BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: SARS-CoV-2

Comparing Saliva Tests to Nasopharyngeal Swabs

Although many college campuses have closed within the past couple of weeks, for the few months they were in session, the general public was introduced to a new procedure for COVID-19 testing: Saliva tests. There are multiple reasons why a saliva test would be more ideal for campuses to use, and it’s not just because the nasopharyngeal swab testing is extremely uncomfortable.

A nasopharyngeal swab is basically a biological term for the COVID-19 test that goes all the way up your nose. News-Medical actually came out with an article going through the testing procedure, and how the SARS-CoV-2 is detected. The purpose of the swab test is to reach the nasopharynx, which is where nonpathogenic and pathogenic bacteria and viruses lie. It’s also used to test the flu and pneumonia. In fact, UC Davis published that they have just come up with a rapid test that could detect both the flu and COVID-19 in one nasopharyngeal test. This makes it the most convenient method, but it’s more expensive; making this harder to upscale for mass testing). It also requires more supplies, and puts health care workers in close contact with infected individuals. Saliva tests would be a lower cost, but there was uncertainty in its accuracy. The Scientist highlights three main experiments that help better our understanding of saliva testing.

The first experiment was led by Yale epidemiologist, Anne Wylie. Wylie and her colleagues tested the accuracy of swab testing using 70 suspected COVID-19 patients admitted to the Yale-New Haven Hospital. They found that saliva samples contained more copies of the SARS-CoV-2 than swabs. The group concluded by saying that they see potential in the saliva swab; however, this was only tested in one controlled area, and the patients at this point were showing symptoms.

The second experiment, led by Mathieu Natcher, took place throughout the French Guiana. There were 776 participants ranging from (wealthier) villages, forests, and more poor neighborhoods. Natcher discovered that the SARS-CoV-2 virus was still present within saliva for a long period of time, despite climbing temperatures, which makes this idea for situations where testing needs to happen in areas where temperature can’t be regulated. The one downside noticed during this experiment was that saliva testing was less sensitive than nasopharyngeal swabs, which means that it can be harder to pick up the bacteria, if there is less in their system. Therefore, saliva testing may not always be as efficient for asymptomatic carriers or people who just became infected.

Pharmacologist at the University of South Carolina helped develop the school’s saliva test, and reported her findings after school came back in session. She noticed that although saliva may be less sensitive, the repetition of testing these students makes it more possible to catch the infection shortly after it comes. She also ran an experiment on two students living together: one of which had a confirmed COVID-19 diagnosis, and the other was at risk. Both students got tested daily using the nasopharyngeal and saliva swabs for the two weeks. She found that the amount of the virus detected in both tests for the positive patient were the same, leading her to conclude that saliva and nasopharyngeal tests both have the same sensitivity. Banister also explained that not the lower sensitivity coming from the saliva test in comparison to the nasopharyngeal test could be due to the fact that saliva turns over quickly in the mouth, while the nasal cavity and lungs hold the virus for longer. Banister also said because of this saliva tests might be a more accurate depiction of who is actually infectious, because the virus stays in the lungs even after the patient is no longer infectious.

We have come a long way since this article was initially posted, and saliva tests have been released to more of the public for a longer period of time. It is interesting to see how these preliminary tests played a role in whether or not to further release saliva tests.

So we beat SARS and MERS… Why haven’t we beat COVID-19?

Many people, especially those who were alive during the SARS and MERS outbreak, may be wondering why we haven’t beat the Coronavirus yet if we beat the SARS and MERS outbreaks, two very similar viruses to COVID-19 or Sars-CoV2. This is a question many people have been facing everyday as the Coronavirus disease has caused a shift in the entire globe’s day to day life unlike SARS and MERS. 

SARS, MERS, and COVID-19 are all part of the coronavirus family. “Coronaviruses are a large family of enveloped RNA viruses” that can be found in a variety of bat and bird species. While this makes the three viruses similar, they all have specific differences causing unique results in terms of outbreaks and how the specific viruses have spread. What is so powerful or different about the coronavirus causing COVID? 

