BioQuakes

AP Biology class blog for discussing current research in Biology

Tag: Virus (Page 2 of 2)

A Super Self-Assembling Vaccine Booster to the Rescue!

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On October 15, 2020

In Student Post

Vaccines: a topic on the forefront of the minds of scientists, researchers, and the general public. With the novel coronavirus and fiery online debates led by coined “anti-vaxers” about the effectiveness and dangers of vaccination, biologists are racing to discover more methods to improve these life-saving injections. An essential component of many vaccines, including ones used to prevent cervical cancer, influenza, and hepatitis is the adjuvant: a “booster” ingredient that helps the vaccine create a longer-lasting, stronger immune response in the patient. Recently, a team of scientists in Japan discovered a new adjuvant—a molecule called cholicamade—that was equally as effective in treating influenza in mice as its predecessor, Alum. The emergence of this new ingredient is exciting, but the real novelty lies in the process these biologists used in discovering chloicamade: looking at molecules that could self-assemble.

What is the self-assembly of a molecule, or multiple molecules? Multiple molecules are said to self-assemble if they are able to organize into a defined pattern without the intervention of an external source, such as heat. These molecules will form ionic or hydrogen bonds with each other, similar to the joining of water molecules, since they don’t share electrons equally, as we learned in AP Biology. Identifying molecular structures that self-assemble is a common practice in materials science, but not often used in researching adjuvants. This team of biologists and chemists hypothesized that utilizing molecules that form in this fashion for disease treatments may be effective because pathogens in viruses also form through self-assembly. They wondered if a similar method in structural formation between a treatment and its virus would trigger a similar immune response.  

And it did! Cholicamide self-assembles through ionic bonds to create a structure which looks almost identical to a virus, triggering the same immune system cells to react. The structure of the molecule

An image of the influenza virus, which the treatment would attempt to replicate.

lends itself to the formation of ionic bonds because of its inherent polarity and electronegative elements. The molecule can be injected directly into vacuoles that will connect it with the specialized receptors which will trigger the appropriate immune response. A vacuole’s ability to store water and other nutrients (as we learned in AP Biology) as well as transport these nutrients throughout an animal cell is vital in ensuring the treatment binds to the correct receptors. Uesugi, a leading scientist in the study, hopes “the new approach paves the way for discovering and designing self-assembling small molecule adjuvants against pathogens, including emerging viruses.” What do you think about this new method in discovering vaccine treatments? How do you see the future of vaccines changing as more adjuvants are researched? I believe there is nothing more exciting than not only confirming the effectiveness of a new treatment, but also conducting the research with a new approach or perspective.

 

 

 

New anti-CRISPR Proteins Serving as Impediments to this Miraculous System.

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On March 17, 2019

In Student Post

CRISPR-Cas9 systems are bacterial immune systems that specifically target genomic sequences that in turn can enable the bacterium to fight off infecting phages. CRISPR stands for “clusters of regularly interspaced short palindromic repeats” and was  first demonstrated experimentally by Rodolphe Barrangou and a team of researchers at Danisco. Cas9 is a protein enzyme that is capable of cutting strands of DNA, associated with the specialized stretches of CRISPR DNA.

Diagram of the CRISPR prokaryotic antiviral defense mechanism.

Recently, a blockage to the systems was found by researchers which are essentially anti-CRISPR proteins. Before, research on these proteins had only showed that they can be used to reduce errors in certain genome editing. But now, according to Ruben Vazquez Uribe, Postdoc at the Novo Nordisk Foundation Center for Biosustainability (DTU), “We used a different approach that focused on anti-CRISPR functional activity rather than DNA sequence similarity. This approach enabled us to find anti-CRISPRs in bacteria that can’t necessarily be cultured or infected with phages. And the results are really exciting.” These genes were able to be discovered by DNA from four human faecal samples, two soil samples, one cow faecal sample and one pig faecal sample into a bacterial sample. In doing so, cells with anti-CRISPR genes would become resistant to an antibiotic while those without it would simply die. Further studies found 11 DNA fragments that stood against Cas9 and through this, researchers were ultimately able to identify 4 new anti-CRIPRS that “are present in bacteria found in multiple environments, for instance in bacteria living in insects’ gut, seawater and food,”  with each having different traits and properties.  “Today, most researchers using CRISPR-Cas9 have difficulties controlling the system and off-target activity. Therefore, anti-CRISPR systems are very important, because you want to be able to turn your system on and off to test the activity. Therefore, these new proteins could become very useful,” says Morten Sommer, Scientific Director and Professor at the Novo Nordisk Foundation Center for Biosustainability (DTU). Only time will tell what new, cool, and exciting discoveries will be made concerning this groundbreaking system! What else have you guys heard? Comment below!

