AP Biology class blog for discussing current research in Biology

Author: asteraceae

Big Cat, Little Bird

A fishing cat in a bird's nest

Credits: Allama Shibli Sadik & Muntasir Akash / De Gruyter


Cats don’t hate water, contrary to popular belief. In fact, there is a species of wildcat evolved to hunt in water. 

Aptly named “fishing cats,” Prionailurus viverrinus is a species of South Asian cat that has evolved to fish. Unlike other felines, they have slightly webbed forepaws and double layered water-resistant fur. This gives them an edge over others as it means they won’t freeze when they fish, giving them an opportunity to pass this trait down and allows them to stay reliant on their fishing diet, unlike other cats who primarily rely on land prey. They are medium sized cats with yellowish fur, and black tabby stripes that gradiate into mottled spots.

They catch their prey by idling on the edge of a body of water, and scooping the fish out of the water. Very rarely do they wade in and put their head underwater to fish.

But their diet does not solely consist of fish. They are also known to eat small rodents, lizards, amphibians and birds in addition to fish.

The only problem is that with the monsoon season, it is nearly impossible to fish as the land prey is gone, and their usual waters are flooded or destroyed. These cats live in areas prone to flooding and the lack of infrastructure means that the prey cannot flee (also fish cannot sustain on land).

So what does the brilliant cat do?

It climbs trees and preys upon the bird colonies. It has been seen preying upon waterbirds (ie. herons, moorhens, cormorants) high within the tree canopy, snapshotted with camera traps.

This might just be its secret to success since the local population also relies on the fish and (since people have more power than these felines) will deter (and kill) these cats. These waterbirds are not just the cats’ benefit, but the benefit of the locals as well!

Unfortunately, due to brackish waters and the urbanization of wetlands, the clever species is slowly dying out. But that’s another article.

There isn’t a lot known about these guys, but there are ongoing research projects with them.

CRISPR and Sickle Cell Disease

A blood smear of someone with sickle cell disease under a microscope

Scientists are starting to use genetic editing tools to edit out genetic diseases, starting with sickle cell disease.

Sickle cell disease is a non-dominant genetic disease that is the result of the red blood cells becoming well, sickle shaped. These cells then die early, and catch on things in veins, resulting in clots.

In addition, the cells aren’t able to properly deliver their cargo to cells- oxygen. The recipients then also promptly die early, resulting in a multitude of complications, many of which are potentially fatal.

CRISPR (short for “clustered regularly interspaced short palindromic repeats”) technology utilizes Cas9 proteins, guided with a sliver of RNA, and it will comb through the DNA and clip the matching strands off, in which it will either be forced to mutate, or function correctly (should it be a mutation that we are seeking to eliminate). 

In this case, CRISPR is being used to alter the genes that cause this disorder (that without morality, natural selection would have done its work in weeding it out) as a replacement for the support (i.e. blood transfusions) . 

Before the actual editing process, the patient’s stem cells are collected and the patient undergoes high dose chemotherapy to clear the existing bone marrow so that the edited cells can take prevalence

Casgevy, the name of one of the gene editing drugs, does exactly that. Blood is drawn, the blood is treated, then the now edited blood is reinserted into the patients bone marrow. It is currently approved for people 12 and over, but that is likely a base number and one’s doctor would properly evaluate for.

29 of 44 treated patients had achieved 12 consecutive months within the span of 24 months without SCD complications, and all 44 treated patients had successfully accepted the mutated stem. 

Common side effects included low platelet and white blood cell levels, mouth sores, headaches, itching, febrile neutropenia, vomiting, abdominal pain, and musculoskeletal pain.

How many other genetic diseases can CRISPR edit out?

How is Omicron still a problem?

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.

Using Mosquitoes’ Greatest Asset Against Them

What if mosquitoes were not a threat anymore? The most deadly animal known to man, harmless?

Aedes aegypti CDC-Gathany

Even today, even with deaths down 31% from 2010 to 2019, mosquitoes still kill around 1 million people a year. According to the CDC, in 2020 they killed over 600,000 to malaria alone. Excluding other viruses such as dengue or West Nile virus.


But scientists intend to turn their affiliation with viruses into an advantage. By implanting their own virus into mosquitoes, one that can limit the transmissibility of other ones.


Wolbachia. A virus preexisting in an abundance of other bugs to the point of it not harming the ecosystem. A virus that can suppress the transmission of viruses. A virus that will be passed down the generations.


In Medellin, Colombia, a mosquito factory exists solely for this purpose. To breed enough of the Aedes aegypti mosquito, that will propagate this virus throughout the town. Rather than the insecticide trucks barrelling through the streets, spraying the air and killing the water, mosquito eggs are injected with incredibly fine needles, nurtured, then released. And there were results. Mosquitoes who picked up a virus were less likely to transmit it to humans. In Yogyakarta, Indonesia it worked too.


Whilst the A. aegypti mosquito originally originated from Africa, they escaped via the slave trade, and later, would follow the paths of troops in World War II. And now many communities are affected by it.


So the introduction of something to suppress these fatal diseases is good, right? 


This program is too new. The Wolbachia might work now, but it’s only a matter of time before these viruses mutate and harness the power of the increased number of mosquitoes. “Mosquito populations are increasing and additional methods are needed to control the mosquitos during their adult stage,” the EPA states in regards to the mosquito population in Puerto Rico. And they do not mention the added mosquito populations. If say, dengue mutates, changes even the slightest bit of its genetic code, and Wolbachia no longer works, then we have simply increased the problem, kicking that can down the road.

There is a chance that a virus will mutate every time it duplicates its RNA/DNA, and since it occurs quite frequently, there is a solid chance for a mutation that ignores Wolbachia to become prevalent in mosquitoes. If the epitope (the spike protein that antibodies recognize) in one of the viruses Wolbachia seeks to prevent changes significantly, Wolbachia’s gift will turn back into its weakness. Akin to how old Covid vaccines no longer work, but I digress.

I cannot say for certain that this may occur, but then viruses are like elusive fish: nearly impossible to predict or ensnare, yet still so prominent in its effects. 


Please tell me if you think this will work. These studies feel a little too optimistic, but I hope I’m wrong.


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