BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: #COVID (Page 1 of 4)

Nature’s Blueprint: Harnessing the Morpho Butterfly’s Light Manipulation to Create More Efficient Cancer Diagnosis

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On March 7, 2025

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Researchers at the University of California San Diego have developed an innovative method for cancer diagnosis inspired by the Morpho butterfly’s wing structures. The butterflies are known for shimmering blue wings, which are derived from microscopic structures that manipulate light rather than pigments. This is incredibly useful for cheaper, invasive-free cancer diagnosis.

Morpho Butterfly

One way that the degree of someone’s cancer is evaluated is through analyzing someone’s Fibrosis, which is the accumulation of fibrous tissue. In oncology, evaluating the extent of fibrosis in a biopsy sample can help determine whether a patient’s cancer is in an early or advanced stage. However, it is currently difficult to distinguish stages of fibrosis using current clinical methods, which includes physical exams, blood tests, bone marrow tests, genetic tests, and imaging tests. Existing techniques rely on staining tissues to highlight key structures in tumor biopsies, but interpretations can vary between doctors. While advanced imaging technologies offer greater detail, they require costly, specialized equipment that many clinics lack.

 

This is where the Morpho butterfly plays a crucial role. The researchers found that placing a biopsy sample on a Morpho butterfly wing and examining it under a standard microscope allows them to determine what phase tumor’s structure is currently at without requiring stains or expensive imaging equipment. This is critical because many clinics can’t afford the highest quality equipment. Also, the research team claims “It’s also more objective and quantitative than current methods,” which is amazing for patients. 

The researchers discovered that the microscopic and nanoscopic structures of the Morpho butterfly wing respond strongly to polarized light, which is a type of light that moves in a specific direction. Collagen fibers, a key structural component of fibrotic tissue, also interact with polarized light, but their signals are typically weak. By placing a biopsy sample on a Morpho butterfly wing, the researchers amplified these signals, making it easier to assess the density and arrangement of collagen fibers. To quantify these findings, the team developed a mathematical model based for analyzing polarized light. This model translates light intensity into a measurable indicator of collagen fiber density and organization, providing an objective metric to assess fibrosis in the tissue. 

This breakthrough is significant because early cancer detection is challenging in many parts of the world due to limited resources. This simpler and more accessible tool can help diagnose patients before the cancer reaches advanced stages. This current study focused on breast cancer, but they plan to expand their research to other tissue and parts of the body. 

This connects to AP Biology because in many organisms, color arises from pigments, molecules that absorb certain wavelengths of light and reflect others. For example, chlorophyll in plants absorbs red and blue light while reflecting green, which is why leaves appear green. However, the Morpho butterfly does not rely on pigments for its brilliant blue color; instead, it uses its structure, where microscopic structures manipulate light to produce color. These structures interact with light to show their color. In addition, collagen fibers, long, fibrous proteins that make up part of the extracellular matrix. Collagen is a structural protein composed of amino acids, forming a triple helix structure that gives the fibers strength and flexibility. The collagen also interacts with polarized light, but their signals are typically weak. By placing a biopsy sample on a Morpho butterfly wing, the wing’s nanostructures amplified these weak signals, making it easier to analyze the tissue without using chemical stains. To me, the most compelling part of this research is that it is simply utilizing a phenomenon of a species. What other species could we try to utilize in research like this? What are your thoughts on this new discovery and its potential implications?

Two Infectious Paths Collide and Collude

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On January 24, 2025

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Recently a new variant of Covid known as XEC was discovered by researchers in Berlin who deemed that not only was this new strand of covid a descendant of Omicron but also a recombinant of strains KP.3.3 and KS.1.1. Both KP.3.3 and KS.1.1 are descendants of Omicron which then mutated into Sub-variant BA.2.86 which then further mutated into JN.1. Where it gets interesting is that JN.1 splits into KS.1.1 and KP.3 which further evolves into KP.3.3. All of the strains are slight variants of omicron however two of the variants recombined to form XEC. This process takes place where genetic material from two organisms combines to in theory make a more successful organism.

Transmission and life-cycle of SARS-CoV-2 causing COVID-19.

The process of recombination takes place through the reconstruction of DNA using enzymes known as Restriction Enzymes. In relation to what we learned in AP Bio DNA acts as substrate which in turn binds to the active site on said restriction enzyme. Every Restriction enzyme can only bind to a very specific active site. This binding then leads to the removal of the target substrate from the DNA chain therefore isolating it. It is then possible to transfer this isolated piece of DNA to another cell where it can then be fit into the DNA of said cell by using an enzyme to break apart the alpha helix of the new DNA and inserting the new strand. This reaction is only easy to produce into organisms with non nucleic DNA because the process of recombination in organisms with nucleic DNA is much more complex and requires additional steps. For example, in eukaryotic cells, the presence of a nucleus and tightly wound chromatin makes accessing and modifying DNA more challenging. Scientists must use more sophisticated techniques, such as using CRISPR-Cas9 systems or other gene-editing tools, to accurately target and integrate new DNA segments.

The process of recombination in viruses like COVID-19 is somewhat different, as viruses rely on host cells to replicate and do not have their own nucleic machinery. In the case of XEC, the recombination likely occurred when two different strains—KP.3.3 and KS.1.1—infected the same host cell simultaneously. This co-infection created an opportunity for their genetic material to mix during replication. The resulting recombinant variant, XEC, may have acquired advantageous traits from both parent strains, potentially enhancing its ability to spread, evade immune defenses, or cause illness.

Understanding this process is critical in tracking the evolution of variants and developing effective countermeasures, such as vaccines and treatments. This is important to us at friends academy because covid is still raging in our world harming people. Therefore we need to do anything we can in order to prevent the spread, learn how to  By studying the molecular mechanisms behind recombination, scientists can better predict the emergence of new variants and assess their potential impact on public health. If you have any questions about the nature of covid strains or covid vaccines feel free to reach out or leave a comment. Your feedback is much appreciated. Thank you for reading.

 

 

 

The Structural Effects of COVID on the Teenage Brain

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On January 24, 2025

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It is a well-known fact that COVID-19, the virus that took the world by storm in 2020, had a significantly destructive physical impact on those who contracted it. However, new research suggests that the coronavirus also had physical effects on individuals, specifically teenagers, who quarantined and successfully avoided infection altogether.

The study that produced much of the data responsible for the findings of this research was conducted by three researchers from the University of Washington. The initial objective of their research was to examine the changes in brain structure over the normal adolescence period. The researchers gathered MRI data from adolescents aged 9, 11, 13, 15, and 17 in 2018, expecting to gather the group and a second data set in two years. However, due to the pandemic, the participants were unable to return for the second MRI scan in 2020, so they returned a year later, providing the researchers with an unprecedented opportunity to dive into research on how the COVID quarantines effected brain development in adolescents.

Cerebral Cortex location

The thickness of the cerebral cortex, the brain’s outer layer of tissue which controls functions such as reasoning and decision-making, naturally thins as we age. The researchers used MRIs to measure the difference in the density of the cerebral cortex in each of the participants in order to examine the effects of the COVID quarantine on the adolescent brain; more specifically, they sought to discover the aging effects of this isolation on the teens. Their research found that all subjects experienced accelerated cerebral cortex thinning, with females experiencing more widespread aging while males showed thinning in only two regions. Additionally, the female brain showed an average age acceleration about 4.2 years older than their age while male acceleration averaged at about 1.2 years older. The majority of the thinning in females’ brains occurred in areas of the brain that contribute to social cognition, an area of intelligence that was highly impacted during the pandemic due to the lack of social interaction during quarantine. Male participants’ brains proved to be affected most prominently in areas involved with face processing.