Message Intercepted – Commence attack on bacteria!

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On January 14, 2019

In Student Post

Tevenphage – Photo credit to Wikimedia Commons

While experimenting, a group of scientists noticed that a A virus, VP882, was able to intercept and read the chemical messages between the bacteria to determine when was the best time to strike. Cholera bacteria communicate through molecular signals, a phenomenon known as quorum sensing, to check their population number.  The signal in question is called DPO.  VP 882, a subcategory of bacteria’s natural predator, the bacteriophage, waits for the bacteria to multiply and is able to check for the DPO.  Once there is enough bacteria, in the experiment’s case they observed cholera, the virus multiples and consumes the bacteria like an all-you-can-eat buffet. The scientists tested this by introducing DPO to a mixture of the virus and bacteria not producing DPO and found that that the bacteria was in fact being killed.

The great part about VP 882 is it’s shared characteristic with a plasmid, a ring of DNA that floats around the cell. This makes it easier to possibly genetically engineer the virus so that it will consume other types of bacteria. This entails it can be genetically altered to defeat other harmful bacterial infections, such as salmonella.

Ti plasmid – Photo credit to Wikimedia Commons

Current phage therapy is flawed because phages can only target a single type of bacteria, but infections can contain several types of different bacteria.  Patients then need a “cocktail” with a variety of phages, which is a difficult due to the amount of needed testing in order to get approved for usage.  With the engineering capability of using a single type of bacteria killer and the ability to turn it to kill bacteria, phage therapy might be able to advance leaps and bounds.

As humans’ storage of effective antibiotics depletes, time is ticking to find new ways to fight bacterial infections.  Are bacteriophages and bacteria-killing viruses like VP 882, the answers?

Learn From the Greeks: The “Trojan Horse” Method to Cure Ebola

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On October 16, 2017

In Student Post

The study to find a cure for the dangerous virus Ebola has resulted in a promising new find: a new strategy has shown positive results.  This new technique involves the placement of antibodies into the cell with the Ebola virus and then it binds to the NPC1 protein before the virus can, essentially rendering it useless.

To understand exactly how these special rainbow unicorn antibodies work, it is essential if we know how the Ebola virus spreads.  The different strains of the Ebola virus (Sudan, Zaire, Tai Forest, Bundibugyo, and Reston) are genetically a little different but they do the same thing.  The virus enters the cell through glycoproteins and gets engulfed into a lysosome. Once inside a lysosome, the virus transforms into a new state where it can bind to a human protein called NPC1.  Once bound to this protein the virus can eject its information into the cytoplasm of the cell and spread.

The solution lies in the binding of the special antibody.  The antibody ZMapp can effectively destroy the Ebola virus, but it is only effective on the Zaire strain. The other strains of Ebola are a little genetically different that the ZMapp antibody does not detect the other strains. Thus, a different approach is required to fight the virus.  The virus can be stopped if an antibody is able to enter the cell with the virus and either bind to the NPC1 protein before the virus does or bind to the virus to disable its ability to bind to anything else.

When the Ebola virus is in a cell’s lysosome it structurally alters itself to enable it to bind with the NPC1, and an advantage that scientists have discovered is that between the different strains of Ebola virus, the transformed versions are very similar, thus an antibody can be made that can bind to all of the different strains.  The problem with this, however, is that antibodies cannot enter the cell the same way that viruses can.

Ebola Virus

The solution that the researchers came up with stems back to the Trojan Horse story from Ancient Greece. The researchers added an extra arm to the antibody, enabling it to latch onto the virus and hitch a ride with it into the lysosome.  Once in the lysosome with the virus, the virus alters and the antibody can then bind again and disable the virus.  This method can potentially be a cure for all of the strains of the Ebola virus, causing an end to a very dangerous virus.

A Cure for Zika? Scientists successfully test a DNA-based Zika Vaccine

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On October 16, 2017

In Student Post

The Zika virus, widely known for its 2015 Latin and North America outbreak, is a mosquito-borne and transmitted virus that develops neurological complications and birth-defects in those infected. The Zika virus is able to be transmitted from a pregnant woman to her fetus, causing microcephaly– abnormal development of the brain. Currently, there exists no vaccine that would fully treat the virus, however, a solution may be in the works.

