AP Biology class blog for discussing current research in Biology

Author: DNAva

Can We Alter Mammals Social Behavior Using CRISPR Gene Editing Mechanisms?

At Georgia State University a team of researchers led by professor H. Elliott Albers and Professor Kim Huhman put gene editing mechanisms to the test to determine if it was possible to alter hamsters behaviors. The hamsters that were utilized in this experiment were Syrian hamsters. These hamsters have been extremelGolden hamster front 1y important in many scientific experiments that look into social behaviors, aggression and communication. Furthermore, hamsters are widely used in scientific research due to the fact that their social skills resemble most similarly to humans.


In this experiment, professor H. Elliott Albers and Professor Kim Huhman utilized CRISPR-Cas9 technology to deactivate neurochemical signaling pathways that play a major part in controlling mammalian social behaviors. The regulators of the social phenomena that controls pair bonding, cooperation, social communication, dominance and aggression are the hormone vasopressin and the receptor it acts on, Avpr1a. VasopressinSek

After the gene editing and the observation of the hamsters were complete, the researchers were shocked by their unexpected results. As stated by Professor H. Elliott Albers,  he “anticipated that if we eliminated vasopressin activity, we would reduce both aggression and social communication. But the opposite happened.”

Instead of reducing the hamsters’ aggression and social communication, the absence of the receptor that activates the vasopressin led the hamsters to demonstrate increased levels of social communication behaviors than when observed prior to the gene editing. Furthermore, it was observed that the differences in opposite sex aggression were removed. Both the male and female hamsters showed aggression towards other same-sex hamsters.  

This shocking finding led the researchers to a different conclusion than foreseen. Because it is known that vasopressin correlates with the increase of social behaviors, it can be concluded that the Avpr1a receptor is inhibitory

Moreover, confirming this study done at Georgia State University, another study published in the Proceedings of the National Academy of Sciences, finds that that eliminating the Avpr1a receptor in hamsters windes up deactivating the vasopressin’s action on the receptor, therefore changing the social behavior of the hamsters drastically in ways one would not expect.

Overall, Professor H. Elliott Albers contends that this study is of extreme value as it helps researchers understand the“neurocircuitry involved in human social behavior and our model has translational relevance for human health. Understanding the role of vasopressin in behavior is necessary to help identify potential new and more effective treatment strategies for a diverse group of neuropsychiatric disorders ranging from autism to depression.”

Connection to AP Biology 😀

This study is connected to our AP biology class as we have learned about regulation of gene expression. Without the presence of the Avpr1a receptor, the vasopressin has no way to be mediated, thus enhancing its social behavioral effects. And with the presence of the Avpr1a receptor, the vasopressin is still active, however, muted. 

A Pathway to Possible Hay Fever Treatments: Targeting Streptococcus Salivarius Bacteria

For many people that suffer from hay fever, it has been found that there is a certain type of bacteria found in the nasal passages that make hay fever symptoms worse. People with seasonal allergies understand the struggle of the never ending runny and stuffy nose, and these symptoms make the allergy seasons quite unbearable. If doctors are able to target this bacteria that makes these runny nose symptoms worse, this can be a pathway to treat the constant runny nose. 

Hay fever, also known as seasonal allergies, come about when certain allergens such as pollen or mold triggers an inflammatory reaction in the nasal passages. This reaction leads to an overflow of mucus, itchiness and sneezing.Depiction of a person suffering from Allergic Rhinitis

A team of researchers set up a study in which they analyzed the microbial population in the nose of people who have hay fever and those who do not. After examining the noses of these patients they found that the people that had hay fever had little diversity in the nasal biome as opposed to the non-hay fever patients. It was actually found that there was an abundance of a particular species of bacteria called streptococcus salivarius in the patients who had hay fever. In fact, the S. salivarius bacteria was found to be 17 times more abundant in the nose of people with allergies compared to those without. This major difference in the amount of  S. salivarius bacteria plays a major role in arousing allergy symptoms. To further understand the role that the S. salivarius bacteria plays in provoking allergy symptoms, an experiment was conducted where researchers studied allergen-exposed cells that line airways. And in examining these allergen-exposed cells, they found that the S. salivarius boosted the cells’ production of inflammation promoting proteins. Due to the fact that hay fever is an inflammatory reaction and this bacteria helps produce inflammatory promoting protein, it exposes the link between hay fever and the S, salivarius bacteria. A common symptom of hay fever is the overproduction of nasal discharge, and it was found that S. salivarus is good at binding to airway-lining cells that are exposed to allergen cells covered in mucus, which therefore produces more mucus. Furthermore, the binding of the S. salivarius bacteria and the air-way lining cells is the major factor in why this bacteria worsens the effects of hay fever.

