AP Biology class blog for discussing current research in Biology

Author: rnase

How a Unique Type of T-cell Can Protect Against Pneumonia

We’ve all probably heard of pneumonia, or even know someone who has had it. Pneumonia is a lung infection that can be caused by bacteria, viruses, or fungi. This infection causes the lungs’ air sacs to fill with fluid, making it hard to breathe. The majority of cases of community acquired pneumonia are linked to Streptococcus pneumoniae (the pneumococcus). Because there is a significant chance of developing bloodstream infection in these cases, the fatality rate is high. Even with antibiotic treatments and vaccines, the fatality rate is 20% for young adults and 60% for the elderly. Although the reason why some individuals are more susceptible to this disease and why others are not has been a mystery for decades, scientists have discovered a cell that may provide some answers.

At the University of Liverpool, the Bacterial Pathogenesis and Immunity Group has identified a subset of white blood cells in mice known as TNFR2 expressing regulatory T cells (Tregs).

In class, we learned that T cells were involved in the cell-mediated response of adaptive immunity. During the immune response, T-helper cells are activated by interleukin to recognize the antigen and trigger the cell-mediated and humoral responses. T-memory cells are created to confer future immunity while T-killer cells are created to kill infected or cancerous cells. A subset of T-cells called regulatory T cells also regulate the immune system. During pneumonia infection specifically, these cells are involved in bacteraemic pneumonia resistance through maintaining and controlling frontline immune responses during infection in the lungs. T Regulatory Cells

When these cells are not functioning correctly or are missing, there is excessive and uncontrolled inflammation that results in tissue damage. This allows the bacteria to enter the bloodstream through the disrupted lung tissue barrier and cause sepsis, which is the body’s life-threatening response to infection.

Professor Aras Kadioglu, the leader of the Bacterial Pathogenesis and Immunity Group, stated, “This is a significant finding, which opens the door to potential new therapies which may target and modulate these subset of Tregs to prevent and treat severe invasive pneumococcal diseases.”

This article caught my attention because I have never heard of this subset of T cells before. Given how severe pneumonia is, it will be interesting to see how scientists will use this information to create new life-saving treatments.

Why does COVID-19 cause death in some people and no symptoms at all for others?

COVID-19 can have a variety of effects on the human body, ranging from no symptoms at all to death. Researchers have been investigating what factors such as demographics, pre-existing conditions, vaccination status, and genetics, may contribute to the severity of COVID-19 symptoms.

Researchers already know that older people and unvaccinated people are more likely to have complications. According to August data from the US Centers for Disease Control and Prevention, those unvaccinated and over the age of 50 were 12 times as likely to die than those who had received two or more booster shots.

Pre-existing conditions can have a significant impact on the symptoms COVID-19 can cause. For all ages, conditions like heart disease, kidney disease, chronic obstructive pulmonary disease, diabetes, and obesity can exacerbate COVID-19 symptoms. Cancer patients on immunosuppressants, however, are particularly vulnerable. Getting infected may cause a cytokine storm. In AP Bio, we learned that if a pathogen has managed to get past the barrier defenses, macrophages secrete cytokines as part of the innate cellular defense. Cytokines then attract other phagocytes called dendritic cells, as well as smaller phagocytes called neutrophils to digest pathogens and dead cell debris. A cytokine storm is harmful as it can trigger inflammation that damages organs and tissues. Fimmu-11-01648-g001

Scientists have also found that certain genes may predispose individuals to be more susceptible to COVID-19. Studies have shown that some genes from Neanderthals could protect against COVID-19, while other genes could raise the risk of developing severe symptoms. Additionally, scientists discovered that people with variations in the gene called toll-like receptor 7 (TLR7) are 5.3 times more likely to have severe symptoms from COVID-19. Proteins produced from this gene are involved with interferons to alert other cells to raise anti-viral defenses when a virus has invaded. Interferons essentially interfere with the virus. Conversely, having variations in another gene called TYK2 can protect against infection. TYK2 is involved with producing interferons. However, there is a genetic trade-off. Although having more interferons can help fight COVID-19, having more interferons when there is no infection may cause the immune system to attack its own body. Therefore, variations in TYK2 may also increase the chance of developing autoimmune diseases like lupus.

Even with all this research, scientists can not determine the risk that one individual has of having complications with COVID-19. The only factor we can control is our own habits. We should continue to wash our hands, wear masks in crowded spaces, and stay up-to-date with vaccinations. I thought this topic was very interesting because many of us at school do not perceive COVID-19 to be a serious disease anymore. However, we should remain vigilant in preventing the spread of SARS-CoV-2 and other viruses as there are others outside our community that are vulnerable.

Omicron: The Most Infectious COVID Variant Yet

Omicron has become the most infectious variant of COVID yet, even managing to re-infect people who already had COVID. According to researchers in Botswana and Africa, omicron’s ability to spread so easily is due to its 60 genetic mutations, which include 42 changes to its spike proteins.

In class, we learned about a form of endocytosis called receptor-mediated endocytosis. Receptor-mediated endocytosis occurs when ligand bind to receptor proteins on the cell membrane that match their shape. This process triggers the cell to let in the virus in a coated vesicle. In this case, the ligands are the COVID spike proteins are the receptor proteins are called ACE2. The omicron spike protein is shaped like a claw machine. Most antibodies attack the claw fingers, however, omicron keeps its “knuckles” bent to hide the parts the antibodies target. Omicron can also stick out one positively charged finger to grab onto the negatively charged receptor. This electrical attraction in omicron is three to five times greater than that of the delta variant, greatly contributing to its ability to infect the cell.Coronavirus. SARS-CoV-2

Researchers also suspect that omicron uses a mechanism unlike previous variants to enter the cell. They believe that omicron uses a backdoor compartment called an endosomes, sorting organelles part of the endomembrane system, and a protein called cathepsin L to drop its genetic material. We discussed in class that the endomembrane system also included vesicles, nuclear envelope, the Golgi body, plasma membrane, and the ER. Through this method, omicron is able to enter the cell without killing it. This is particularly significant as the virus can use the host cell to create even more of the virus to spread. Another mutation that aids the virus is a sugar molecule on the spike protein. This modification makes it difficult for antibodies to attack the virus. For these reasons, omicron has managed to evade very effective vaccines. In one case, it was found that two doses of the Moderna vaccine was only 44% effective at preventing omicron infection between 14-90 days after getting the vaccine, and only 23.5% effective between 3-6 months after getting the vaccine.

I was interested in this topic because I’ve noticed that many of my classmates have gotten infected with COVID recently, even after receiving multiple vaccines or having already being infected with COVID. We can only hope that the next mutations will not lead to a more virulent form of the virus.

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