(Photo from Wikipedia Commons)

David B. Weiner, Ph.D., an executive vice president of The Wistar Institute and a developer of the Zika vaccine notes that, “Synthetic DNA vaccines are an ideal approach for emerging infectious diseases like Zika”. Synthetic DNA vaccines are vaccines with genetically engineered DNA. They work in the same way as regular vaccines, inciting cells to produce specific antigens for immunological responses. Synthetic DNA vaccines can also have potential benefits over traditional vaccines, including a higher predictability, stability, and ability to be manufactured and distributed safely and rapidly.

The current Zika vaccine in development, GLS-5700, houses multiple strains of genes with DNA instructions that tell a hosts’ cells how to react and fight off a Zika virus antigen. In late 2016, researchers tested the vaccine on 40 participants. Two groups of 20 received different does of the vaccine at zero, four, and twelve week intervals. At the end of the experiment, researchers found that all participants had developed Zika-specific antibodies and 80 percent of the participants developed neutralizing antibodies against the Zika virus.

Zika 2015-2016 Outbreak (Photo from Wikipedia Commons)

Although rare in the United States, Zika continues to threaten millions living in South and Central America. Despite being in its last stages of development, GLS-5700 and other Synthetic DNA vaccines are still prohibited from being used in the United States- although this may change with the introduction of the Zika vaccine. The future of Synthetic DNA vaccines and viral disease prevention lies in the success of the GLS-5700.

 

 

 

 

XRN1: The Virus Hitman

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On October 12, 2016

In Student Post

When I think of the words killer and assassin, my mind drifts to shady men in all black equipped with sniper rifles. However, recent research conducted by the University of Idaho and the University of Colorado Boulder has indicated that I should expand that mental list to include XRN1, a gene in saccharomyces cerevisiae which, according to a recent study, kills viruses within the yeast. Upon stumbling onto this subject, I was intrigued because it was a fairly simple procedure that led to a huge discovery. To grasp the significance of such a discovery, one must understand it on a molecular level. XRN1’s duty in yeasts is to create a protein which breaks down old RNA. The image below shows the generic process of the creation of a new protein through gene regulation.

Wikipedia- Regulation of Gene Expression

Wikipedia- Regulation of Gene Expression

Yeasts also contain viral RNA since practically all yeasts are infected by viruses. When scientists removed XRN1 from the yeasts, the viruses within yeasts replicated much faster, and when they expressed high amounts of XRN1, the virus was completely eradicated. This is because the XRN1 gene was inadvertently breaking down the viral RNA, mistakenly taking it for the yeast’s RNA. Scientists continued the research by using XRN1 from other saccharomyces yeast species. The virus continued replicating rapidly but the XRN1 did continue its job of breaking down the yeast’s RNA. This shows that the XRN1 from each yeast species evolves to attack the specific viruses that occur in its host while still maintaining their basic role as the RNA eaters. Scientists are hopeful about this study’s human health implications. Viruses such as Polio and Hepatitis C work by degrading XRN1 and not allowing it to break down RNA, respectively. Dengue Fever also occurs when XRN1 is unable to perform its function of RNA breakdown. These studies on Dengue Fever and Hepatitis C elaborate on the implications of XRN1 not breaking down RNA. Scientists hope that this discovery could lead to the triumph of XRN1 over these viruses. Could this really be the discovery that leads to the first ever Hepatitis C vaccine? Do you think that XRN1’s success against virus in yeasts guarantees eventual success against viruses in humans?

 

Original Article: http://phys.org/news/2016-10-yeast-gene-rapidly-evolves-viruses.html

 

HIV Resistance to CRISPR/Cas9

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On May 1, 2016

In Student Post

A recent study, described in the Science Daily, shows that researches who used the CRISPR/Cas9 to mutate HIV-1 within cellular DNA found that the mutation led to unexpected resistance.

When HIV enters a cell, its RNA genome is converted into DNA and becomes intertwined with the cellular DNA. So the goal for the CRISPR/Cas9 is to target a DNA sequence and cleave viral DNA. The problem is HIV is too good at surviving and thriving despite new mutations, making it more difficult for the CRISPR/CAS9 to target.

PDB_1wj9_EBI

Photo Source

Chen Liang, Senior Investigator at the Lady Davis Institute at the Jewish General Hospital, noted that when they sequenced the viral RNA of escaped HIV, they were surprised to see that majority of the mutations the virus had, instead of resulting from the errors of viral reverse transcriptase, were rather introduced by the cellular non-homologous end joining machinery when repairing the broken DNA.