The synaptic connections made when teenagers interact with one another were exactly what was missing during this time of lockdown and isolation. During adolescence, the brain is still forming new neural pathways and developing, and the quarantine teens experienced during the COVID-19 pandemic prevented them from practicing the skills they needed to develop the synaptic connections that allow them to interact with and relate to peers. This lack of social activity is thought to be one of the reasons for the premature thinning of the brain in these young participants. The concept of neural and synaptic pathways connects to what we’ve learned in AP Bio this year about how neurons function. We know that the dendrites are the part of the neuron that receive stimuli, and when those dendrites receive highly stressful stimuli (such as the isolation and loneliness experienced as a result of a lack of social interaction), the brain’s development is thought to shift toward premature maturation in order to protect the synapses related to emotion, learning, and memory. This development can protect the individual and their brain in the moment; however, the period of prolonged exposure to stressful stimuli can later lead to mental health effects such as anxiety and depression.

Long Covid: a Hazy Mind, and a Hazier Definition.

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On January 12, 2025

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Novel Coronavirus SARS-CoV-2 (49680675977)

The term “long COVID ” has been thrown around frequently without a clear definition. In fact, it has no straight definition and is just as foggy as its symptoms suggest. New research on long COVID has revealed just why this syndrome is so nebulous and how to effectively avoid it.

The definition of long Covid varies between different public health bodies. Still, overall, it shares the idea that it is a condition characterized by unexplainable symptoms well after an initial COVID-19 infection. Such symptoms can commonly include memory issues (“brain fog”), cough, headaches, problems with taste and/or smell, and chronic fatigue. While the pathological mechanisms for long COVID aren’t entirely understood, research has pointed to the virus’s ability to disregulate the immune response. A dysregulation in the immune response would allow the virus to remain inside the body’s tissues long after the initial infection and prevent it from being adequately dealt with.

In AP Biology, we learned about the exact biochemical and cellular pathways essential to the immune response. Helper-T cells carry the information of an infection into the lymph and signal B-cells and other T-cells to divide. Cytotoxic-T cells destroy infected cells, and cytokines are biochemical transmitters that allow cells to communicate with each other. Long COVID attacks these basic functions by exhausting the Helper-T cells and preventing them from effectively signaling other cells. The virus also elevates the number of cytokines and cytotoxic-T cells, overwhelming the immune system with unneeded information and expending more energy on unnecessary cytotoxic-T cells that may start attacking uninfected cells. These attacks therefore weaken the immune system and allow for the effects of long COVID.

Currently, there is no specific treatment for long Covid, but there is a way to prevent it altogether. Avoiding infection by COVID-19 means that the effects of long COVID can never set in, so the best way to prevent these terrible symptoms is to stay as vigilant as possible and keep ourselves healthy. Do you know anyone with long COVID? If so, what have they done to cope with their symptoms? Let me know!

Leaky Blood Vessels and Long COVID

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On January 9, 2025

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Earlier this year, researchers in Dublin, Ireland, found that brain fog from long COVID is associated with blood-brain barrier disruption. COVID-19 is an infectious disease that causes symptoms lasting for two to six weeks, depending on the severity of the case. Long COVID, on the other hand, is a lingering illness that can cause one’s COVID symptoms to last for months. This lingering illness consists of prolonged COVID symptoms after initial infection, with patients reporting fatigue, dizziness, impaired taste and smell, and brain fog. Cognitive impairment, or brain fog, is a particularly devastating symptom of long COVID, as it causes the affected individual to experience mental exhaustion and forgetfulness. The team of researchers in the aforementioned article set out to find the root cause of brain fog in people with long COVID. They used dynamic contrast-enhanced MRI (DCE-MRI), which specifically measures tissue vascularity and permeability, to study patients’ brains. The researchers found that a significant percentage of long COVID patients who self-reported symptoms of brain fog also had increased blood-brain barrier permeability. The blood-brain barrier (BBB) is a protective layer that lines the brain’s blood vessels. In an earlier AP Bio unit, we learned that cell membranes are semi-permeable and filter out harmful substances. The function of the BBB is practically identical to that of a cell membrane: it is a semi-permeable bilayer that filters out harmful substances. Both the cell membrane and the BBB are structured with phospholipids, and both have transport mechanisms, include pumps, to filter substance in and out.

This research study ultimately suggests that long COVID disrupts the BBB and causes systemic inflammation. Systematic inflammation causes the body to experience irregular temperatures, increased heart and breathing rates, and produce an abnormally high amount of cytokines. This response ultimately leads to structural changes in the brain that cause brain fog. 

Novel Coronavirus SARS-CoV-2

While I don’t know of anyone in my personal life who has or had long COVID, I do know how awful it is to have regular COVID, so I can’t imagine how horrible it would feel for those symptoms to linger for months on end. Have you or someone you love ever experienced long COVID? What was it like for you or them to live with those symptoms?

Rogue Antibodies: Unraveling the Mystery of Long COVID’s Lingering Pain

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On January 9, 2025

In Student Post

Rogue antibodies could contribute to some of the symptoms of long COVID such as a heightened response to pain and decreased pain tolerance as they begin attacking people’s own nerves. Autoantibodies were previously thought to be possible causes of long COVID, a chronic condition that can cause symptoms and conditions to last over weeks after the initial COVID-19 infection, by scientists and these studies confirm their hypothesis. Autoantibodies are antibodies made by a person’s own immune system that have malfunctioned and target their own cells rather than viruses and bacteria. Scientists Hung-Jen Chen’s team and Akiko Iwasaki’s group found that mice injected with antibodies from patients with long COVID-19 antibodies could tolerate standing on a hot plate for a shorter time compared to the mice that received antibodies from healthy people.SARS-CoV-2 without background However, there is no firm evidence that the hypersensitivity to pain resulted only from the long Covid as those mice received antibodies from patients with chronic pain. Overall, the increased sensitivity is predicted to be due to the rogue antibodies attacking people’s own tissues which is enough to start the various symptoms. These results could give comfort to those who have long COVID as there is now an explanation as to their symptoms and can understand the causes of their pains. Nevertheless, symptoms for COVID are immensely high with there being more than 200 documented symptoms. Scientists believe that autoantibodies could be a large cause of these symptoms as there is an increased amount of autoantibodies in the blood during a SARS-CoV-2 infection and the autoantibodies are shown to linger in people with long COVID even after the initial illness has passed. Nonetheless, if the cause of long COVID can be confirmed to be due to the autoantibodies then doctors could try and reduce the amount circulating in the blood which could really benefit a number of patients, especially those who have long COVID.

 

As someone who has gotten covid before I wondered what the longer implications could be. Additionally, I have family friends who still had bad symptoms months after initially contracting COVID-19 and so it fueled my interest in learning more about long COVID. I am happy to learn that there is finally research that can provide a greater explanation for some of the conditions of COVID-19 and can support a possible solution. Moreover, while the severity of COVID-19 has decreased it is not completely gone and so it is important to remain educated and safe during this time. If you have ever had COVID do you think you ever experienced an enhanced sensitivity to pain? If so, do you think you have any symptoms of long COVID? Lastly, antibodies are very interconnected to the immunology topic in AP Biology as they generally help fight against viruses and bacteria. Normally, when a person gets infected with a virus the innate immunity immediately kicks in before the adaptive immune response activates. The adaptive immune response subsequently triggers the humoral response, and B-plasma cells secrete antibodies that bind and neutralize the pathogen so that macrophages can engulf and destroy the antibody-coated pathogen. However, the antibodies involved in the long-term symptoms of COVID seem to be malfunctioning antibodies which are in turn attacking the healthy cells of the person.

