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Dear Joseph, Gandalf—a monkey confined to a laboratory at the University of Pittsburgh (Pitt)—was so desperate for affection that he presented his back to passersby and gestured desperately to try to get them to groom it. But he received no affection or warmth—only torment. After a severely stressed monkey caged nearby bit Gandalf's hand down to the tendons, the veterinarian on call refused to examine his injury. Instead, she just prescribed ibuprofen—a woefully inadequate treatment for such a serious wound. He was then forced to undergo an experimental surgery. Three weeks later, he was euthanized and sealed in a biohazard bag after experimenters took tissue samples from his corpse. Today, there are hundreds more monkeys trapped in cages at Pitt, while tens of thousands more languish in other laboratories, experiencing pain and fear as Gandalf did. If you and I don't help them, who will? Please, be one of the 1,000 donors we need to pitch in just $5 or more by April 30 to help support PETA's vital work to end cruel, deadly experiments on animals. PETA's eyewitness observed other monkeys in the laboratory slowly losing their minds: pacing, rocking, and displaying other repetitive behavior often seen in stressed animals held in captivity. Since our investigation, news reports broke that a monkey who may have been infected with a dangerous pathogen escaped from a cage at the same university and that staff allegedly attempted to cover it up—potentially putting animals and humans alike at risk. Powered by committed PETA supporters like you, our work to end experimentation on animals has helped reduce the number of monkeys, rabbits, and other animals suffering each year:
But as long as even a single animal is suffering in a laboratory, we must push forward to end the neglect and abuse—and we can't do it without your support. Our goal is for 1,000 generous supporters to make a donation by midnight on April 30. We're making good progress, but we need you with us, too. Give your gift of $5 or more now and help prevent more animals from suffering in laboratories and cruel experiments! As always, thank you so much for all that you do for animals—every step we take toward a kinder world is only possible with your dedication and compassion. Kind regards, | |||||||||||||||
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Saturday, February 5, 2022
They deliberately infected volunteers with Covid.
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Wednesday, January 19, 2022
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Nelson, |
Last week, we asked you to call on Canada and other global governments to finalize a strong Global Ocean Treaty at the UN this March.
We’re going to be releasing lots of crucial updates about this campaign in the lead-up to the UN meeting set to begin on March 8th—the best way to make sure you’re receiving them is by following Greenpeace on social media. (Also, following us on socials is the best way to guarantee a regular dose of quality penguin content to your timeline.) |
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Tuesday, January 18, 2022
What if TIPS can be converted to work against SARS-CoV-2 and the Omicron variant?
TIPs: Therapeutic Interfering Particles
A New Paradigm for HIV Treatment and Prevention
Therapeutic Interfering Particles, or TIPs, could represent a fundamentally new approach to stopping HIV and other infectious diseases. The theory behind TIPs is this: Since viruses are dynamic—that is, they mutate and spread—our approach to controlling them must also be dynamic. But until now our approach has been static—we develop drugs that do not mutate or spread. As a result, HIV continues to evolve and outwit us, rendering our treatment strategies limited at best—and, at worst, ineffective.
TIPS, however, are designed to both spread and evolve alongside the viruses they attack, including HIV. As a result, TIPs have the potential to dramatically reduce the lethality of HIV and slow its spread, or stop it completely, on a global scale. There is more research to be done, but the promise of TIPs is being diligently pursed as a part of Gladstone’s broader goals to better prevent and treat—and ultimately cure—HIV/AIDS.
What are TIPs?
TIPs are genetically engineered HIV particles that have been stripped of all their harmful material. What’s left is an empty “outer envelope” that has no infectious qualities but is able to piggyback onto HIV, allowing it evolve to and spread with HIV. This empty envelope (or therapeutic particle) interferes with HIV by disrupting the way the virus replicates, thereby eliminating its power to destroy cells.
How do TIPs work?
To understand TIPs, we must understand what makes HIV so effective and so lethal. And that is, HIV inserts itself into the very DNA of our cells—specifically, the white blood cells in our immune system. In doing so, it turns these cells into mini “HIV factories” that busily produce more and more HIV particles. Eventually, the cells die, releasing HIV into the bloodstream where the virus infects and kills yet more cells. This process repeats millions of times, eventually destroying our immune system.
TIPs beat HIV at its own strategy by hijacking the virus. In other words, once inside a cell, TIPs piggyback onto HIV and transform the cell from an “HIV factory” into a “TIPs factory.” Instead of producing HIV, the cell produces more and more interfering particles. Like HIV, these TIPs then spread into other HIV-infected cells, hijacking those factories.