The mutations to the sequences caused by the HIV were unrecognizable to the Cas9. Thus the resistant viruses just continued to replicate.

This study serves as a cautionary tale for scientists hoping to apply CRISPR/Cas9 as an antiviral. Liang does not believe these efforts are useless, however, as he is hopeful about strategies that could overcome this roadblock. One such strategy would be to target multiple sites with CRISPR/Cas9 or use other enzymes besides Cas9. After the solution is identified, the next step will be figuring out ways to deliver the treatment to patients. Liang is confident that CRISPR/Cas9 will open doors for finding a cure for HIV-1 and many other viruses.

More Info:

http://www.genengnews.com/gen-news-highlights/hitting-hiv-with-crispr-cas9-can-arouse-resistance/81252590/

http://www.techtimes.com/articles/148378/20160409/crispr-cas9-gene-editing-is-not-good-enough-to-beat-hiv-whats-next-in-humanitys-fight-against-the-deadly-disease.htm

 

 

This new tropical virus is not as fun as it’s name sounds!!!

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On February 29, 2016

In Student Post

Although it may be fun to say, the Zika Virus is no laughing matter.

16735-close-up-of-a-mosquito-feeding-on-blood-pv

According to the U.S. Centers for Disease Control and Prevention the number of Zika Virus infections has increased to 147 in recent months (only 107 of which are from international travelers from Zika-infected areas). Moreover 117 more cases of Zika were reported from Puerto Rico after the CDC released those aforementioned numbers. The CDC urges that people refrain from traveling to highly infected areas like Puerto Rico and especially Brazil for the 2016 Summer Olympics.

The 2016 Olympics in Rio de Janero, Brazil is a hotspot for Zika infection through mosquito bites

The 2016 Olympics in Rio de Janero, Brazil is a hotspot for Zika infection through mosquito bites

 

Zika is spread through the bite of an infected female mosquito (typically of the Aedis Aegipty type) and 80% of the infected showed a variety of the following symptoms: mild fever, skin rash around area of bite and other, conjunctivitis (pink eye), muscle and joint pain that last for approximately 1 week, and fatigue.

 

Now you may be asking yourself, “What’s so dangerous about a virus that sounds like it should be a Pokémon? People get over viruses every day?” Well the answer is not with Zika itself, but rather with what Zika causes.

 

Several studies have emerged that claim Zika is directly connected to Guillain-Barre Syndrome and Microcephaly. Additionally, the PAHO (Pan American Health Organization) claims there is no evidence that Zika can cause death, but there have been several reports of it worsening pre-existing medical conditions.

CDC_map_of_Zika_virus_distribution_as_of_15_January_2016

Areas of Zika Virus infection and density of cases (the darker the purple the more amounts of cases in that area)

Guillain-Barre Syndrome – an extremely rare disorder in which your body’s immune system attacks the nervous system, systematically destroying it over a long period of time. Although weakness and tingling to extremities are first symptoms, they can quickly spread eventually leading to full-body paralysis. Most people with the rare disease must be immediately hospitalized for rigorous treatment.

 

Microcephaly – a rare neurological condition in which an infant’s head is significantly smaller than average. Most often it can be detected at birth and sometimes avoided with late-stage abortions but recent U.S. laws have prevented such actions. Microcephaly results in abnormally low brain function and development (not growing enough in the womb and not developing at a normal pace after birth.) Children with Microcephaly have severe developmental issues and there is no treatment or cure.

 

Microcephaly can be caused by Zika if a woman contracts the virus in the first and second trimester of the pregnancy. 9 cases of pregnant women contracting Zika have been recorded and of those 9 cases, two women had miscarriages, two women terminated their pregnancies, one woman had a baby with very severe Microcephaly, and most other women contracted the virus in the late stages of the pregnancy and had generally healthy babies

 

In conclusion, if you are a pregnant woman try not to travel to exotic and/or tropical areas where Zika-infected mosquitos usually live.

 

Original Article: http://news.yahoo.com/factbox-why-zika-virus-causing-alarm-202231278.html;_ylt=AwrC1jHwztFW5m0AGIHQtDMD;_ylu=X3oDMTBydWNmY2MwBGNvbG8DYmYxBHBvcwM0BHZ0aWQDBHNlYwNzcg–

Do Viruses Make Us Smarter?

