AP Biology class blog for discussing current research in Biology

Author: angenetic

Fighting Cancer with CRISPR

For many years the treatment of cancer has remained difficult and uncertain. Though there are many treatment methods such as chemotherapy and bone marrow transplants, these methods are never guaranteed to work. However, a teenage girl named Alyssa diagnosed with T-cell acute lymphoblastic leukemia (T-ALL) has been successfully treated with a new experimental treatment. T-ALL is a type of cancer where cancerous T-cells overpopulate healthy T-cells, leaving the patient susceptible to disease. In this form of cancer, T-cells also mistake each other as threats. CRISPR illustration gif animation 1Due to the nature of this cancer, in order for treatment to be effective, T-cells would have to appear foreign to the patient’s immune system. This is made possible through the gene editing system, CRISPR. For Alyssa’s treatment, doctors utilized and altered donated T-cells. Using CRISPR, the donated T-cells were stripped of CD7 protein, a common T-cell protein, and CD52 protein, a protein recognized by cancer treatment.  Additionally, donated T-cells received a receptor that gave them the ability to target cancerous and healthy T-cells by having the ability to recognize CD7. All of these changes were made through a process called base editing with CRISPR. During base editing, individual letters, or bases, in the T-cells’ DNA code were altered. These minor alterations have the ability to change the nature of the cell. Thanks to this new treatment, Alyssa’s cancer is now undetectable.


I found T-ALL cancer and its destructive nature relatable to the way that viruses take over human body cells, however, our adaptive immunity uses antigens to recognize an intruder. T-cells contain specific proteins which make them recognizable to other T-cells, including cancerous ones. T-ALL destroys the body’s own T-cells which is why this specific treatment needed to use altered T-cells that did not contain recognizable proteins. WheT Lymphocyte (16760110354)n the body is infected by a virus, memory T and B cells use antibodies, a little piece of the virus, to remember and recognize the virus if it were to enter the body again. 


Pick Me Up… Or Put Me Down

We all know those mornings. You stayed up too late studying, playing video games, or binging your favorite series. You wake up drowsy and distressed, then remember you have a test today. For a moment you panic, but you quickly realize you have the luxury of indulging in a hot cup of coffee. Your preconceived impression is that the coffee will cure your exLatte and dark coffeehaustion– it’s almost too good to be true. Suddenly, you notice that you have become reliant on a beverage to take the place of quality sleep several days a week. But is this notion accurate? How well can caffeine mask a lack of sleep

The reason people feel drowsy at any time of the day is due to a buildup of adenosine in the bloodstream. Adenosine is produced when the body consumes its central energy source (ATP). Adenosine in the bloodstream binds to adenosine receptors. Once bound, these receptors trigger a release of proteins that inhibit neuron activity, leading to drowsiness. 

Caffeine’s solution to the abundance of adenosine acts as a temAdenosinporary patch-up. Caffeine has the ability to block adenosine receptors, therefore preventing adenosine from causing drowsiness. The problem, however, is that caffeine does not stay bound to adenosine receptors for very long, so tiredness will likely kick in at some point later in the day. Since caffeine is just “patching up” the problem, it will never be nearly as effective as sleep which allows for the breakdown of adenosine. 

I have noticed the effects of caffeine are much greater later in the day compared to consuming it in the morning. This is because caffeine tends to raise cortisol levels. Upon waking up, cortisol levels are already high. It is also the case that adenosine levels grow as the day progresses. These two factors explain why caffeine has stronger effects later in the day. There is a more drastic change caused by caffeine on cortisol levels and the “control” of free adenosine. 

I found the process of caffeine binding to adenosine receptors to relate to our cell communication unit. When caffeine enters the bloodstream, it acts as a competitive inhibitor by preventing adenosine from binding. A competitive inhibitor takes the place of a substrate in an enzyme directly at the active site. This prevents a chemical reaction from occurring. In this case, caffeine is blocking a receptor that causes drowsiness when activated. If caffeine is blocking it, adenosine which would have caused drowsiness is unable to attach to the receptor. If the adenosine were to attach to this receptor, it would trigger a signal that is sent through neurons to cause the sensation. 