And because TIPs are essentially empty envelopes, they reproduce and spread more quickly than HIV, which is laden with genetic material. Think of a race car zipping alongside an overloaded 18-wheeler truck. Eventually, the roadster (TIPs) overtakes the more sizable HIV and speeds ahead, producing more and more TIPs—and causing HIV production to plummet.
How do TIPs help someone who already has HIV?
Because TIPs interrupt the way HIV reproduces, the amount of HIV virus in an individual person—that is, their viral load—drops considerably. This allows the immune system to remain robust, helping the person stay strong and healthy. This also makes it much more difficult for the virus to spread from person to person, because lower viral loads mean lower transmission rates.
So TIPs serve two absolutely essential functions: they reduce the amount of HIV in an infected individual and make it harder transmit the virus to others.
How could TIPs stop HIV on a global scale?
Remember, TIPs piggyback onto HIV and spread with it. So if an HIV-infected person with TIPs spreads the virus, he or she is also spreading a treatment. In this way, TIPs can spread throughout a population and gradually reduce both the prevalence and virulence of HIV.
Gladstone researchers expect that this approach can reduce the global spread of HIV—including the world’s hardest hit areas, such as sub-Saharan Africa, where HIV infection rates range from 15–30% of the population. For any strategy to work on this scale, it must overcome what epidemiologists call the “universal barriers” to stopping infectious diseases:
Access—getting the drugs and vaccines to the target populations;
Adherence—getting people to stick to the regimen and take their meds;
Resistance—treating viruses that mutate and can become treatment-resistant; and
“Superspreaders”—reaching small groups of individuals who engage in behaviors that are likely to transmit the virus and have a disproportionate impact on the spread of the disease.
Unlike current treatment-and-prevention strategies—including lifesaving antiretroviral medications—TIPs leap over each of these barriers:
Access—TIPs are a single-dose treatment that spread the same way HIV spreads.
Adherence—TIPs’ one-time exposure eliminates the need to adhere to lifelong
drug-treatment regimens.
Resistance—TIPs piggyback onto HIV and evolve with it, undermining HIV’s ability to become treatment-resistant.
“Superspreaders”—Because TIPs spread alongside HIV (i.e., by those sharing needles and/or having unprotected sex with someone who has HIV), they will reach this otherwise difficult-to-identify and treat population, thereby dramatically reducing HIV prevalence.
What is the potential impact of TIPs?
Gladstone scientists project that if just 1% of the population in sub-Saharan Africa were to receive TIPs, the prevalence of HIV in 10 years would drop to less than 10% of the population. In 50 years, the prevalence rate would drop to less than 2% of the population. In short, these game-changing results are vast improvements over even the most optimistic projections for reducing HIV prevalence through antiretroviral medications or an effective vaccine.
What is next for TIPs at Gladstone?
Our researchers are poised to take TIPs from the petri dish, where it so successfully interrupts HIV, into lab animals, the essential next-step in researching both its safety and efficacy. Gladstone investigators are actively seeking funding to advance this research as quickly as possible.
We invite you to get in touch with Gladstone to discuss how you can help support our TIPs research, as part of our goal to improve HIV/AIDS treatment and prevention—and to ultimately cure this disease.
Contact Leor Weinberger, PhD, Director and Bowes Distinguished Professor, at leor.weinberger@gladstone.ucsf.edu.
Monday, January 17, 2022
GENTLE PEOPLE: 
AS OF THIS DATE, MONDAY JANUARY 17, 2022, THE OMICRON VARIANT OF THE SARS-COV- 2 VIRUS IS NOT UNDER CONTROL AND IT CONTINUES TO MAKE PEOPLE SICK! IT ALSO KILLS!
WE NEED ANOTHER VACCINE AIMED SPECIFICALLY AT THE OMICRON VIRUS AND TO WAIT IS TO RISK THE CHANCE OF OMICRON DOING MORE DAMAGE THAN THE ORIGINAL SARS VIRUS. WE KNOW IT SPREADS FASTER AND NOW CANADIAN MEDICAL STATISTICS ARE PROVING IT KILLS!