The Brain Drain: How The Pandemic Has Aged The Brains Of Teenagers

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On January 9, 2025

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Covid-19 changed the world in many ways, but, according to a new finding, one of the most surprising consequences lies hidden inside teenage brains. Did you know that stress can physically alter your brain, affecting decision-making and emotional regulation? Recent research reveals a stark reality about how pandemic-induced isolation and stress impacted the neurobiology of teenagers. 

Recent research has revealed that the premature aging of teenage brains has become an unsettling consequence of Covid-19. A study conducted by the University of Washington’s Institute for Learning & Brain Sciences (I-LABS) found that pandemic-related disruptions, such as social isolation and school closures, accelerated brain aging by up to four years in adolescents. This discovery emphasizes the deep effects of chronic stress on young brains and raises important questions about long-term consequences.

Using MRI scans of 160 teens before and after the pandemic, researchers observed significant thinning of the cerebral cortex, which is the brain’s outer layer responsible for decision-making and reasoning. Although natural thinning is normal and occurs with age, the stress caused by the pandemic appeared to accelerate this process. The effect was especially pronounced in girls, whose brains aged an average of 4.2 years compared to 1.4 years for boys. Some researchers believe this gender difference might arise from the unique ways boys and girls process stress, with girls depending heavily on social interactions for emotional support.

The premature aging of the cortex could help researchers explain the rise in anxiety and depression among adolescents during the pandemic. Thinner cortices are related to slower processing times and reduced flexibility in thinking. However, experts stress that the findings do not mean these effects are permanent. They believe that recovery is possible if teens regain social connections and emotional support.

human brain on white backgroundIn AP Biology class, we explored how nerve pathways and receptors work together to transmit signals throughout the body. These signals begin with action potentials, which are caused by the movement of sodium ions (Na+) into the neuron through sodium channels. After this  an outflow of potassium ions (K+) goes through potassium channels. This wave of depolarization goes down the axon. When the signal reaches the synapse, it triggers the release of neurotransmitters from vesicles into the synaptic cleft. These neurotransmitters then bind to receptors on the next neuron’s membrane, causing ligand-gated ion channels to open and either causing or inhibiting a new action potential. This connects directly to our learnings, as the accelerated thinning of the cerebral cortex observed in teens during the pandemic could relate to disrupted nerve signaling. Nerve pathways in the brain are intricate and complex, so they depend on precise signaling, including the balance of sodium and potassium ions, for higher-level and important functions like decision-making. Prolonged isolation and stress may have impacted neurotransmitter release and receptors, leading to changes in how signals are processed and are received.

Another study by Stanford University found similar cortical changes during COVID-19 regulations, further supporting the connection between isolation and brain aging. This research suggests that prolonged stress during formative years can have lasting effects, emphasizing the need for support and social opportunities for teens.

As a teen girl who had lived through the quarantine, this research resonated with me. The loss of daily interactions with friends and not being able to go to school was hard. It’s heartening to know that recovery from these issues is possible, but it also highlights the importance of addressing mental health as we all try to recover from the pandemic. How can we ensure that young people’s social and emotional needs are met if similar things occur in the future?

What do you think about these findings? Should schools and communities invest more in emotional support programs? How can families support teens in rebuilding their social skills? I’d love to hear your thoughts in the comments below.

Persistent alterations in gray matter in COVID-19 patients experiencing sleep disturbances: a 3-month longitudinal study

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On December 19, 2024

In Student Post

In a fascinating study done by Kaixuan Zhou and his team inspected the brain’s structural changes with sleep disturbances caused by COVID-19 during the acute phase, or the phase where the recipient experiences symptoms.  The team also investigated to see if the symptoms persisted after 3 months. The team hypothesized that the indirect damage of SARS-Cov-2 during the acute phase leads to “indirect neurological damage” that causes sleep deprivation. The team designed an experiment where 26 of the COVID-19 patients with sleep disorders and 27 COVID-19 patient SARS-CoV-2 without background

without sleep disorders were recruited. The team then took blood samples and asked the patients to “return for follow-up evaluations after 3 months, enabling a longitudinal analysis.”  The team’s findings suggested that “COVID-19 patients with SD exhibited significant brain structure changes in various brain lobes and that these were correlated with sleep quality.” The alteration the team found during the “acute phase and at a 3-month follow-up” displayed the neurological impact of COVID-19. The affected regions of the brain were the hippocampus (which is critical for memory formation), the prefrontal cortex (which is crucial for decision-making), and the insular cortex (which is responsible for sleep regulation).  In the end, the team discovered necessary evidence to show that COVID-19 during its acute phase alters parts of the brain, which therefore leads to many problems including sleep disturbances.

As someone who knows that sleep is crucial for one’s well-being and believes that a lack of sleep can lead to decreased immune function, this article regarding a lack of sleep caused by COVID-19 interested me. However, my hunch that sleep can cause a lack of sleep can be backed up scientifically. Zhou’s research article connects to Unit 4 of our AP Biology course, which was the immune system. According to the Mayo Clinic, when one is deprived of sleep there is a “decrease in production of these protective cytokines.” Cytokines in general are crucial to the immune process, as they start many processes that help fight off infections and viruses. Notably, they start the adaptive immune reaction, as the release of cytokines from the Helper T-CellsImmune response 1  after binding to the antigen attached to the MHC on the dendrite activates the cytotoxic T cells, memory T cells, plasma B cells, and memory B cells. From there, the cytotoxic T-cells kill infected cells and the plasma-B cells release antibodies to neutralize the antigens. Therefore, when one has a lack of cytokines, the processes induced by them are not in as great a quantity and are weaker overall, leading the adaptive immune system to weaken.

The study done by Zhou and his team has many future implications. Firstly, the study emphasizes that after recovering from COVID-19, patients should be continually monitored, as this study shows that there are long-term effects of COVID-19 on brain health. But more importantly, the fact that COVID-19 can alter brain structure makes clear that more studies need to be done to understand the full scope of COVID-19’s effect on the brain’s structure and overall function over time. What do you think doctors and researchers will study next regarding COVID-19’s effect on brain function?

 

 

 

 

The Lingering Shadow: How SARS-CoV-2 Spike Protein Haunts the Brain

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On December 18, 2024

In Student Post

Covid impacted everyone’s life during the pandemic and become something we might come into contact on a semi regular basis, so it is crucial to understand the long-term effects of SARS-CoV-2. A recent study by Erdem et al. has shed light on some of the longer term effects, explaining how the virus’s spike protein persists in the brain even after viral load dissipation. This blog post dives deep into these findings, and also finds connections with our curriculum.

 

The research by Erdem et al. (2024) details how the SARS-CoV-2 spike protein does not simply vanish after the virus is cleared from the body but instead lingers in the skull-meninges-brain axis. Also, in the cerebral spinal fluid, there were elevated levels of neurodegeneration. There were even dysregulated inflammatory pathways and neurodegeneration-associated changes in the brain. All of these symptoms are “long” after covid has exited the system. Giving a possible cause of all the chronic neurological symptoms seen in long-COVID patients. Interestingly, the study found in mouse samples that the injection of just the spike proteins was enough to cause neuroinflammation and modified behavior. Vaccination does, luckily, reduce the lingering spike proteins. However, it does not completely destroy them. 