Streptococcus salivarius

 Now, with this research in mind, the next step is to discover how to specifically target this bacteria to help lessen the effects of hay fever. Researchers are now finding a way to find methods that block the adhesion of the S. salivarius bacteria to the allergen exposed cell. Hopefully they come up with a method in the near future because that will for sure make the spring season more pleasurable for me!

Connection to AP Biology 😀

This connects to our AP biology class as we went into depth about our immune systems and their different defense mechanisms. Our immune system protects the body against pathogens such as viruses and bacteria. In our biology class, we learned about 2 different immunity systems: innate and adaptive immunity. In this blog, inflammation and overflow of mucus are recurring topics as they are the main symptoms of hay fever. These responses come from our innate immunity which is a defense that is an immediate reaction upon infection. This reaction is nonspecific and it is a rapid response. when a pathogen can go beyond the barrier defenses, such as your skin, that is when the innate cellular defense is triggered. Most of these triggers lead to an inflammatory response. So, with this in mind, it is clear that after pollen gets past an individual with hay fever skin barrier, that triggers the innate cellular defense which then results in inflammation and an overproduction of mucus.  


How Having Allergic Asthma Can Protect an Individual From COVID-19

Scientists have found that individuals with asthma are, in fact, less susceptible to COVID-19. One could question how a pre-existing health condition could actually aid in fighting off a virus? It is accurate to assume that an individual with allergy asthma would be at more risk than a perfectly healthy individual. 

Allergic asthma occurs when your airways tighten when an allergen is inhaled. The same immune system proteins that are involved with excess mucus production and the tightening of airways are used to form barriers around exposed airway cells (immune system mechanism for people with allergy asthma). This information is the basis behind the studies that explains the reasoning behind why people with asthma are less susceptible to COVID-19. 

Asthma attack-airway (bronchiole) constriction-animated

When a patient has asthma, usually the development viruses such as the Flu and Strep Throat are more dangerous for them, and still these patients with asthma are at more risk when they are infected with COVID-19. The difference lies between asthma and allergic asthma. Researchers were able to identify that people with allergic asthma were not showing major symptoms to COVID-19, which was not what one would expect. Why is that? 

Protein Protection

The differentiating factor that sets allergic asthma from regular asthma is a specific protein called interleukin-13 (IL-13). The normal function of IL-13 is to help fight off parasites. Normally, specific T-Cells release this protein. In response to the release of IL-13, the body produces a sticky mucus substance and compacts airways. This traps the parasite until the immune system finishes the job by killing the parasite. 

However, when an individual has allergic asthma, the body mistakes harmless matter such as pollen for a parasite, and uses IL-13 when it is not needed. The researchers now need to determine how, exactly, IL-13 is protecting patients from COVID-19.

Protein IL13 PDB 1ga3

No IL-13 Present Study

Researchers conducted a study in which they would compare how cells that haven’t  been treated with the IL-13 protein react when healthy and when infected with coronavirus. 

It was found that the healthy cells  grew in lawns that nearly resembled grassland. This area is made Bronchiolar epithelium 3 - SEMup of a hair-like substance called cilium. The cilia move in waves which aids in mucus movement and the excretion of anything stuck in the mucus.

On the other hand, the cells that were infected with the coronavirus had a much different reaction. The cilia lawn was no longer clear. The cilia was covered with mucus and many bald spots that seemed as if infected cells died. The infected cells were compressed out of the lawn of the cilia, and in that process they become inflated. This inflation occurs due to vacuoles in the infected cells getting blocked up with viruses. Once the infected cell gets filled up with viruses past its capacity, it explodes and releases all of the viruses that had been in the cell. 

