This article reviewed the rise indrug resistance in the treatment of viral, bacterial, fungal and protozoaninfections. In order to better understand drug resistance in these differentclasses, researchers have been analyzing the current drugs to develop anddesign new drugs to combat the resistance. Researchers have also been spendingthe time to going back to the original models to get a better understanding ofhow each model’s cellular mechanism works. This article offers a foundation tounderstand the complexity of drug resistance and all of it’s components,specifically mutation rates and fitness effects. HIV waschosen as the model virus because it has a high spontaneous mutation rate,genetic variation that may be controlled. Pathogenic bacteria were chosen asthe model bacteria because of how horizontal gene transfer and spontaneousmutations causes resistance. Pathogenic fungi was chosen as the model for fungibecause the fungi only have a limited horizontal gene transfer amount whichcauses the fungi resistance to become dominantly dependent on mutation rates.
Plasmodium falciparum was chosen as the model virus for protozoan becauseresistance to drugs is due to point mutations. Human cancer was also chosen toreview because it does not spread from person to person and the chromosomalinstability causes rise to drug resistance. Animportant factor in understanding drug resistance is the fitness costs. Thearticle stated that the fitness cost of HIV is dependent on the subtype.
Thefitness cost of bacteria can sometimes be cost free. The fitness cost in fungiis very large enabling it to invade the host. Cancer tends to have a morecomplicated fitness cost because of its chromosomal instability. These fitness costs can becompensated for by mutations. In HIV and bacteria multiple mutations reduce thefitness cost, in fungi it is difficult to reduce the fitness cost. In cancercells, the fitness cost is not compensated for because of the diversity in themutations of the cancer.Bacteria, fungi, protozoa andcancer cells have also evolved mutation supply rates in which they are able tokeep a large population and high rate of horizontal gene transfer.
Thesefactors have contributed to creating protection of the Bacteria, fungi,protozoa and cancer cells. Specifically, cancer cells thrive off the bloodsupply causing an increase in the cells, which enlarges the tumor creatingprotection for the cancer. The article also examines the use of multiple drugs.They found that resistance to one drug could either increase resistance orincrease susceptibility. In conclusion, this articledetermined that resistance occurred in bacteria, fungi, protozoa and cancercells, with differences and similarities between each. The results were veryuseful because they demonstrated the differenced between the classes and thevarious drugs.
By comparing these different classes, it established a goodfoundation to better understand how drug resistance occurs and gives a betterunderstanding of the current research being done to overcome these obstacles. I overall agree with this articlein that understanding drug resistance is much more complex than it might appearand that many factors go into the process. I did find that some sections weremore detailed in certain classes than others. Cancer and fungi were topics thatseemed to be lacking in detail and examples, this may be because there still isnot enough research done on that class yet. The article did go into a lot ofdetail on HIV and bacteria, with many examples and detailed procedures.