Erdem et al. (2024) December 11, 2024

Further investigation showed by Takahashi et al. (2024) that there is a strong correlation between the duration of spike protein presence with the severity of neurological symptoms. Fontes-Dantas et al. (2023) showed that viral presence was not necessary at all for the presence of neurological symptoms, and there is, in fact, a specific genotype: GG TLR4-2604G>A (rs10759931), which has been associated with bad neurological outcomes after covid spike exposure.  

 

This topic connects to AP Bio in a few ways. The first is how the spike protein’s interaction with ACE2 receptors on cell surfaces is a real-life example of receptor-mediated endocytosis. The second obviously is the immune response, in which the spike protein’s persistence challenges the immune system’s ability to regulate inflammation, which we explored when discussing the roles of different immune cells, particularly how macrophages can become activated, leading to both protective and sometimes harmful effects. Finally, the stability and functionality of the spike protein expose the critical nature of protein folding and its impact on function.

 

Understanding the effects of SARS-CoV-2 and specificly the role of the spike protein in neurological damage, allows for both future research and treatment. As we learn more, studies like these highlight the importance of vaccination and early interventions, because we truly didn’t know the full affect of covid. Long covid was just a rumor for years, during the pandemic. By unraveling the mechanisms behind these symptoms one by one, we, as a society, move closer hopefully curing long-COVID for millions of affected peoples worldwide.

 

I choose to write about this topic because my dad has been effected by long covid, and im interested in what caused it and could be done to fix it. To me the idea that just a viral protein could independently cause damage is both fascinating and alarming. 

What do you think about the long-term effects of COVID-19 and how science can help address them? Do you see ways we can better prepare for similar challenges in the future?

Squeaking Ahead: Mice Take the Lead in COVID-19 Research

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On December 17, 2024

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Researchers at The Jackson Laboratory and Trudeau Institute discovered that a specific mouse type, called the “CAST” mouse, naturally shows severe COVID-19 symptoms without requiring genetic changes. Previously, mice required genetic modification in order to experience severe responses to COVID-19, which both helped and hindered research. This finding, alongside the broader research it’s a part of, offers exciting possibilities for studying the disease and advancing treatment development.

The CAST mouse, which was part of a study on eight genetically diverse mouse strains, was uniquely vulnerable to COVID-19. Unlike other strains that experienced mild symptoms or recovered fully, the CAST mice exhibited severe illness from all of the COVID-19 variants that significantly affected humans. Their distinct susceptibility to the virus is highly valuable for research.

 

The CAST mice serve as this excellent model for studying severe COVID-19 symptoms in humans because they aren’t genetically modified. When infected, they display high viral loads in their lungs and show lung damage similar to the hyperinflammatory response seen in severe human cases, without involving brain infections, which was an issue in earlier genetically modified models. These brain infections, alongside other effects from genetic modification, severely impact our ability to understand the virus. However, this new development in the CAST mice allows researchers to closely study human-like responses to the virus on a clean genetic backdrop, which will advance understanding and treatment development.

 

The CAST mouse provides critical insights into the acute effects of COVID-19 and researchers hope to use the mice to better understand the long-term impacts of the virus. Unlike traditional or engineered models, it mimics human-like responses, making it invaluable for studying the disease. Further research on these mice may lead to a deeper understanding of COVID-19, improved vaccine development, and better preparedness for future outbreaks.

 

This research ties into AP Biology by examining infection and vaccines, which are part of the immune system unit. When the body fights an infection, the adaptive immune response causes macrophages and dendritic cells to present the antigen, triggering the release of interleukins that activate helper T-cells. These helper T-cells then stimulate other T-cells to divide into T-memory and T-killer cells. Additionally, they stimulate B-cells to split into B-plasma and B-memory cells. All of these cells work together to fight the infection by killing or neutralizing the pathogen and creating immunity for future exposures. Vaccines are important because they introduce a non-lethal form of the antigen to the body in order to initiate this first immune response.  As a result, the body can mount a stronger and quicker defense upon subsequent exposure to the same infection. While there are ethical considerations, I wonder which other animals could be used to study COVID-19. What are your thoughts on this new discovery and its potential implications?

 

Vaccine vs. Long COVID: The Ultimate Showdown

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On December 17, 2024

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As the world continues to battle the COVID-19 pandemic, new insights into how the virus affects the body are shaping the future of treatment and prevention. Research into long COVID, the phenomenon where symptoms persist long after the acute infection has passed, has revealed underlying biological mechanisms that could lead to better treatments. Simultaneously, studies focusing on the effectiveness of vaccines against emerging SARS-CoV-2 variants are helping scientists refine their approach to vaccination and booster strategies. Together, these advances offer a promising outlook for controlling the virus in the long term and improving outcomes for individuals with persistent symptoms.

Long COVID is a complex condition that affects a significant number of people who recover from the acute phase of COVID-19. While the exact causes remain unclear, recent research has begun to uncover potential mechanisms behind the persistent symptoms, which can include fatigue, brain fog, and difficulty breathing. These findings could pave the way for targeted therapies.

One major area of focus is the possibility of lingering viral reservoirs in the body. Studies suggest that even after the acute infection resolves, viral RNA may persist in tissues such as the brain, lungs, and intestinal lining, continuing to trigger immune responses. This suggests that SARS-CoV-2 might not be entirely cleared from the body, contributing to ongoing inflammation. Another key theory involves autoimmune responses, where the body’s immune system, after being activated by the virus, begins attacking its own tissues. Both these mechanisms could help explain why some individuals suffer from long-lasting symptoms.

Research also highlights the role of microvascular damage in long COVID. Evidence shows that the virus can damage the tiny blood vessels throughout the body, reducing oxygen supply to tissues and contributing to chronic fatigue and other symptoms. Understanding how COVID-19 causes these persistent symptoms may help scientists develop more effective treatments for long COVID, potentially targeting these viral reservoirs or blood vessel abnormalities.

Another major focus of current COVID-19 research is the evolution of SARS-CoV-2 and how vaccines can continue to provide protection as new variants emerge. The Omicron variant, for example, has raised concerns because of its ability to evade immunity induced by both previous infection and vaccination. However, research has shown that booster shots significantly restore protection, particularly against severe disease and hospitalization.

Scientists are now exploring multivalent vaccines, which target multiple variants at once. Early studies show that these vaccines may provide broader protection, potentially preventing infection from a variety of SARS-CoV-2 strains. Some researchers are also looking into universal vaccines that aim to target more conserved regions of the virus, such as the spike protein, to provide long-lasting immunity against both current and future variants.

População do DF conta com 47 tipos de vacinas e soros

Research on COVID-19 vaccines has focused on improving their effectiveness and how booster doses can extend immunity. Over time, the immune response from the initial vaccination wanes, but booster doses effectively “re-energize” the immune system, increasing levels of neutralizing antibodies and T-cell responses. This ensures vaccines remain effective as the virus evolves. Interestingly, vaccination not only reduces the severity of acute COVID-19 infections but may also lower the risk of developing long COVID. Preliminary studies suggest that vaccinated individuals who experience breakthrough infections have less severe long COVID symptoms compared to those who are unvaccinated, and vaccination might even prevent the condition by preventing an overactive immune response or reducing viral persistence.