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On January 18, 2015

In Student Post

5284032560_4812d29f9f_o

Sanofi Pasteur

A study conducted at the Lund University shows that “inherited viruses” that are millions of years old play an important role in building up the complex networks that characterize the human brain.” It is well known that retroviruses are make up about five percent of our DNA. Research under Johan Jakobsson indicate that retroviruses may play a critical role in the basic functions of the brain, “in the regulation of which genes are to be expressed, and when.”

Studies of neural stem cells show that these cells use a particular molecular mechanism to control the activation processes of the retroviruses. Findings have shown to have increasingly gained control in our cellular machinery. Because tumors are unable to form in nerve cells, different from other teachers, viruses are activated specifically in the brain. The results open up potential for new research paths concerning brain diseases linked to genetic factors.

“I believe that this can lead to new, exciting studies on the diseases of the brain. Currently, when we look for genetic factors linked to various diseases, we usually look for the genes we are familiar with, which make up a mere two per cent of the genome. Now we are opening up the possibility of looking at a much larger part of the genetic material which was previously considered unimportant. The image of the brain becomes more complex, but the area in which to search for errors linked to diseases with a genetic component, such as neurodegenerative diseases, psychiatric illness and brain tumors, also increases”.

Original Article: http://www.biologynews.net/archives/2015/01/12/do_viruses_make_us_smarter.html

For More Info:

http://www.sciencedaily.com/releases/2015/01/150112093129.htm

The Buzzing Battle of the Bees

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On January 17, 2015

In Student Post

Bee

http://commons.wikimedia.org/wiki/File:Bees_on_sunflower.JPG

 

There is a species of bees called “commercial” bees. These bees are kept by beekeepers to pollinate crops such as tomatoes, sweet peppers, and oilseed. This population of managed bees is coming down with “fast evolving viruses”, according to the University of Exeter in Science Daily News.

Then there are “wild” bees, free to fly around, not employed by beekeepers. The viruses that the commercial bees have are starting to spread to the wild bee population. Currently, researchers are “calling for new measures” to protect the wild pollinators, and confine the commercial, diseased population. In the article, Dr. Lena Wilfert said this can be controlled by beekeepers keeping a vigil eye and monitoring the commercial bees they own. It is their “responsibility” to do so. Also, interesingly enough, the international transport of these commercial bees must have more checks and security. They must be screened better, in order to get a better sense of how many have a disease, so they know not to set any of the commercial bees free into the wild.

The major cause of the spread is the Varroa mite. This spreads viruses, such as the Deformed Wing Virus, and may increase the power of the viral spread. It significantly weakens bees, causing their RNA to deteriorate. The article says that it has been “identified as an emerging disease in pollinators,” and there is a connection between wild bumblebees who have it, and commercial honeybees.

The poor management of the commercial bee community is the cause of this horrible break out of diseases among innocent wild bees. In the future, researchers plan to investigate which species of commercial bees are the major cause of the breakout and spread. The wild bee population is extremely important for our environment, and beekeepers need to realize that, and make sure their bee farm does not spread disastrous diseases.

 

*Additional information is found through the last two hyperlinks.*

*Original article is the first hyperlink.*

The Continued Spread of Ebola

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On October 19, 2014

In Student Post

 

Ebola_virus_em

The most recent epidemic that is spreading through Africa is Ebola. It has taken the lives of over a thousand people, but it could get much worse. Without proper isolation and treatment of the infection scientists predict the number of infected individuals could increase to more than 20,000 in just six weeks. Some scientists are even predicting more than a million deaths due to Ebola if  treatment and containment is not improved. Ebola is generally transmitted from animals to humans, who then pass the virus t each other by contact. Symptoms generally include fever, fatigue, muscle pain, headaches and a sore throat, which is then followed by vomiting, diarrhoea, rash, and finally impaired kidney and liver function. The fatality rage for this contagion is about 70%. As of right now there is no vaccine for this virus, and the best way to stop the spread of it is to simply isolate those experiencing symptoms. This virus is currently being closely monitored as it is unknown whether the situation in Africa will get worse, and begin to spread to other countries, infecting people by the thousands. Hopefully scientists are able to discover a vaccine that will halt the spread of this deadly virus, saving the lives of thousands of individuals

The Ebola Epidemic: When Will it End?

