This article reviewed the rise in
drug resistance in the treatment of viral, bacterial, fungal and protozoan
infections. In order to better understand drug resistance in these different
classes, researchers have been analyzing the current drugs to develop and
design new drugs to combat the resistance. Researchers have also been spending
the time to going back to the original models to get a better understanding of
how each model’s cellular mechanism works. This article offers a foundation to
understand the complexity of drug resistance and all of it’s components,
specifically mutation rates and fitness effects.

            HIV was
chosen as the model virus because it has a high spontaneous mutation rate,
genetic variation that may be controlled. Pathogenic bacteria were chosen as
the model bacteria because of how horizontal gene transfer and spontaneous
mutations causes resistance. Pathogenic fungi was chosen as the model for fungi
because the fungi only have a limited horizontal gene transfer amount which
causes the fungi resistance to become dominantly dependent on mutation rates.

Plasmodium falciparum was chosen as the model virus for protozoan because
resistance to drugs is due to point mutations. Human cancer was also chosen to
review because it does not spread from person to person and the chromosomal
instability causes rise to drug resistance.

important factor in understanding drug resistance is the fitness costs. The
article stated that the fitness cost of HIV is dependent on the subtype. The
fitness cost of bacteria can sometimes be cost free. The fitness cost in fungi
is very large enabling it to invade the host. Cancer tends to have a more
complicated fitness cost because of its chromosomal instability.

These fitness costs can be
compensated for by mutations. In HIV and bacteria multiple mutations reduce the
fitness cost, in fungi it is difficult to reduce the fitness cost. In cancer
cells, the fitness cost is not compensated for because of the diversity in the
mutations of the cancer.

Bacteria, fungi, protozoa and
cancer cells have also evolved mutation supply rates in which they are able to
keep a large population and high rate of horizontal gene transfer. These
factors have contributed to creating protection of the Bacteria, fungi,
protozoa and cancer cells. Specifically, cancer cells thrive off the blood
supply causing an increase in the cells, which enlarges the tumor creating
protection for the cancer. The article also examines the use of multiple drugs.

They found that resistance to one drug could either increase resistance or
increase susceptibility.

In conclusion, this article
determined that resistance occurred in bacteria, fungi, protozoa and cancer
cells, with differences and similarities between each. The results were very
useful because they demonstrated the differenced between the classes and the
various drugs. By comparing these different classes, it established a good
foundation to better understand how drug resistance occurs and gives a better
understanding of the current research being done to overcome these obstacles.

I overall agree with this article
in that understanding drug resistance is much more complex than it might appear
and that many factors go into the process. I did find that some sections were
more detailed in certain classes than others. Cancer and fungi were topics that
seemed to be lacking in detail and examples, this may be because there still is
not enough research done on that class yet. The article did go into a lot of
detail on HIV and bacteria, with many examples and detailed procedures.



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