This research connects directly to concepts I’ve learned in AP Biology, especially the adaptive immune system’s use of B-cells and T-cells to respond to pathogens. In class, we studied how vaccines help the immune system recognize the virus’s spike protein, prompting the production of antibodies and memory cells. This mirrors the process of clonal selection, where specific B-cells produce antibodies to neutralize pathogens. Vaccines essentially train the immune system to respond more quickly and effectively in future encounters, which ties into the primary and secondary immune responses we’ve discussed.

As research continues, clinical trials are exploring treatments for long COVID, including drugs to target inflammation and immune system modulation. Other trials are testing booster regimens to ensure vaccines remain effective against emerging variants. Additionally, rehabilitation programs for long COVID patients, including physical and cognitive therapies, show promise in alleviating lingering symptoms and improving quality of life.

The progress made in understanding both long COVID and vaccine development provides hope for the future. While much work remains, the ongoing research into COVID-19’s long-term effects and the continued evolution of vaccines and treatments are essential in shaping how we will manage this disease moving forward. In the coming years, advancements in universal vaccines and more refined treatments for long COVID could revolutionize our approach to combating the virus.

I’m passionate about the recent breakthroughs in COVID-19 research because of their potential to transform public health. The progress being made in understanding long COVID and improving vaccines offers real hope for both immediate and long-term solutions. I chose to write about this topic because it’s inspiring to see how these innovations could not only help control the pandemic but also improve the lives of millions affected by the virus.

What are your thoughts on the recent advancements in COVID-19 research, particularly in relation to long COVID and vaccine development? Do you think we’ll see even more groundbreaking discoveries in the coming years? I’d love to hear your opinions in the comments!

What is worse: COVID-19 or Post COVID-19?

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On December 17, 2024

In Student Post

 

Since the begining of the  COVID-19 pandemic, society has seen a significant rise in cases of chronic pain. During the pandemic, researchers constantly expressed their fear of COVID-19 resulting in more health issues within individuals.

SARS-CoV-2 without background

When the pandemic first began and everyone went on lockdown, researchers announced their potential concerns with the world shutting down. During the lockdown phase, which lasted about 4 months, people refused to go out since they were afraid of getting COVID-19. Researchers felt that the pandemic would lead to more issues like limited access to health care, less physical activity, and lasting effects of COVID-19 within humans.

Researchers were correct with their predictions as there was a major increase in physical health issues, but especially mental health within many individuals. Many developed depression due to being isolated for such a long period of time. Many of these health issues which began during the pandemic are still a current issue.

Chronic pain is seen within many individuals as a result of the pandemic, and Long Covid definitely contributes to it. Long Covid is when an individual had Covid and still deals with the symptoms. This can cause many problems such as fatigue, brain fog, and body aches.

Scientists believe the reason people encounter Long Covid is due to the virus still being in the body which causes inflammation and immune system dysfunction. Researchers are close to developing a drug that can help treat or prevent this as it may be released soon.

Finally, researchers have seen how the pandemic has negatively influenced society‘s health as a whole as it has led to many consequences. Additionally, as a society, we were unprepared for COVID-19 which highlights the need for better healthcare strategies to help combat these challenges. Although COVID-19 still has lingering effects within individuals, solutions and treatments are in the process of being introduced. These solutions would contribute to an easier and speedier recovery.

COVID-19 relates to what we have learned in AP Biology so far since we have learned different viruses. COVID-19 is caused by the SARS-CoV-2 virus, which is a pathogen that goes into the body and starts an infection. The immune system detects antigens, which activate T helper cells. T helper cells act as a defense mechanism for the body. They also signal other immune cells, like B cells, to produce antibodies. The antibodies neutralize and surround the virus to prevent the production of more infected cells. At the same time, T helper cells also help activate cytotoxic T cells, which kill infected cells, and also stops the spread of the virus. This ultimately fights off the infection and prevents severe illness.

 

The COVID-19 Heart Mystery

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On December 16, 2024

In Student Post

A study supported by the National Institutes of Health (NIH) has discovered that SARS-CoV-2, the virus causing COVID-19, can damage the heart without directly infecting heart tissue. The virus is believed to be spread from person to person through droplets released when an infected person coughs, sneezes, or talks. The research specifically focused on individuals with SARS-CoV-2-associated acute respiratory distress syndrome (ARDS), a potentially fatal lung condition. ARDS occurs when lung swelling causes fluid to build up in the tiny elastic air sacs in the lungs, preventing the lungs from filling with air. The study revealed that the virus causes lung damage through systemic inflammation.

File:SARS-CoV-2 without background.png

Researchers observed that this systemic inflammation was caused by cardiac macrophages that shifted from performing their normal routine of maintaining heart health to an inflammatory state. The macrophages normally sustain the heart’s metabolism and clear out harmful foreign substances. The macrophages’ change of function due to infection can weaken heart function and lead to death.

To understand this process in more depth, the researchers compared the heart tissue samples of 33 people who died of non-COVID causes with individuals who died of SARS-CoV-2-associated ARDS. The researchers discovered that SARS-CoV-2 led to a larger amount of cardiac macrophages and caused them to become inflammatory rather than performing their normal function, ultimately contributing to cardiovascular complications in extreme COVID-19 cases.

To get to the bottom of whether the virus was directly infecting the heart or whether the dysfunction was caused by the immune response, researchers implemented mice in their studies. They infected mice with SARS-CoV-2 and studied the impact of their cardiac macrophages. Other mice were not infected by the virus but were exposed to significant lung inflammation similar to that caused by COVID-19. This experiment helped the researchers determine if lung irritation, without the virus, might elicit the same immune response. Before you read further, what do you think the outcome of this experiment will be?

The findings of the researchers showed that even in the absence of the virus, significant lung damage was sufficient to cause the inflammatory shift in cardiac macrophages, indicating that systemic inflammation, not the virus, was predominantly responsible for the heart damage. This finding shows that the immune system’s response to the virus, particularly the inflammatory signals from the lungs, can cause remote organ damage, including the heart, which was previously thought to be damaged solely by the virus. How interesting!

By using the mouse experiment described above, researchers also investigated the possibility of inhibiting the inflammatory response with a neutralizing antibody. They discovered that this intervention stopped the movement of inflammatory macrophages to the heart, ultimately preserving cardiac function. While this treatment has not yet been tested in humans, it suggests that targeting the inflammatory pathways activated by SARS-CoV-2 may be a potential strategy for preventing cardiovascular complications for individuals with COVID-19. Hopefully, this will help a lot of people! Do you think this neutralization method could be effective?

This article relates to AP Bio because the article shows the importance of macrophages. Macrophages are key immune cells that perform essential functions. Their primary role is phagocytosis, where they recognize, engulf, and digest pathogens, dead cells, and other debris. This process begins when macrophage receptors detect pathogens that are floating freely. These macrophages help perform the bridge between the innate immune response and the adaptive immune response, promoting pathogen clearance, and initiating tissue repair. Once the target is identified, the macrophage engulfs it into a vesicle called a phagosome, which then fuses with a lysosome to degrade the contents using enzymes. The degraded pathogen fragments, antigens, are then displayed on the outside of the macrophage for T-Helper Cells to bind to and continue the immune response. The macrophage will also secrete cytokines to activate the T-Helper cell that can then activate other cells such as B-Cells and T-Cells to differentiate. Later on in this process, the differentiated B-Plasma Cells secrete antibodies to neutralize the foreign substance. The macrophage will then engulf and destroy this foreign substance. In addition, macrophages add in the process of clearing dead or apoptotic cells, which helps prevent excessive inflammation and tissue damage.