ROLL UP YOUR SLEEVES BECAUSE WE NEED ANOTHER VACCINE AND WE NEEDED IT YESTERDAY! THE FIRST THREE VACCINES DO CREATE SOME PROTECTION AS THEY WERE CREATED FOR THE SPIKE PROTEINS OF THE ORIGINAL VIRUS. THE PROBLEM IS THE OMICRON VARIANT MAY BE ABLE TO SIDE STEP THE VACCINES. IT IS NOT THE SAME VIRUS AND IT IS EVASIVE AND DANGEROUS AND IT HAS DEVELOPED MANY MORE SPIKES.
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OTTAWA -- Health Canada's chief medical adviser says variant-specific vaccines can be approved faster than the general ones first issued to combat COVID-19, but one targeting the Omicron strain still likely won't be ready in time to help with the latest wave.
Dr. Supriya Sharma said what is really needed are vaccines that can possibly stop more than one variant at a time, including those yet to come.
Omicron became the dominant variant in Canada in just over two weeks, and the Public Health Agency of Canada said Friday it's now believed to be responsible for more than 90 per cent of all COVID-19 cases.
How is the omicron variant different from the delta variant and others?
It has a lot of mutations in its genome. Compared to the original coronavirus, the delta variant has fewer than 20 genetic changes to the gene for the spike protein. The omicron variant has more than 30 genetic changes. It’s almost double.
The more changes there are in the spike protein gene, the more likely the vaccines and the therapeutic drugs could lose their efficacy. It’s not good news, especially for those who have not been vaccinated.
It’s no surprise that we’re seeing this at the starting point of the winter. The outbreak really intensifies during the holiday season because places become more crowded due to travel and shopping. It’s the perfect time for omicron to start emerging and it has the potential to become another big variant.
Is the omicron variant more dangerous or more contagious than delta?
There are not enough data or cases reported to know yet.
The danger is that we are always two steps behind the virus. First of all, the variant is already circulating in the population by the time we detect it. The second reason we are behind is because we have to then characterize the virus’ behavior. We’re trying to assess how infectious it is and that takes a longer time. By the time we figure these answers out, the virus is already widespread.
The good thing is we learned a lot from delta, so we’ve had a more proactive response to the omicron variant. But to put a stop to other variants emerging, people have to get vaccinated and reduce transmission, which is what enables the mutations.
Do our current vaccines protect against it (including the booster)?
Most likely, yes, and here’s why. The vaccine creates two “arms” of immunity: the humoral arm and the cellular arm. The humoral immune response triggers the creation of antibodies to neutralize the virus. But changes to the virus can impact the effectiveness of the antibodies, which means that the vaccinated can still get COVID-19 and spread it.
Now, cellular immunity is different. It’s more important when it comes to preventing severe disease. Our cells are trained to recognize the virus, and they help keep the virus from causing severe damage to our bodies. Those who are vaccinated will likely not get that sick if they contract the variant.
The problem is we have a vaccine that was created almost two years ago for a virus that appeared two years ago. Once we have a vaccine that is based on the current variant, we can catch up with the virus.
Should we prepare for states and cities to shut down again?
I think it is highly unlikely, being that people are so tired of being locked down. Also, we have other preventive measures. We can have people get vaccinated and get the boosters, and we can have people wear masks. We know those measures work beautifully.
Why are countries from Australia to Israel closing their borders so quickly?
It’s more political than anything. Closing borders can only slow down the virus for a few weeks or a couple of months. The problem is once you’ve identified the virus, it’s already too late. It’s already widespread. So, closing the borders is not effective. The virus is already there.
Can we expect to have COVID variants from now on?
Yes, until we are able to get the entire human population vaccinated. It’s not just about the United States. We’re talking about the entire human population. A lot of the new variants come from areas where there are not a lot of vaccines available.
Hypothetically speaking, if the whole world got vaccinated, would that keep other variants from forming?
I believe it will most likely go away or it will become a very mild virus. It will not cause severe disease anymore. It will become like the common cold.
I feel like the latter is more of a possibility, considering that the virus has already widened its spread and has already adapted to humans. I think it will likely be here to stay even if you vaccinate the entire population, but it will not cause severe sickness or death anymore.
What are the symptoms of omicron?
It’s not much different than those of the other variants: cough, loss of smell, diarrhea, fever, runny nose and headache. The symptoms may vary, but we don’t have enough data yet to know how.
What is the most sensible thing for people to do at this point?
We should continue doing what we have been doing. We should continue to wear masks and get vaccinated. Those who have already been vaccinated should make sure they get their booster. Make sure your kids are vaccinated and continue to protect our loved ones and ourselves. We just can’t let down our guard at this point.