COVID-19 on the Genetic Level

Similar to any other virus, the symptoms of COVID-19 are amplified in patients who are of old age, have additional complications, or are unvaccinated. For instance, researchers found that unvaccinated individuals ages 50 and older are 12 times more likely to die from COVID-19 than individuals who are vaccinated with boosters (Hesman Saey). Additionally, cancer patients, especially those who are immunosuppressed, are at a higher risk of facing the serious impacts of COVID-19. Research suggests that baseline immunosuppression increases the risk of a cytokine storm. Cytokine storms result in extreme immune responses towards a pathogen which can result in harmful conditions for the body or inSARS-CoV-2 without background​​​ some cases death. 

These factors play an important role in the severity of COVID-19, however, there are still some severe cases that are unaccounted for. Throughout the COVID-19 pandemic, one question that has perplexed many scientists is: why do certain healthy patients contract severe cases of COVID-19 while others merely experience the symptoms of the common cold? Recent research has found that genetics may be the answer. Studies have revealed that genes passed down from our ancient ancestors can both help and hurt individuals infected with COVID-19. A global study that took DNA samples from 28,000 patients infected with Covid-19 and about 600,000 healthy patients confirms this theory.

The two main genes taken i3D Structure of Legumin Proteinnto account are toll-like receptor 7 (TLR7) and TYK2. Variants in these genes are what can control the severity of a COVID-19 case. TLR7 is a gene whose protein is responsible for initiating an immune response by sending signals to other cells that a pathogen has invaded the body. If this process is not operating correctly, it is more difficult for the body to defend against a virus. So, if SARS-CoV-2 enters the body, a variation in TLR7 can cause a more severe case of COVID-19. TYK2 is responsible for producing interferons. A variation in TYK2 can cause an overproduction of interferons. When there is a virus present, such as SARS-CoV-2, the production of interferons can be helpful in the body’s defense. 

The processes impacted by TRL7 and TYK2 directly relate to the body’s innate immune process. Innate immunity is the body’s first line of defense once a virus has passed through our innate immune system. The innate immune process involves mast cells which release histamines and macrophages which release cytokines. Interferons work in a similar way. All parts of innate immunity are focused on keeping the pathogen from advancing. Cell signaling is central to innate adaptive immunity, so any alterations in it would result in a less effective defense and therefore a more severe case of COVID-19. 

I found this COVID-19 study to be intriguing because this past January a few members of my household were infected with COVID-19. However, only one experienced extreme symptoms. Since all were vaccinated, it may be possible that the alterations in TLR7 and TYK2 are the reason for the differences in reactions among my family.

How Do Ancient Viruses Still Impact Humans?

When one thinks of the similarities between modern and ancient humans, one will probably think of the basic genetic material that determines our physical structure. However, what is not so obvious are the viruses that infected them yet remain in our genes. It is known that DNA containing these ancient viruses make up about eight percent of the human genome (Ancient Viruses). These viruses have previously been believed to be insignificant, however, recent research has disproved this theory. 

The viruses that have been genetically passed down are known as retroviruses. Retroviruses spread by making copies of themselves through the production of RNA which contains instructions for its DNA and replication. This reproduction process, called transcription, is similar to that which is done in the nucleus of eukaryotic cells. However, in this case, the synthesized DNA is then placed in the DNA of the cell it occupies. With that in mind, For the genes containing these viruses (or any gene) to be activated, they must contain specialized RNA with the information for its reproduction and it must be revealed by a protein called the transcription factor. Ácido desoxirribonucleico (DNA)

Using data from the Genotype-Tissue and Expression project, scientists Aidan Burn, Farrah Roy, Michael Freeman, and John M. Coffin searched for these active virus genomes in healthy tissue. They specifically sought out HML-2 which is a relatively new virus. They also looked for the RNA which would indicate its activation. This virus was found in all of the tissue they examined and they found the highest activity of it in the cerebellum. 

Though they were once harmful to humans, these viruses found within healthy cells and tissues no longer serve as functioning viruses. They are now known as Endogenous Retroviruses (ERV). They cannot infect, but rather they serve us in our immune system. Their activation has been shown to have a vital role in embryonic development and aid in the detection of cancer.

I found the origination of ERV in human genomes to be similar to that of mitochondria and chloroplasts’ origin in eukaryotic cells. It is likely that mitochondria and Chloroplasts were engulfed by bacteria cells and are now able to carry out their functions (reproduction) within them while also benefiting the cell (providing it with ATP). Similarly, at some point during human evolution, the virus entered humans andMitochondria 8 -- Smart-Servier was then able to utilize its environment (the host cell) to reproduce. I would also describe the relationship between ERV and modern-day humans as symbiotic due to the recent research which has revealed their benefits.

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