In the example of the SARS-CoV-2 article, the cardiac macrophages were made inflammatory due to systemic inflammation triggered by lung damage. This inflammation prevented them from performing their essential functions, such as clearing harmful substances, maintaining heart health, and other functions stated above. The macrophages’ inability to perform these functions ultimately caused damage to the heart.

Well, coming off from Thanksgiving, I certainly am thankful for my functional macrophages!

 

 

 

There is a 7% Chance that You had COVID for a Long Time

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On December 16, 2024

In Student Post

Yes, you read the title right. About 7% of adults (above age of 12) have had long COVID. Many of us have heard about  this weird phenomenon of COVID’s symptoms persisting for a long period of time, sometimes months or even years. This is called long COVID. This sounds awful, and it is. Thankfully, Pam Belluck’s article from the New York Times goes more in depth on the new research regarding Long COVID. In this blog post, we will go through the new research regarding long COVID, including the diagnosis, symptoms, treatments, and science of it.

The research conducted actually stems from government intervention. The Social Security Administration, in 2022, requested a group of relevant and talented experts meet to research the implications and long-term health effects of long COVID. In 2024, the large team of experts published their findings in a fluent 264 page report.

Long COVID, according to the National Academies of Sciences, Engineering, and Medicine, remains a prominent problem in our society, and continues to harm people’s lifestyles. So, how is it diagnosed?

Actually, that’s the first problem. Long COVID doesn’t show up on any COVID test, and there is no concrete way to diagnose someone with it. Every person that gets long COVID experiences it slightly differently than all the rest, making it a challenging diagnosis to make to a patient. This is especially concerning because people’s lives could be degraded every day by long COVID and not they nor their doctor know they even have it. Often, however, the diagnosis is made based on some common symptoms and personal history with COVID. 

Long term covid-19

Generally, a patient with long COVID has symptoms (more listed here) for more than three months after their initial COVID diagnosis, which include lack of energy, brain fog, inconsistent smell or taste, anxiety, and frequent headaches. There are a plethora of additional symptoms any one individual may experience as well. The problem again lies in the fact that everyone experiences long COVID differently. Differently well beyond that of how different people’s symptoms of normal COVID, the flu, or a common cold are. These symptoms last, as in the name “long” COVID, for a very long time, in some cases taking more than two full years for a full recovery, according to the researcher’s report. The report also commented that children can get long COVID too, but their symptoms are less severe and they recover faster.

Also investigated were the risk factors associated with acquiring long COVID. Most evidently, those who get a bad case of COVID initially are more likely to accumulate long COVID. If you were hospitalized for COVID, the report concluded, then you are up to three times more likely to get long COVID than one who had COVID but wasn’t hospitalized for it. However, due to the significantly larger number of mild COVID cases, most long COVID cases are from mild original cases, despite the lesser likelihood of one attaining long COVID after a mild initial response. For currently undetermined reasons, the report found that women were approximately twice as likely to develop long COVID than men. This could relate to possible hormone discrepancies, but there is no sufficient, unconflicted literature to completely validate this hypothesis. Unvaccinated people were also more likely to get long COVID. 

Recovery is slow, especially after the first year, the report said. Treatments depend on the person and their symptoms. There is no long COVID vaccine or cure, either.

Long COVID is a true phenomenon, but there are no such “impossibles” in science, there is always an explanation. Let’s take a closer look at each hypothesis of long COVIDS cause through an AP Biology lens.

One theory is that COVID causes chronic inflammation, which leads to the symptoms previously discussed. Chronic inflammation is caused by the body turning on its inflammatory response, and in this case never turning it completely off after COVID. We learned that the inflammatory response, most importantly, includes mast cells releasing histamine. Histamines “dilate local blood vessels” and “cause the area to swell with fluid,” which ultimately leads to what we see as inflammation. Other parts of the inflammatory response we learned about include macrophages release of cytokines, which attract neutrophils and dendritic cells, helping to consume dead cell debris. With all these processes occurring all the time with chronic inflammation, the body uses immense amounts of energy for no valid reason. This is why the most elicited symptom of long COVID is fatigue.

Another theory put forward by the report is that small fragments of COVID remain in an organ of the body. In AP Biology we learned the common process of B and T cell’s roles in fighting disease as a part of the adaptive response. Mainly because of B and T cell replication, just like chronic inflammation, this process takes large amounts of energy and resources to carry on continuously, even at a small scale.

Knowing all this, think back to the couple months after you had COVID last. Personally, my dad had long COVID and couldn’t taste or smell for months after he got over COVID initially. Did you have any symptoms persist? If so, share in the comments your experience with long COVID. I hope you better understand how it works and why you may have experienced it yourself, or why someone you know has.

COVID-19 Pneumonia: A Lasting Impact on the Lungs

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On December 16, 2024

In Student Post

COVID-19 pneumonia occurs when the SARS-CoV-2 virus causes severe inflammation in the lungs, leading to symptoms like difficulty breathing, low oxygen levels, and persistent coughing. In serious cases, the infection damages the tiny air sacs (alveoli) in the lungs, making it harder for oxygen to pass into the bloodstream. This condition can require hospitalization and even mechanical ventilation to help patients breathe. While many patients recover fully, a significant number experience long-term effects or long term COVID-19 pneumonia, even years after infection. These effects are especially concerning for those who had severe pneumonia, as their lungs often suffer from fibrosis—scarring that makes it harder for the lungs to expand and contract properly.

Recent studies have shown that about half of patients who were hospitalized with COVID-19 pneumonia still have lung abnormalities like ground-glass opacities (hazy spots on CT scans) and areas of scarring more than a year after recovery. These changes can cause ongoing symptoms such as reduced lung function and trouble breathing, affecting daily life.

 

Fibrosis is the main cause for long-terSARS-CoV-2 without backgroundm lung damage, and it forms when the body’s immune response to COVID-19 pneumonia becomes excessive. When the immune system encounters severe inflammation, it attempts to repair the damage by producing fibrous connective tissue. However, an overactive immune response can result in too much fibrous connective tissue being deposited, which alters the lung’s structure. The stiffened lung tissue makes it difficult for oxygen to pass efficiently into the bloodstream, which can lead to shortness of breath and reduced exercise capacity.

Similarly, in AP Biology when inflammation as an immune response becomes excessive it can become harmful in the long term. Furthermore, oftentimes when the body overreacts to pathogens the body can be negatively affected. A fever as an immune response can also be harmful because as pathogens can die from the high heat, the enzymes in our body can also denature. This loss of structure leads to function loss, which has implications for our energy levels. For example, the denaturation of enzymes involved in cellular respiration  causes essential energy processes to slow. 

Understanding the long-term effects of COVID-19 pneumonia is critical as researchers work to develop treatments that target scarring and improve lung health. These advancements could offer relief to the many patients still grappling with the lingering impacts of this disease, giving them a better chance at full recovery. As a recent patient of pneumonia, I’ve understood its complexity and danger!

Unraveling the Mystery of Cytokine Storms: New Insights into COVID-19’s Deadly Immune Response

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On December 16, 2024

In Student Post

Researchers from Johns Hopkins and other institutions discovered a new cause of “cytokine storm,” a dangerous immune response that can increase the risk of death in COVID-19 patients. Their findings were published in the Proceedings of the National Academy of Sciences on November 27, 2024.