First of all, let’s talk about how viruses hijack our bodies. Viruses are microscopic parasites, much smaller than bacteria, that contain key elements that make up all living things such as nucleic acids and DNA or RNA, but are unable to replicate and access this information encoded in their nucleic acids, meaning they cannot self replicate. In order to reproduce, they rely on the genetic material of host cells (our own cells). As we talked about in class, viruses are able to bind to our cell surface receptors and trick our cells to “let them in”. The viruses are then able to hijack our cells by releasing their genomes, or that information they couldn’t previously access, resulting in our cell making millions of copies of that genome to spread throughout the body in order to infect other cells and / or other human hosts. This is how all three of the coronaviruses hijacked our bodies and communities. Let’s hear what happened once this step occured.

SARS stands for Severe Acute Respiratory Syndrome. The SARS outbreak began in the Guangdong province in China in 2002. The coronavirus that caused SARS, called SARS-CoV, was likely spread to humans, in the China wet markets, from civets or other animals who acquired the virus from horseshoe bats. The World Health Organization (WHO) issued a global alert after identifying an atypical pneumonia spreading amongst hospital staff and later names the virus SARS based on the symptoms people began to express. The epidemic was controlled on July 5th 2003 and only four cases have been reported since, 3 of which being in a lab setting dealing with the specific coronavirus. The reason why SARS was able to be contained so quickly was due to the fact that one could only spread the virus if he/she had symptoms and if one expressed symptoms it was easy to self isolate, therefore not spreading the virus to others. In addition, SARS has a fatality rate of 9.6% meaning a good number of people who contracted SARS were likely to pass on and therefore not pass on the virus to others. 

MERS stands for Middle Eastern Respiratory Syndrome. As we learned in class, viruses are no longer named by their place of origin, but this was not the case in 2012 during the outbreak of MERS. Similar to SARS, MERS is a zoonotic virus, meaning MERS was passed from an animal, in this case a camel who contracted the virus from bat once again, to humans in Saudi Arabia. Although 27 countries have reported cases of MERS since 2012, transmission among people is rare and MERS has a fatality rate of 34.3%, making it even more deadly than SARS and therefore making it even harder to spread. 

The first case of COVID-19 or SARS-CoV-2 was reported in Wuhan China in December 2019. By the end of January 2020 the WHO had declared a public health emergency of international concern and by the beginning of February the WHO had declared a pandemic. So what makes the coronavirus disease so much worse than the other ones? How did COVID-19 spread so quickly and to the entire globe? And why are our daily lives changed forever or at least until we can get a handle on the virus?

First of all, the COVID-19 causing coronavirus SARS-CoV-2 is very similar to SARS-CoV, but with very unique and important differences. What we have all learned about SARS-CoV-2 is that you don’t need to be experiencing symptoms to transmit the virus. This is very different from SARS-CoV where you needed to have symptoms in order to transmit the virus. Also, while the transmission rates are lower for MERS and SARS because the fatality rates are higher, in the case of COVID-19, the fatality rate is approximately 1-3%, meaning more people are surviving COVID-19 making it easier for this virus to survive and pass on to other people that it has yet to infect. In addition, as we talked about in class, we have evidence that “viruses can naturally mutate to mimic host biology so as to ensure successful viral propagation” and as a result “a host of high frequency mutations have resulted in a least 5 differentiated SARS-CoV-2 strains to date” making it even harder to develop a successful vaccine to target and eliminate the coronavirus disease.   

So, will we ever be able to put a stop to the spread of the coronavirus disease and therefore the pandemic? The answer is yes, but we first need to figure out how to stop the spread of the virus. The truth about COVID-19 is that unfortunately, as stated above, it is much easier to transmit than SARS and MERS, and COVID-19 has been able to get on planes and travel the world unlike the previous coronaviruses. While it is easier to transmit it is also more survivable than the other coronaviruses that have impacted our communities thus far.

