“Aspergillus fumigates: virulence genes in a street-smart mold” Synopsis

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This article tells us about how Aspergillus fumigates has certain virulence factors that are unique to itself. This type of fungus is able to adapt to different environments. The "street smart" idea in this article is due to the fact that this fungus is able to act quickly upon changes. It has its own little ways to detect and therefore adapt to different situations.

The main way to get A. fumigates is by inhaling its spores which are known as conidia. Because these spores can be cleared out in healthy individuals, it is more of a problem in the immunosuppressed.  This mold is most commonly found in these individuals. Conidia germinate into hyphae which then grow to damage the epithelial barrier. From there, the fungus is then able to penetrate into blood vessels. Once there inside blood vessels, hyphal fragments are able to move to other locations in the body.  By the time these fragments have dispersed throughout the body, curing the infection is much harder. Once in the host, it has to constantly get nutrients and this is done by special enzymes and proteases. To continue living inside the host, A. fumigates have certain gene products that help it to adapt to changes in environment.

Fluctuating temperatures inside the body are a cause of death to many microorganisms. Some just can't take the high temperatures of the host. A. fumigates has the ability for this not to be a problem for it. It has this special characteristic called thermotolerance, which is ability to withstand heat. There have been three genes identified that contribute to this thermotolerance. If any one of those genes is disrupted, thermotolerance will be affected.

In addition to thermotolerance, they have a unique cell wall. It is made up of complex substances that give them much strength. There are genes that also contribute to a rigid yet permeable cell wall. Even if there is a reduction by half of a certain gene, our "smart" mold will be able to still keep its homeostasis. One key ingredient of their cell wall is chitin, which contributes to the cell wall strength. Chitin helps provide structural integrity for it. This strong barrier is an integral component of the organism, which is why it has seven different chitin synthase genes (just to ensure a "backup"). Since this chitin cell wall is specific to fungi, it is the target of many anti fungal treatments. So, since there is a target in place, the next question is how to disrupt the target.

Another "smart" technique this fungus has is the ability to secrete metabolites, such as gliotoxin, that can actually protect against predators. A study was done on this specific toxin and it was shown that the toxin can increase virulence levels when some neutraphil function is present. This can imply that the major target of this toxin are neutraphils.

Stress is when there is some type of disruption in a normal process. Stress for A. fumigates can be something like a temperature change or nutrient availability. But nevertheless, they are equipped to deal with these situations as well. Their signal transductions pathways send signals to enzymes which then can deal with certain situations. And when nutrient levels change, they can adjust their metabolism to make sure their needs are met.

I really think that these adaptations and resistances that A. fumigates has are a result of evolution. I think that throughout time genes were mutated to better fitness of this organism. So, therefore they didn't just have these genes to begin with, but instead have acquired these genes. From being able to adapt to different environments such as making sure its chitin cell wall will always be made, nature gave protection to the best characteristics of this fungus. Physical protection like the chitin and also another type of protection was given, and that is resistance. Chitin has evolved to have this special and very important characteristic.

Even something like the thermotolerance could have been evolved. Maybe the earlier A. fumigates couldn't have withstood heat from the body of its host. Throughout time, it could have evolved its genes in such a way so that it built up a tolerance to this death factor.

It's already established that the chitin in its cell wall is integral. This allows it to live outside the host body and not just inside, like other microorganisms. Most microorganisms can't grow on top of skin, because there is a lack of nutrients. There only thing to eat there is chitin, which is perfect for fungi. And when it goes through difficult situations, homeostasis is still met.  Even our drug therapies are chitin based. Since this characteristic is unique to fungi, it creates an easier identifiable target for us in getting rid of an infection.

There is an importance to these findings of these characteristics.  These studies have shown the resistance and /or manipulation that this fungus has.  It's evolving to better itself, therefore to increase survival. Experiments and studies done on this topic can be helpful with trying to manipulate this "smart" mold.  However, an underlying problem still exists, and that's the ability of this organism to adapt to different environments and mutate to become resistant.  So even if research and experiments are done, the fungus can still "out smart" us.  And that's why A. fumigates is one of the most damaging organism that causes systemic mycoses.

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