Cytokines, as discussed in class, are small proteins released by macrophages that help control the immune system and fight infections.  A “cytokine storm”occurs when the body releases too many cytokines too quickly, leading to severe inflammation and damage to multiple organs.

File:Cytokine release following SARS-Cov-2 infection resulting in ARDS related to COVID-19.png
By Razaghi, Ali, Attila Szakos, Marwa Alouda, Béla Bozóky, Mikael Björnstedt, and Laszlo Szekely. 2022 – https://doi.org/10.3390/diagnostics12112789, CC BY-SA 4.0, Link

To find out what triggers cytokine storms, the researchers analyzed tissue samples from 40 patients who died of COVID-19. They looked at samples from various organs, including the lungs, heart, liver, kidneys, lymph nodes, and the nasal cavity.

They identified about 50 immune genes that were more active in the nasal swabs and continued to investigate these genes in the other tissues. Many of these genes are part of the “inflammasome,” a group of proteins that are a part of a signaling network that help the body fight off viruses and bacteria.

The researchers found that when these genes stay active instead of turning off, they can cause a cytokine storm.

In COVID-19 patients, immune genes in the nasal cavity (where the virus enters) send signals through a system called the renin-angiotensin-aldosterone system (RAAS) – this is a hormone system that usually helps regulate blood pressure, body fluids, and electrolytes.

In COVID-19, RAAS goes into overdrive, pushing the immune response into an overreaction. The belief is that this overreaction of RAAS may be responsible for causing the cytokine storm and preventing the inflammasome proteins to be turned off.  This impairs the infection-fighting function of the lymph nodes and severely damages the lungs, kidneys, heart, liver, and other organs. This may be the reason that some people were more likely to die from COVID-19.

Interestingly, the researchers believe that gene markers of this inflammatory response can be detected in the blood!  This can help identify patients at risk for severe COVID-19.  The researchers also believe their findings may help understand “long COVID,” a condition with lingering symptoms after the initial infection. This area remains a focus of ongoing research.

In biology, I have learned about cytokines, which are small proteins that help regulate the immune system and fight infections.  They are secreted by various cells, including immune cells like macrophages, B cells, and T cells. Cytokines help regulate immune responses by promoting or inhibiting inflammation, guiding immune cells to infection sites, and stimulating cell growth, differentiation, and repair.

This made me think of other components to getting infected with the virus.  For example, what other factors make you more susceptible to the body’s response to a covid 19 infection?  Does age play a role, other underlying health issues, or is it all written in our genes?

Clearing the Fog: Exploring the Relationship Between COVID-19 and Cognitive Impairment

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On December 16, 2024

In Student Post

Have there been moments where you’ve lost your train of thought? Or forget something you just heard? Or did your brain just feel “foggy?” At some point, we have experienced these “Brain Fog” moments. 

But for those recovering from the SARS-CoV-2 infection, this “fog” can be more serious and more frequent. Those who experience long COVID (a COVID-19-related medical condition after three months post-infection) may experience a symptom of cognitive impairment. These include memory loss, difficulty learning, and fatigue. 

Previously, there had been limited information and research about the link between cognitive impairment and SARS-CoV-2. However, Sarah Lutz and her University of Illinois Chicago team decided to investigate mice and solve the ultimate question: Why does a COVID-19 infection trigger these neurological issues?

First, the team infected a sample of mice with the SARS-CoV-2 virus. Then they chose to examine the infected mice’s blood-brain barriers (BBB). 

But what is a blood-brain barrier? Well, it’s a semipermeable membrane formed by endothelial cells. Its purpose is to allow cerebral blood vessels to regulate the movement of molecules in and out of the brain. It’s also responsible for maintaining neuronal function homeostasis and preventing harmful substances circulating in the bloodstream from entering the brain. As part of our Cell Communication unit, we learned about positive and negative feedback loops and their reactions. We learned that negative feedback loops are a response to a type of change or disturbance in a biological system and create a reaction to return to the target set point or equilibrium. The blood-brain barrier system resembles negative feedback loops because once there is a disturbance in the barrier, a regulatory response is activated to quickly try and repair it and revert conditions back to normal. Both negative feedback loops and the blood-brain barrier have the same goal: maintaining homeostasis.

Usual pattern of radiopharmaceutical distribution in brain parenchyma.

Focusing back on the experiment to ensure her results accurately reflect the population, Lutz mimicked her research on current health conditions and patterns. For instance, the team specifically tracked mice with mild infections rather than severe ones since most of the COVID-19 cases in humans today are mild due to vaccines. They also focused on older mice as subjects for their research to account for age being a risk factor for cognitive impairment in COVID-19-infected humans.

Then, the team infected the mice with SARS-CoV-2 (the virus that causes COVID-19) and examined their blood-brain barriers. They discovered that after receiving the infection, the mice’s BBB vessels became less strong and more leaky, providing less protection for the brain. In addition, the infected mice also displayed signs of memory loss and cognitive impairment, the research team found. 

Several studies have been conducted that mirror these results. For example, an analysis of the U.S. Current Population Survey showed that after the start of the pandemic, an additional one million U.S. residents of working age reported having difficulty remembering, concentrating, and making decisions than at any time in the preceding 15 years. A further study used an online assessment tool to test cognitive impairment. They gathered 800,000 people who experienced COVID-19 symptoms for over 12 weeks. Subjects with mild symptoms, on average, scored three fewer IQ points than the control group. Those with unresolved persistent systems had a 6-point deficit. 

Furthermore, the National Library of Medicine connects damages in the blood-brain barrier to conditions such as stroke and epilepsy and neurodegenerative diseases such as Alzheimer’s, highlighting its relation to memory and reasoning problems. 

Interestingly, the infected mice both had leaky BBBs and exhibited signs of cognitive impairment. Is there some type of relationship between the two? 

While further examining the mice’s blood vessels and the specific genes, Lutz noticed a significant decrease in the signaling pathway, Wnt/beta-catenin. The Wnt pathway stabilizes beta-catenin, allows it to interact with transcription factors in the nucleus, and triggers specific cellular responses, including cell growth and division. It’s a significant pathway in brain development during embryonic development, and damage to it can lead to cancer or brain tumors. Another function is to improve the health and maturation of the BBB, which is what the Lutz team focuses on. 

These findings about the Wnt pathway opened the door for another test: whether stimulation of the Wnt/beta-catenin pathway could change the composition of the BBB after Sars-CoV2 infection. 

The team explored a specific gene therapy to activate the pathway and tested if it could improve the cognitive impairment of the infected mice. The results supported their hypothesis- the mice had less blood-brain barrier leakage and enhanced memory and learning!

Ultimately, Lutz’s study provides an important link between the blood-brain barrier and the effects of cognitive impairment due to long COVID. Since there is still limited information, the team believes that more research should be conducted about the blood-brain barrier, the whole brain in general, and its relationship to COVID-19 since it can prevent further complications and issues. However, these results are a stepping stone in the right direction. To one day create a therapy to prevent humans from experiencing cognitive impairment post-SARS-CoV2 infection!

The results of this study make me very hopeful for the future as well. Several of my family members have experienced Long COVID and have experienced Long COVID and have experienced symptoms, including problems with taste and smell. Luckily, no one in my family has experienced neurological problems such as memory loss as a symptom; however, many people I know do have loved ones who unfortunately have developed severe cognitive impairment as a result of COVID-19, and it’s hard seeing these changes develop in the people you love the most. Through research such as this, maybe one day, this problem of leaky blood-brain barriers could be eradicated, and no one will ever have to experience these pains after a COVID-19 infection again. 

