaria can change the way you smell, making you more attractive to mosquitoes, according to a new study. The work. Conclusions and Recommendations: Malaria is making a dramatic comeback in The disease, caused by mosquito-borne parasites, is present in and there have been recent reports of drug resistance in people infected with P. . These brief scenarios give a sense of the diverse ways that malaria can affect people. By establishing the attractiveness of these compounds to malaria mosquito vectors .. For all IACs, we found a quantitative relationship: The majority of individuals .. and the antennal tips were guided into the recording electrode to complete.
The mosquitoes showed no preference between two pairs of socks collected at different times from children who never showed a sign of malaria. To learn what caused the different response, scientists sent foot odor samples from 56 kids through a device that analyzed which chemicals were present, then puffed each chemical one at a time over mosquito antennae attached to tiny electrodes.
The test zeroed in on a handful of chemicals that activated the antennae and that also were found at higher levels in infected children. The chief ones were from a class of chemicals called aldehydes, including heptanal, octanal, and nonanal. Those chemicals easily vaporize and are common additives in perfumes. Researchers at Durham University in the United Kingdom are studying whether dogs can be trained to sniff out people with malaria.
Odom John is investigating the potential for a breath test to identify malaria infections. The new body odor work could also help lead to a diagnostic tool, or improve mosquito traps, Logan says.
Malaria infection creates a ‘human perfume’ that makes us more attractive to mosquitoes
But getting the right chemical cocktail is tricky. The new paper found small tweaks in labmade scents influenced whether mosquitoes were enticed. For those that do live, size can be a critical factor.
Often, the smallest adults die before they have a chance to mate or eat. If adults make it to a sunset swarm to hunt for a mate, subtle factors can affect their success.
Males use a complex sensory organ to track and amplify the sound of a female's whine. Both a female's ability to produce the right tones and a male's capacity to track them are crucial to successful pairing.
Despite these complexities, wild mosquito populations are often exceedingly dense. Millions of mosquitoes can hatch daily in a single village.
Pushing a bio-engineered trait into such a vast wild population would be an uphill struggle. In a recent review of the existing studies of mosquito reproduction and survival, Charlwood estimates that, assuming a highly fit malaria-resistant mosquito can be produced, it would take many decades for the resistance trait to come to dominate a wild population through normal genetic inheritance.
And complete population replacement is the goal: In any human-designed mosquito hatchery, the insects are bound to be subject to adaptive pressures that differ from those in the outside world. Any tweaks to their innate timing systems could render transgenic mosquitoes useless in the wild.
In nature, mating takes place during a precise minute window at dusk. Colonies that breed indoors, where the lights are either on or off, are likely to undergo selection for insects that will mate after dark. Even a slight delay in the biological clocks of human-reared mosquitoes could leave them unable to find wild mates.
Antimalarial transgenes themselves make mosquitoes less likely to survive in the wild. In a paper published in Science in AprilBruce Hay, Chun-Hong Chen, and their colleagues at the California Institute of Technology describe a genetic trick that accomplishes this task in Drosophila, and they hope it will translate with relative ease into the mosquito genome.
Hay's group has designed a genetic element they've dubbed Medea, a set of genes that spreads quickly through a population not because it makes individuals more fit, but because it kills the competition. The other way is to whack them in the knees. That's the way Medea works, through everyone's favorite behavior: Beeman hypothesized that this trait was actually a pair of genes, one a toxin that poisoned every egg cell a mother beetle produced, the other an antidote that rescued only the offspring carrying the selfish gene set.
Hay and his group read Beeman's studies and began to brainstorm ways to design a system in Drosophila that could replicate this pattern. Hay's group tinkered with the installation of various toxin genes but could not find a workable system. Either the toxins were so powerful they killed every oocyte before it could be fertilized, or so weak they had no significant effect at all.