Can your common cold help you beat vicious COVID-19?

Season colds are quite common, and while they are inconvenient and make us feel icky, they may be our advantage for our battle with COVID-19. 

To start off, when reading this article, I noticed that the author used the term “coronavirus” more casually. He referred to a “coronavirus” as a common cold, which of course left me confused. So I dug a little deeper…

Here’s a fun fact that I learned from this:

Many of us having been thinking that COVID-19 is the same as what we call the “coronavirus.” After reading an article differentiating the difference between the terms, I found that the term coronavirus is actually the broad term to describe a whole range of viruses. SARS-CoV-2 is the specific virus that causes only COVID-19 and is causes what doctors call a respiratory tract infection.

Basic biology tells us that while there are many cells that make up our body, they are all interconnected. A pathogen, like the SARS-CoV-2 virus, is an enemy to the cell. We learned about how things enter the cell in biology: the pathogen enters the cell, travels through the cytoplasm, and enters the nucleus. Because the virus has genes, it is able to rapidly produce copies of itself to infect the other cells. And of course, we know how scary these infected cells are when they start spreading to the lives around us given our situation with a global pandemic.

What we now know is that the SARS-CoV-2 virus, our “bad guy,” can actually induce memory B cells. These memory B cells survive for quite a long time; they are important in identifying pathogens, and creating antibodies to destroy such pathogens. So when we got sick during the winter last year, chances are these memory B cells fought them off. The key part of the memory B cell in our fight against COVID-19 is the cell’s ability to remember the antibodies it created from past illness for the future.

What does this mean?

The belief is that anyone infected by COVID-19 already has the memory B cells from past common colds to fight the virus off.  Taking a further step, it is believed that since everyone already has the memory B cells, anyone who has had COVID-19 in the past is unlikely to get it a second time. If the SARS-CoV-2 virus were to enter your body a second time (which is likely considering the virus has not gone away and is literally all around us), our bodies would be prepared with former knowledge of the antibodies used to fight and win this time.

A study performed at the University of Rochester Medical Center is the first to demonstrate how this may be so.

Mark Sangters, Ph.D., is a research professor of Microbiology and Immunology at URMC; he has backed up his findings by comparing different blood samples. When looking at 26 blood samples of recovering moderate COVID- 19 patients (people who have had it for their first time now), it seems that many of them had a pre-existing pool of memory B cells that could recognize the SARS-CoV-2 virus and rapidly produce antibodies to destroy it. He also studied 21 blood samples of healthy donors, collected years before COVID-10 existed. What he found was that these B cells and antibodies were also already present.

When we are sick with a common cold, our antibodies are created by memory B cells to attack the Spike protein. This protein is what helps viruses infect our cells. What Sangters noticed, is that although each Spike protein is different for each illness, the S2 portion of the Spike protein is the same throughout all sickness. Our antigens can not differentiate the parts of the S2 subunit, so they attack the Spike protein regardless. This was his final piece in his conclusion that our common colds that caused our memory B cells to make antibodies, could be used to fight against COVID-19.

The Long Road Ahead:

My concern with this article is that this is the biggest issue we face with COVID-19 is patient outcome. As of right now, there is no way to fully prevent everyone from COVID-19 because it is still all around us. The issue the world is facing, is how to treat those who have already contracted the virus. This information just simply is not enough to help. How will these memory B cells help those who are currently sick? The answer: Scientists are unsure. There is still the uncertainty of the future vaccine and study of these memory B cells for a possibility of milder symptoms or shorter length of illness from COVID-19.

 

Despite all of this concern, this is still a step in the right direction. Any information about this terrorizing virus is still helpful given how little we know about COVID-19. If we were to expand more on this information, we could save the lives of those around the world!

 

 

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