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On September 25, 2014

In Student Post

Ebola Virus

The Ebola epidemic in West Africa has captivated international audiences the last few weeks.  Ebola Virus Disease is an often fatal disease which is systemic meaning it attacks all organs and tissue in the body. It can be spread through any human to human contact, making this disease highly contagious. The countries of Liberia, Sierra Leone and Guinea have been heavily affected by this disease. On tuesday September 23th the Center for Disease Control (CDC) based in Atlanta Georgia released new projections on the Ebola epidemic in Africa based on computer modeling.  The CDC released a best-case scenario being that if proper measures are taken the disease could be eradicated by January 2nd and a worse-case scenario that if disease is left unmonitored and continues as is, there will be approximately 1.4 million cases by January 2nd.   Doctor Thomas R. Frieden, the director of the Ebola epidemic, has stated that since the data was received in August conditions have improved slightly due to increased aid to the affected regions. Another report was released by the World Health Organization (WHO) which stated more conservative figures but also acknowledged that there could possibly be more due to unreported cases. The WHO report brings about the idea that the epidemic may not end and the Ebola virus will perpetuate in West Africa. It is obvious to health officials, such as Dr. Jack Chow, that even in a medium case scenario the amount of hospital beds and aid are rapidly being surpassed by the number of cases. The CDC does acknowledge this impending lack of bed and isolation unit crisis. One solution to this problem is to educate citizens on home care and send home care packages to support this movement.  Although some are dubious, Frieden states that home care had been effective in the smallpox crisis in the 1960s in Africa.  In addition to homecare, Doctor D. A. Henderson explains that funds and food play a huge roll in the containment and elimination of disease because when you give victims money and food there is no need for them to beg or go out to the market for food where they might encounter other human contact. How should this epidemic be handled? Is homecare an effective solution? Where should money be allocated, homecare or hospital expansion?

 

Link to Article:

http://www.nytimes.com/2014/09/24/health/ebola-cases-could-reach-14-million-in-4-months-cdc-estimates.html?ref=health&_r=1

 

Protein Structure May Lead to Cure for Ebola

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On September 21, 2014

In Student Post

For those who haven’t been keeping up with the latest in viral outbreaks, Ebola has been spreading throughout West Africa and has already taken the lives of 2,600 people since the outbreak in March 2014.  According to the World Health Organization , there are currently no certified vaccines or treatments for Ebola but a new breakthrough may have answers to developing a cure or vaccine for the deadly disease

Scientists at the University of Virginia have gotten their hands on a crystalized structure of the Ebola Nucleoprotein C-Terminal domain, which is an important protein used in replicating the virus.  The tertiary fold of the C-terminal is “unique in the RNA virus world,” claims structural biologist Dr. Zygmunt Derewenda, and this unique fold could ultimately lead to the foundation of drugs to prevent further infections.

The team was able to produce the protein by using E Coli as the protein factory.  So far, the protein demonstrates traits that are extremely unique and unlike other known proteins.  Evidence thus far has shown that the viral nucleoapsid is self assembled by the domain.  Insights and new research that the UVA team is conducting is paving the way to an Ebola anti-viral drug.

 

Ebola Virus Particles

 

Osmosis Jones: Fact vs. Fiction

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On March 10, 2013

In Student Post

 

The Cells of the Immune System
Photo from: http://commons.wikimedia.org/wiki/File:Innate_Immune_cells.jpg

Osmosis Jones is the story of a white blood cell police officer, Ozzy, who teams up with a cold pill, Drix, to save Frank from a deadly virus. Of course being a children’s movie Osmosis Jones isn’t a completely accurate depiction of the human immune system, or body in general, but just how accurate is it?

In the movie the major conflict arises when Frank, the human, eats an unsanitary egg. On this egg lives the virus, Thrax, who is a deadly pathogen. So far the movie checks out. In the human immune system the first line of defense are barriers between the inside of the body and the outside world. Some of these barriers include the skin, mucus membranes, tears, saliva, sweat and stomach acid. In the movie the virus does penetrate one of these barriers, in this case the mouth, to enter the body. This is accurate to how a virus may enter the human body.

After this the movie becomes less and less accurate to how the human immune system functions. Although there is detection of a pathogen the only response Frank’s immune system has in the movie is through the use of the police force, the white blood cells. This is completely inaccurate to how the human body fights off a pathogen. When the body detects a pathogen (virus or bacteria) mast cells release histamines to dilate the blood vessels (this is never shown in the movie, especially because the blood vessels are shown as highways, but thats another matter altogether). The next step in the immune response is macrophages come and engulf infected and dead cells and they release cytokines that attract other immune cells to the area. Neutrophils and natural killer cells then kill the infected cells. The closest thing to this second line of defense is the police force and their communication. They have radios and ways to communicate to call for backup, although it is extremely inaccurate to the way the immune system really functions.