Instead of adding the expression of a poisonous protein, we could silence a gene needed for normal embryonic development. The next step is to apply this work from Drosophila to A. The mosquito's entire genome was recently sequenced, but it remains little known compared with Drosophila's genetic code, which has been explored and tinkered with by a multitude of researchers. Still, early oogenesis and embryogenesis in the mosquito is similar to that in Drosophila.
The hope is that bioengineers will be able to use the counterparts of the genes identified in Drosophila to build a Medea element in mosquitoes, then link it to malaria-resistance genes. Now we need to go do it in a real insect, the mosquito, and we want it to fly not only in a nice simple lab environment but [also] in the wild, where it's exposed to uncontrolled temperature, humidity, predators, and genetic diversity.
Any releases of transgenic mosquitoes are expected to be limited to males, which don't feed on blood and so have no direct contact with people.
Your Guide to Malaria | Everyday Health
If the plan succeeds, the right gene driver could replace an entire population of wild mosquitoes with offspring bearing the antimalaria transgene in the course of a year or two. He acknowledges that any factory environment would probably select for traits that reduce mosquitoes' fitness in the wild, but he believes an effective gene driver can overcome the problem. Recent work by geneticists Ken Vernick and Michelle Riehle, of the University of Minnesota, in collaboration with field researchers in Mali and Kenya, shows, for the first time, that the majority of A.
Biologists in Mali captured wild female mosquitoes resting on the walls of huts in a malaria-affected village. The mosquitoes had mated in the wild, and their young were reared in a laboratory, then fed on blood from malaria-infected people in the same village.
A few days later, the researchers dissected the mosquitoes and found that a majority had been able to kill the parasites they had ingested. They've homed in on a single gene locus coding for a leucine-rich protein, APL1, similar to molecules known to work in antipathogen responses of plants and mammals. The study, published in Science inis unique in that it examines malaria resistance in mosquitoes that are the offspring of natural matings by wild parents in a malaria-endemic area.
Most work on transgenic malaria resistance uses colonies of mosquitoes not only removed from the selective pressures of the wild but also tested by their response to rodent, rather than human, malaria. Anything you develop in the lab, where all the insect's needs are taken care of, is very artificial.
The same mechanism of immunity seems to exist in A. Riehle believes building a malaria control strategy around this natural immune response is a much safer bet than relying on transgenes. The finding that resistant mosquitoes dominate wild populations is both encouraging and daunting: One potential weapon for tipping the balance against malaria-bearing mosquitoes is a fungus, endemic to Africa, that attacks adult insects.
The fungus weakens and kills more malaria-infected mosquitoes than malaria-free mosquitoes. Willem Takken is one of a group of researchers exploring the use of the fungus, already commercially produced for use against agricultural insect pests, as a way of knocking down mosquito populations in African villages. Fungal spores mixed in oil, sprayed on sheets of fabric, and then hung on the walls of homes killed a significant number of mosquitoes within days of their first blood meal.
Even if the insects were susceptible to malaria, they died before they'd had time to incubate the contagious form of the Plasmodium parasite in their bodies. The advantage is that the fungus is naturally present in Africa, and mosquitoes may be regularly exposed to it in the wild. Resistance traits evolved in nature are less likely to cause unforeseen problems than completely novel, laboratory-built genes.
That kind of artificial boost may be able to wipe out the minority of the A. If transgenic mosquitoes are ever released into the wild, it will only be after a long series of experiments. Researchers will have to slowly move their bioengineered insects from the lab to carefully sealed outdoor cages to study the effects of natural temperature, humidity, and light regimes.
They'll need to find ways to mass-produce designer insects. Bioengineered mosquitoes will face many legal and ethical hurdles: Some scientists working in the field acknowledge that African health officials are wary of the idea of any genetically modified organism being set loose on their turf. But as Scott points out, there are parts of Africa where families don't name their children until they're two years old because so many of them don't survive.
Young children, whose immune systems are not fully developed, are more susceptible than adults to the loss of red blood cells caused by malaria, and they often die from it. They'd like it to stop.
- Malaria Parasite, Mosquito, and Human Host
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