AP Biology class blog for discussing current research in Biology

Tag: endocytosis

Why don’t we have a cure to HIV?

HIV, Human Immunodeficiency Virus, is a severe virus that destroys the body’s immune system, which can later lead to AIDS(acquired immunodeficiency syndrome) if the virus is not treated. Since its discovery in 1981, there have been no proper ways to completely cure this virus, which led many people to wonder the same question: what does HIV do to our body that’s incurable?


Initially, when the virus enters the body, it uses a particular cellular protein called cyclophilin to bind with our cell receptor; it then receives our cell’s information and changes its shape to fit into the compartment. Once that’s done, HIV does a process that we often hear in biology: Receptor-Mediated Endocytosis. To further explain this, the cell is triggered by a specific ligand that matches the cell’s shape. When it’s inside the cell, HIV uses its own DNA and genes to replicate itself. After, the virus Exocytosis gets out of our cells and moves on to infect other cells in our body.

People might question why HIV is incurable? Other viruses do the same thing when entering our bodies, but they can still be cured. To answer this question, we need to go back inside the cells to see what the virus is doing there. While HIV replicates itself and infects cells, it also integrates with the host’s DNA to create reservoirs. When inactivated, the virus inside the pools are remained “silent.” However, once the current virus inside the body is used, a stimulus is sent to those reservoirs to reactivate the remaining virus and start the infection.

Despite its fatality over the years, with modern-day’s medical technology, a person with HIV can live just as long as those who are HIV-negative if the virus is detected early. With that being said, it is crucial to receive early treatments once you have HIV.

How is COVID-19 similar to Yellow Fever

Since the start of the pandemic, COVID-19 has affected millions of people around the globe. It’s an RNA virus that causes fever, cough, and death. Like other respiratory viruses, COVID-19 spreads quickly by particles that come out of your mouth when you sneeze, breathe, and cough.

Novel Coronavirus SARS-CoV-2


One similar virus is Yellow Fever. It’s also an RNA virus that transmits by mosquito bites. Depending on the person’s body, one might react differently from another. Most people either have no symptoms or mild symptoms that can be recovered in a week. However, people with weak immune systems might develop severe symptoms such as high fever, chills, and body aches. In addition, the fatality rate for people to develop severe symptoms is between 30%-60%.


Now you might wonder, what makes those viruses similar? Aside from them being RNA viruses, they also have similarities in symptoms. Still, most importantly, those two viruses both do something that I mentioned in my last post: Endocytosis. When these viruses enter our body, they use their special protein receptors to trick our cells into thinking it’s some proteins that benefit our body. Once viruses enter the body, using receptor-mediated cytosis, it uses its own protein and DNA to replicate themselves, including those false proteins. One thing to note is that those viruses can’t replicate by themselves. They would need to rely on living cells to multiply. Once the viruses replicate themselves, they carry on with exocytosis to exit the infected cell and infect more cells in our body.

Last but not least, Yellow Fever and COVID-19 can’t be completely cured since the viruses mutate so quickly that we don’t have enough time to find what can erase those viruses completely. However, as long as we receive vaccines and take care of our health, those viruses shouldn’t worry us too much.


What is Marburg Virus and why is it so fatal?

Many people probably never heard the term “Marburg Virus” before. Still, it is one of the deadliest viruses humans have ever found, with an average fatality rate of 50%, ranging between 23% to 90%, and there’s still no approved treatment to cure this virus. So what is Marburg Virus, and what does it do to the immune system that causes us to be in danger? To understand all of these, we must first dive into the structure of the Marburg Virus and what “strategies” they use to deceive our immune system and enter our cells.