Sunday, January 16, 2022
COVID-19 daily epidemiology update - Canada.ca
On this page
Key updates as of January 14, 2022, 7 am EST
Thursday, January 13, 2022
Heartless Bastards!!
Sky-Scraper buildings
are warm at night...
With empty floors and Neon Lights
and solid doors locked tight
against helpless poor who's desperate plight
are ignored on sight...
And outside...
Another homeless person dies
in the freezing cold of a
Winter's night...
---------------------------------------
N.J.R.
Wednesday, January 5, 2022
Hello Gentle People:
Apparently the Omicron variant of Sars-CoV2 is more dangerous than even the Delta variant.
Why? Because it spreads faster and sadly it also kills people. Even Three vaccines are not enough to protect us against this vicious virus!
Once again we must do everything to block the damn thing and once again we may need another vaccine. Yes, another vaccine because the Three predecessors were all aimed at the original Covid 19 and the Omicron is a two step variation away from the original.
The deadly Omicron variant spreads faster and even with Three vaccines, you are not protected.
A fourth vaccine and maybe more is needed. Don't let down your guard or your masks until the Hospitals finally give us the all clear signal. Do not be blasé about this virus or you may end up in a body bag.
N.J.R
Tuesday, January 4, 2022
Correct me if I am wrong but this is my THEORY FOR GRAVITY.
What can be said about our Sun?
1. It is a large Hydrogen fusion reactor so hot it creates a giant ball of plasma.
2. Plasma is so intense it breaks apart Atoms into their component sub-atomic particles.
3. When Atoms split they create an explosive chain reaction which releases tremendous amounts of energy but when Atoms are fused together by pressure and heat, they become Plasma and this also releases tremendous amounts of energy.
4. Sub Atomic particles in the form of radiation and Photons blast out into space but much of that energy is sucked back into the Sun by gravity. The gigantic mass of the Sun creates gravity which sucks in any and all elements unlucky enough to be passing near. One of the most abundant elements in the universe is Hydrogen and that is the main fuel for the Hydrogen fusion reaction within the Sun.
5. The explosive force of our Sun is so strong it sends radiation and Photons millions of miles out into space. On Earth we feel the heat and we see the light from our Sun.
6, For every action there is a reaction and so for our Sun the force of drag of an Atom is proportional to the square of the velocity times the mass of the Sun. This force of drag is gravity.
7. Plasma smashing apart Atoms at tremendous speed creates a force of drag reaction. The "drag" is created when newly created sub atomic vacuum holes are quickly filled in with new Atoms.
8. Vacuum holes are created when Atoms are smashed by the heat and pressure of Plasma and then exploded into the Universe. We can assume that the force of drag of sub-atomic particles are also proportional to the square of their velocity multiplied by the mass of the Sun. This creates a force of drag so powerful energy drops or is sucked into it in order to replace lost Atomic particles blasted out into space. We call this force Gravity.
9. Without mass and heat and pressure uniting Atoms or smashing them apart, there is very little gravity created.
10. When an element, such as Hydrogen, falls into the sun it becomes fuel for the Hydrogen fusion reaction which creates Plasma which in turn smashes more Atoms into particles. The particles leave so fast they create sub atomic vacuums that when multiplied by the mass of the sun, becomes gravity and gravity then drags in more Hydrogen Atoms which maintains the fusion reaction.
CONCLUSION: Heat and pressure creates fusion which in turn creates Plasma which destroys Atoms and blasts their sub- Atomic particles into space in the form of light Photons, Radiation and Heat. The quick destruction of Atoms creates sub-atomic vacuum holes and since nature abhors vacuums, the holes are quickly replaced by new Atoms. Since Hydrogen is the most abundant element in the Universe, Hydrogen falls into the Sun and fuels the Sun's Plasma reaction.
Our Sun is a large Hydrogen fusion reactor creating a giant ball of Plasma which is so hot it breaks apart Atoms and blasts heat and light Photons into space. When sub-atomic particles are lost into space, vacuum holes are created. New Atoms quickly replace the particles lost and this replacement process times the mass of the Sun, is gravity.
New Atoms are mostly Hydrogen and they in turn are pulled apart by heat and pressure and their particles blasted out into space. When destroyed, Atoms leave a space much like a truck on a highway creates a vacuum turbulence. Air quickly fills the vacuum space created behind the truck. With Hydrogen fusion high energy Plasma smashes together Hydrogen Atoms and energy is released creating tiny spaces or vacuum holes. These holes are quickly filled in with new Elements (mainly Hydrogen Atoms) falling or being sucked into the Sun and this process we know as gravity. The new Atoms then become part of the massive fusion reaction which creates heat and light for all life on Earth.