The third line of defense that the Human body uses is specific defense. This includes B and T cells and the steps taken to target the pathogen specifically and the infected cells. Through the processes of Cell-mediated response and Antibody-mediated response the immune system targets the infection and destroys it. Both of these processes are not depicted in the movie in any form. This along with the ending (don’t worry I won’t spoil it) are both inaccurate to anything that could happen in the human body.

So Osmosis Jones isn’t the most scientifically accurate movie of all time, but that doesn’t stop it from making a great movie. The inaccuracies in the film can be excused by the fact that it is a children’s movie and not a new theory about the immune system. I mean how many kids would want to sit though a movie that was 100% accurate? You would lose all of the car chases, the drama, the suspense, the mucus filled dams, and the explosions. Overall I really enjoy Osmosis Jones, although I don’t recommend using it to study for your next science test.

 

 

Protein Might Help Fight Deadly Diseases

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On March 10, 2013

In Student Post

The enzyme “Cholesterol-25-Hydroxylase,” or CH25H, might help fight against human viruses such as Rift Valley Fever, Niphah and HIV. CH25H converts cholesterol to an oxysterol called 25HC, which can permeate a cell’s wall to prevent a virus from getting in. The CH25H enzyme is activated by interferon, an anti-viral cell signaling protein produced in the body.  Researchers have known that interferon has been part of the body’s defense mechanism against viruses, though it does not have any antiviral properties itself.

This discovery is revolutionary because other antiviral genes have not been able to be used for treatment of viruses in humans. According to Yang Lui, a student at the David Geffen School of Medicine at UCLA, most antiviral genes are difficult to use in therapy because the genes are difficult for cells to express. However, CH25H is different because it is naturally synthesized.

HIV Replication within a cell

The discovery of CH25H is relevant to the efforts to develop broad antivirals against an increase of emerging pathogens. In a collaboration with Dr. Lee, another UCLA professor, it was discovered that the 25HC produced from CH25H can inhibit HIV growth in vivo. The researchers initially found that 25HC inhibited HIV growth in cultures. When implanted mice with human tissues, the 25HC reduced the HIV in within 7 days and reversed T-Cell depletion caused by the HIV. It was also discovered that 25HC inhibited the growth of other diseases such as Rift Valley Fever Virus and Ebola.

There are still some weaknesses with the study. It’s difficult to deliver 25HC in the large doses needed to fight viruses. Researchers also need to compare 25HC to other antiviral HIV treatments.

Understanding HIV, one protein at a time

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On March 10, 2013

In Student Post

By NIAID/NIH (NIAID Flickr’s photostream) [Public domain], via Wikimedia Commons

In a recent study, scientists at Johns Hopkins University have narrowed down a list of 25 human proteins that HIV viruses target the most. The scientists started by studying the HIV-1virus, which is the most infectious and most common type of HIV. They knew that the virus clings to proteins and membrane as it emerges from an infected human cell in order to disguise itself from the human immune system, but inquired as to whether it was a random process or not. They then searched for types of proteins that they targeted the most, using the HIV-1.

They virus tends to target the CD4+ T cells and microphages which both migrate to sites of inflammation. This makes sense because HIV targets the immune system and  the virus can wait to attack while disguised by these cells. They originally identified 279 proteins that this virus in particular targeted when isolating the HIV-1 with CD4+ T cells, but when they crossed the data from two different cell types, they found that only 25 proteins were shared by viruses from both cell types!

This is an extremely interesting and groundbreaking discovery because of the possibilities behind this discovery. If we can figure out the types of proteins these HIV viruses are hiding behind, we could target and destroy them which could possibly lead to the abolition of HIV.

Is All the Hype Around This Years Flu True, or Is The Government Just Trying To Kill Us?

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On January 10, 2013

In Student Post

In December(2012) 9 polio vaccination workers in Pakistan in were murdered. And just last week 7 men and women that were on their way home from work at a community health center in Pakistan were shot dead.  Do you notice a trend?

Urban legends and conspiracy theories are what provoked people to think that these health workers need to be killed.  Due to various reasons, discussed in this article, people have been lead to believe that there are malicious motives behind their medical acts and patients resist medical treatment in fear of being killed for their organs or being poisoned with a fake vaccine. The illegitimate distrust from the patients can originate because the doctor is foreign(usually Western) or a lot wealthier then the patients.