According to CDC, Marburg is a virus that originated in 1967 in Marburg and Frankfurt, Germany, and in Belgrade, Yugoslavia (now Serbia). It is a virus that attacks your immune system to cause severe fever, Malaise, and diarrhea. In addition to those symptoms, people who get the virus can also suffer severe weight loss, vomit, and even organ failure. The virus was not very active for the past 20 years, but recently, in August 2021, a 46-year-old man from Temessadou M’Boké, a village in Guéckédou prefecture in Guinea, died after hemorrhaging from several natural orifices. Marburg virus

To understand this virus, we must first look at its structure. Marburg Virus(MVD) is an RNA virus that can enter our cells by endocytosis, specifically receptor-mediated endocytosis. Since Marburg Virus is a special type of virus, it has its own attachment proteins; it uses the process of Receptor-Mediated Endocytosis because it triggers a specific receptor in a coated pit. After the virus triggers the receptor on our cell, it gets attached to our cell surface and clusters the receptors. Because Marburg Virus also contains its own protein, our immune system falsely identifies it as something good for our body, which allows them to attach to our membrane and send the virus into our cells. Once it’s in, the virus uses its RNA to provide information to replicate and infect cells using viral proteins. Once a cell is infected by the virus, the virus and its copy use the same process to infect other cells in our body until the majority of our cells are infected. (SARS-CoV-2 uses the same process as Marburg Virus since they both are RNA viruses.)


Now that we know the structure of the virus and how it enters our body, we need to figure out why it is so deadly. We certainly have many RNA viruses that exist in our daily lives, but most of them are not fatal. One of the differences between Marburg and other viruses is that it can cause severe hemorrhagic fever, similar to the symptoms of Ebola. It is a condition that affects many body organ systems, damages the overall cardiovascular system, and reduces the body’s ability to function. Furthermore, the fever will reduce the level of blood-clotting cells in our body, leading to severe internal bleeding and death as the excess amount of blood pressures your organs and tissues.

Advancing Towards a Cure for Mucolipidosis Type II

Mucolipidosis type II—also known as “I-cell disease”—is a rare life-threatening condition in which the heart and abdomens become swollen, bones deform, and the patient typically does not make it past the age of 7. This lysosomal storage disease is heritable and currently incurable.  

Inclusion cells are non-living substances located in the cell that are not membrane-bound. These non-living substances include glycogen, lipids, and pigments. In mucolipidosis, inclusion cells in growing fibroblasts occupy the cytoplasmic space aside the Golgi apparatus—hence the name “I-cell disease.”

Recent research reveals a new gene, TMEM251, that is defective in humans with symptoms of mucolipidosis type II. TMEM251 is crucial in enabling lysosomes to function appropriately. In AP Biology class, we covered how lysosomes are essential to various cell processes, such as digesting food and breaking down old cell parts enclosed in vesicles. Without the lysosome’s function, this waste will build up, unable to be broken down.

Several enzymes inside lysosomes digest worn-out cell parts (proteins, carbohydrates, lipids, and nucleic acids) of which the lysosome recycles. These enzymes require a signal called the mannose-6-phosphate biosynthetic pathway (M6P) in order to enter the lysosome. TMEM251 activates the M6P. When TMEM251 is defective, there is no M6P to allow the enzymes into the lysosome, thus creating an inability for the lysosomes to function

Researchers tested the link between defective TMEM251 and type II mucolipidosis symptoms by knocking this gene out in zebrafish, ultimately yielding defects in the zebrafish’s abdomen, heart, and skeletal development. These symptoms align with those of mucolipidosis type II in humans, concluding the existence of a relationship between TMEM251 and the disease. 

To treat children with mucolipidosis type II, the researchers propose the idea of “enzyme replacement therapy.” They hypothesize that by supplying enzymes containing M6P modification to TMEM251-deficient cells, the enzymes will be able to filter into the cell through endocytosis, delivering them to the malfunctioning lysosomes. Isn’t that neat? In AP Biology class, we learned that endocytosis occurs when the substances surrounding the cell membrane are transported into the cell. Through the process of receptor-mediated endocytosis, specific ligands (i.e. enzymes) bind to receptors that match their shape.  

A depiction of various types of Endocytosis

I believe that enzyme replacement therapy would efficiently treat mucolipidosis in humans, and encourage further study in this area to seek treatment for this deadly disease that robs young children of their bright futures. Would you support further research in this area? Please feel free to share your thoughts in the comments! 


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