Unfortunately, it is not as simple as this singular reaction, not all cells that were in the infected lawn were affected the same way. Researchers noticed that the cells that were attached to the cilia were infected with SARS-CoV-2, but the goblet cells, which are mucus producing cells, were barely affected. The researchers found that a protein called ACE2 is present on the surface of ciliated cells more commonly that goblet cells. With this finding, the researchers can assume that ACE2 is the protein receptor that allows SARS-CoV-2 to enter the cell. 

IL-13 Present 

Now the researchers conducted a second study in which they will coat the cell in  the IL-13 protein and compare how the cell reacts when infected with coronavirus. The celia lawn surface with the IL-13 present has a lot less inflated dying cells on its surface and the movement of the cilia was much less rapid. This decrease in movement indicates that the mucus is present in the cilia for much longer than when IL-13 is not present. It was made clear that the IL-13 protein acted as a protectant towards the infection. 

They later found out that untreated cells, once infected with SARS-CoV-2, release bursts of mucus. Whereas the IL-13 cells keep the mucus stored. Furthermore, it is known that IL-13 proteins produce a sticky mucus that has the ability to trap viruses before they get the chance to infect the cell. So, this excess mucus that is present in the treated cells can make sure the virus is out of the lungs before the damage has been done. Researchers also found A thick layer of keratan sulfate that was developed on the cell’s surface that was treated with IL-13, which protects them against SARS-CoV-2 from coming into contact with the cell.

In addition to protecting the cells, the IL-3 protein causes cells to produce less ACE2. And with less ACE2, not as many SARS-CoV-2 can come into the cell, since ACE2 is the SARS-CoV-2 receptor. 

There is so much unknown about IL-3, and researchers are still trying to determine specific properties of this protein. Scientists are eager to find out more about IL-13 as they think this protein can lead to new treatment findings.

This new information about how people with allergy asthma react to COVID-19 can be looked at as a positive because it’s one thing about having allergy asthma that actually benefited the individual!

Why is it That I Tend to Get More Mosquito Bites Than All Of My Friends?

Have you ever wondered why some people get more mosquito bites than others? To your surprise it is not because they have “sweet blood,” there is actually an odor that our body produces, some more than others, that attracts mosquitoes. Jason Arunn Murugesuu, a reporter for the New Scientist, recently published an article regarding research conducted by Maria Elena De Obaldia at Rockefeller University in New York. In this study, they posed the question of whether body odor affects mosquitos’ attractiveness to an individual.

Aedes aegypti CDC-Gathany

In this experiment, there were two boxes that contained nylon fabric swatches that were worn by two different individuals, and in each box lay the fabrics. The third box held  female Aedes aegypti mosquitoes. The researchers tested which box most attracted the Aedes aegypti. After numerous trials, it was found that their results stayed persistent.

It was determined that nylon fabrics that most attract mosquitoes were worn by individuals that happened to have a higher concentration of carboxylic acids present in their body odor. The bacteria on our skin produce carboxylic acids, which are a result of sebum, a substance composed of lipids that lie on the skin’s surface as a protective barrier.


Sadly, one cannot necessarily prevent the amount of carboxylic acids our body produces to limit the number of mosquito bites. According to De Obaldia, our body’s odor comes down to our genetics, skin microbiome and diet. It is unlikely for body odor to be altered based on mild changes, such as a temporary change in diet. Skin bacteria live deep down in our pores, so it is unlikely that they can be removed, which is why they are a significant factor in our body odor.

Moreover, De Obaldia repeated the study but replaced the  Aedes aegypti mosquitoes with genetically modified mosquitoes that have a weakened ability to sense acids. After this experiment was conducted, the researchers found that some of the mosquitoes had a lessened preference for nylon fabrics that contained a higher concentration of carboxylic acids. 

This study concludes that mosquitoes do, in fact, have a preference as to who they are choosing to bite. Scientists now have a reasonable solution to decrease mosquitoes’ preference for humans and spread diseases, which is to genetically modify the mosquitoes. 

Now, after reading this, if you notice that you are getting more mosquito bites than all of your friends, it is possible that you have a higher amount of carboxylic acids present in your body odor. 


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