But there is some justifiable skepticism about these doctors. In an interview Dr. Jehuda Hiss, head of Israel’s main forensic institute, stated that in the 1990’s, body parts were taken from dead bodies(of Israelis, Palestinians, and others) without consent and were transplanted into Israeli soldiers.  Although the Israeli military said they stopped the illegal taking of organs 10 years ago, people still believe that doctors will let their patients die rather then help them because their organs will be beneficial to them. People have been resistant to getting vaccines since the late 1700’s, after the creation of the smallpox vaccine.The fact that a vaccine injection actually puts bacteria or a virus into your body is scary and illegitimate to many. The article mentions a true incidence of doctor with ulterior motives.  “A Pakistani doctor who was hired by the Central Intelligence Agency to give out a hepatitis B vaccine was actually trying to collect DNA samples from bin Laden’s suspected compound to verify his presence.”

Although there are rare cases of these myths holding truth, a doctors medical assistance will almost always be in the patients’ best interest and health. Do you think the government is keeping things from us and our actual doctors appointments are much more then just a check up?

Medical students and staff at Tripler Army Medical Center

Photographer: Army Medicin
Licensing: http://creativecommons.org/licenses/by/2.0/deed.en

 

Main Article: http://www.livescience.com/26108-medical-urban-legends-kill.html

Secondary Articles: http://www.livescience.com/5955-body-part-theft-truth-myth.html and http://www.dovaccinescausethat.com/

Picture: http://www.flickr.com/photos/armymedicine/6382971901/ and http://creativecommons.org/licenses/by/2.0/deed.en

New Deadly Virus Discoved in Africa

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On October 6, 2012

In Student Post

Recently an article was released summarizing the discovery of a new disease in Africa. In 2009 a fifteen year old boy in a small village in the Democratic Republic of the Congo fell ill. The initial symptoms were malaise and a bloody nose, but quickly the boy developed an acute hemorrhagic fever. Within two days of the showing symptoms the boy died. Approximately eleven days later a thirteen year old girl who went to the same school as Patient One developed similar symptoms, and died three days later. At the local health center which both Patients One and Two visited, a thirty-two year old male nurse began to experience identical symptoms. He was moved to the hospital in Boma, Democratic Republic of the Congo, where the doctors drew blood and began to test for known viruses; they found nothing. However, very recently a research team used deep sequencing to determine the pathogen,which they dubbed “Bas-Congo Virus”, and posted their results in the Public Library of Science Journal. It was discovered that the virus belonged to the Rhabdoviridae family, best known for the Rabies virus. Interestingly enough, though, the Bas-Congo virus only shares 34% of the amino acids found in other Rhabdoviruses, meaning that it is very different. The discovery of this virus may end up being of great importance due to the possibility that the virus may return. In any case, we will have one less pathogen on this planet to identity lest there be another, more deadly, outbreak.

Tricky Viruses

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On January 11, 2012

In Student Post

Photo Credit: Foto_di_Signorina Flickr

           Strong viruses, such as HIV, make the body work for them. Researchers in Copenhagen have been studying how these viruses manage to take over the body. The virus takes over one cell and then uses the RNA to influence the DNA, giving the virus complete control over the cell. The RNA of the virus is similar to the RNA of the cell. Therefore, the ribosomes of the cell copy the sequence from the virus instead of the actual RNA. This causes the cell to produce the virus’ proteins.

                The RNA of the virus has what is called a pseudoknot. Pseudoknots are places on the RNA that the ribosomes must decipher before it can move on. The pseudoknot holds the sequence for key destructive proteins of the virus and once the ribosome deciphers it, those proteins are produced. This is how HIV can spread so rapidly in the body and can take such a hold over the host; it doesn’t do any of the work.

Antibodies to the Rescue!

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On December 4, 2011

In Student Post

Photo Credit: RambergMediaImages Flickr

 

 

HIV is an extremely dangerous virus because our own antibodies cannot effectively attack it. HIV uses a coat of sugars to hide itself from our antibodies. Although the body cannot effectively fight HIV, it does its best by making new antibodies to try and attack this powerful virus. These new antibodies attach to different spots on the sugar coating of the virus. It uses the sugar coat to bind to a site on the virus where amino acids are exposed. Then the antibody attacks the virus from that site, disabling it.

 

The discovery of this antibody and the way it binds to the virus is important because it can lead to advances in a cure and a vaccine. It gave scientists key information about binding sites made out of sugars and amino acids. They can use this information, as well as information from other projects and discoveries to make a more effective vaccine. In fact, some recent tests have shown that the antibodies play an important role in the health of someone infected with HIV.

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