Link to Main Source

 

How Vaccination is Reducing Long COVID Rates With The Rise of New Variants

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On December 16, 2024

In Student Post

As the COVID-19 pandemic has unfolded, researchers have monitored how different variants of the virus impact health outcomes, particularly concerning long COVID. A recent study published in the New England Journal of Medicine examines the rates of long COVID among individuals infected with the coronavirus during different phases of the pandemic. Researchers analyzed data from about 450,000 U.S. veterans who contracted COVID-19 between March 2020 and January 2022. The study highlights a decline in the occurrence of long COVID as new variants emerged, particularly among those who were vaccinated.

Long COVID is a serious condition that can affect anyone who has had a SARS-CoV-2 infection. Symptoms can last weeks to years and may require comprehensive care. According to the study, during the pre-delta phase, 104 out of every 1,000 unvaccinated individuals developed long COVID within a year of infection. This decreased to 95 per 1,000 during the delta variant surge and then it dropped to 78 per 1,000 during the omicron phase. In contrast, vaccinated individuals experienced significantly lower rates of long COVID: only 53 out of 1,000 developed long COVID after delta infections, and 35 per 1,000 did so after omicron infections. This data shows the protective effect of vaccination against long COVID.

The researchers attribute approximately 72% of the reduction in long COVID cases during the omicron phase to vaccination efforts, with the remaining decrease linked to changes in the virus itself and advancements in medical treatments, including antiviral therapies. Despite these findings, the study warns that there remains a risk for long COVID due to ongoing infections and reinfections. The researchers mention that these factors could lead to a large number of individuals potentially experiencing long-term health issues related to COVID-19.

This study’s findings directly relate to what we have learned in AP Biology on the immune system and vaccination. Vaccines are designed to elicit an adaptive immune response by stimulating the production of memory cells that can recognize and combat pathogens more effectively when you are re-exposed to a virus, particularly the production of memory B and T cells. These cells allow for a faster  immune response when exposed to the pathogen again. In the case of COVID-19 vaccines, they allow the immune system to recognize and combat the SARS-CoV-2 virus more effectively, reducing the severity and duration of symptoms, including those associated with long COVID. This highlights the biological mechanisms behind vaccination and their role in controlling infectious diseases and avoiding long-term health consequences.

The findings from the study on long COVID rates are very interesting and encouraging. It’s great to see the positive impact of vaccination on public health, especially as we navigate the challenges posed by new variants. Personally, I feel optimistic about the future as we continue to learn more about the virus and improve our strategies. The potential for long COVID to affect many individuals is a reminder of why vaccination and education are important. I am very interested in public health and well-being, so this topic is especially important to me.

Considering the evolution of SARS-CoV-2 variants and vaccine development, what strategies do you think are most important in addressing immediate and long-term impacts of COVID-19 on public health?

A person, wearing gloves and a surgical mask, handles a COVID-19 Vaccine vial and syringe

How is Omicron still a problem?

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On January 16, 2024

In Student Post

Covid-19 under a microscope

 

Allow me to take you back to the early days of the Covid-19 pandemic. Alpha, and Delta were the primary variants.

And then Omicron stumbled in, and unlike the others, never left.

Unlike the others, who had viciously ensnared others to their deaths, Omicron was more akin to a hard cold, or the flu. Whilst it shared flagship symptoms like parosmia (loss of smell/taste) and other respiratory symptoms, they resulted in less hospitalizations. In addition, we were going stir crazy and had started to unlock the lockdown. 

And Omicron, unlike the others, was a rapidly evolving virus, one variant one second and another the next. The rapid mutations in the epitopes (the spike protein that the immune system uses to distinguish it from other viruses) made vaccines, which are designed to emulate the epitopes so the body can recognize it (hence the potential fever- your body is learning the epitope’s shape so it can catch the real thing faster), next to impossible to settle on. Trying to get a working vaccine for it was like trying to hold a tiny fish in the rain- it just kept slipping away. 

And now again, descendants of Omicron are dominant again.

HV.1 is a descendant of Eris (EG.5) but isn’t really that different from Eris. Vaccines that are designed to target XBB (another offshoot) still work on both of them. HV.1 is only dominant for minor mutations, as vaccines still work.

The real worry is BA.2.86, which has been determined to evade the immune system. It, in comparison to say, EG.5.1 or XBB.1.5, resulted in a lower concentration of neutralizing antibodies, meaning one infected would be infected for longer.

Its descendant, JN.1 might be even better at it. It can be transmitted at low levels due to its highly mutated spike protein, and still evades the humoral response more effectively than its predecessor.

I, for one, think that Omicron isn’t going away. It mutates too quickly to truly be caught. But I think a monovalent vaccine is possible per each set of dominant strains. And to that, I mean it will likely become another vaccine to get annually in the fall.

How COVID-19 Robs Us of Our Sense of Smell

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On January 15, 2024

In Student Post

Led by researchers from NYU Grossman School of Medicine and Columbia University, the study with the pandemic virus, SARS-CoV-2, found that the infection caused by SARS indirectly dials down the action of olfactory receptors (OR), proteins on the surfaces of nerve cells in the nose that detect the molecules associated with odors. This new study not only sheds light on the reason for loss of smell, but also sheds light on the effects of Covid-19 on other types of brain cells, and on other lingering neurological effects of COVID-19 like “brain fog”, headaches, and depression.SARS-CoV-2 without background

The study involved analysis of olfactory tissue from human autopsies and experiments on golden hamsters, a species highly reliant on their sense of smell. The researchers observed that the virus triggers an increase of immune cells, which release cytokines altering the genetic activity of olfactory nerve cells. They suggest that that if olfactory gene expression ceases every time the immune system responds in certain ways that disrupts interchromosomal contacts, then the lost of sense of smell may act as an early signal that the COVID-19 virus is damaging brain tissue before other symptoms presents, and suggest new ways to treat it. However, these cells are not infected by the virus directly. These findings could have broader implications than it first seems. The persistence of immune reactions in the nasal cavity may influence cognitive functions and emotions because these olfactory neurons are connected to sensitive brain regions. The team’s next steps include creating treatments to protect the “nuclear architecture” of these cells and prevent long-lasting implications. This study aligns with many core topics in AP Biology, such as proteins, the immune system’s role in disease response, and the immune system’s interaction with neurons. It offers insight into the understanding of how cells communicate and respond to pathogens. It also delves into gene expression which illustrates how factors like viral infections can lead to changes in a cell’s genetic activity. This study represented a significant step in understanding the broader effects of COVID-19 and opens options for new treatment strategies. The Study also provides valuable insights into the functions of the immune system and neurons during a COVID-19 infection. The increase of immune cells and the release of cytokines in response to SARS-CoV-2 can alter the activity of olfactory nerve cells. This not only affects our sense of smell but also has more affects on brain function. The immune reaction in the nasal cavity could impact cognitive functions and emotional states because of the connection of olfactory neurons to sensitive brain regions. This understanding of how COVID-19 effects immune responses and neuronal changes is crucial as it helps scientists find new ways for treating the long term effects of COVID-19. Now this brings the question of if this study gives insight into how to treat patients with long term issues from Covid and how they will be treated.

 

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