Author: @ Nelson Joseph Raglione
Sunday, December 19, 2021
COVID-19 vaccine: What’s RNA research got to do with it?
A coronavirus uses a protein on its membrane—shown here in red in a molecular model—to bind to a receptor— shown in blue—on a human cell to enter the cell. Once inside, the virus uses the cells' machinery to make more copies of itself. (Juan Gaertner / Science Source) The US Food and Drug Administration recently approved emergency use authorization for a COVID-19 vaccine developed by Pfizer and the German pharmaceutical company BioNTech.
The vaccine made history not only because it reported a 95 percent efficacy rate at preventing COVID-19 in clinical trials, but because it is the first vaccine ever approved by the FDA for human use that is based on RNA technology.
“The development of RNA vaccines is a great boon to the future of treating infectious diseases,” says Lynne Maquat, the J. Lowell Orbison Distinguished Service Alumni Professor in biochemistry and biophysics, oncology, and pediatrics at Rochester and the director of Rochester’s Center for RNA Biology.
COVID-19, short for “coronavirus disease 2019,” is caused by the novel coronavirus SARS-CoV-2. Like many other viruses, SARS-CoV-2 is an RNA virus. This means that, unlike in humans and other mammals, the genetic material for SARS-CoV-2 is encoded in ribonucleic acid (RNA). The viral RNA is sneaky: its features cause the protein synthesis machinery in humans to mistake it for RNA produced by our own DNA.
For that reason, several of the leading COVID-19 vaccines and treatments are based on RNA technology.
A contingent of researchers at the University of Rochester study the RNA of viruses to better understand how RNAs work and how they are involved in diseases. This RNA research provides an important foundation for developing vaccines and other drugs and therapeutics to disrupt the virus and stop infections.
“Understanding RNA structure and function helps us understand how to throw a therapeutic wrench into what the COVID-19 RNA does—make new virus that can infect more of our cells and also the cells of other human beings,” Maquat says.
In the past few decades, as scientists came to realize that genetic material is largely regulated by the RNA it encodes, that most of our DNA produces RNA, and that RNA is not only a target but also a tool for disease therapies, “the RNA research world has exploded,” Maquat says. “The University of Rochester understood this.”
In 2007, Maquat founded The Center for RNA Biology as a means of conducting interdisciplinary research in the function, structure, and processing of RNAs. The Center involves researchers from both the River Campus and the Medical Center, combining expertise in biology, chemistry, engineering, neurology, and pharmacology.
“Our strength as a university is our diversity of research expertise, combined with our highly collaborative nature,” says Dragony Fu, an associate professor of biology on the River Campus and a member of the Center for RNA Biology. “We are surrounded by outstanding researchers who enhance our understanding of RNA biology, and a medical center that provides a translational aspect where the knowledge gained from RNA biology can be applied for therapeutics.”
How does RNA relate to disease?
A graphic created by the New York Times illustrates how the coronavirus that causes COVID-19 enters the body through the nose, mouth, or eyes and attaches to our cells. Once the virus is inside our cells, it releases its RNA. Our hijacked cells serve as virus factories, reading the virus’s RNA and making long viral proteins to compromise the immune system. The virus assembles new copies of itself and spreads to more parts of the body and—by way of saliva, sweat, and other bodily fluids—to other humans.
“Once the virus is in our cells, the entire process of infection and re-infection depends on the viral RNA,” Maquat says.
One of the reasons viruses are such a challenge is that they change and mutate in response to drugs.
That means novel virus treatments and vaccines have to be created each time a new strain of virus presents itself. Armed with innovative research on the fundamentals of RNA, scientists are better able to develop and test therapeutics that directly target the RNAs and processes critical to a virus’s life cycle.
How do RNA vaccines work?
Traditional vaccines against viruses like influenza inject inactivated virus proteins called antigens. The antigens stimulate the body’s immune system to recognize the specific virus and produce antibodies in response, with the hope that these antibodies will fight against future virus infection.
RNA-based vaccines—such as those developed by Pfizer/BioNTech and American biotechnology company Moderna—do not introduce an antigen, but instead inject a short sequence of synthetic messenger RNA (mRNA) that is enclosed in a specially engineered lipid nanoparticle. This mRNA provides cells with instructions to produce the virus antigen themselves.
Once the mRNA from a vaccine is in our body, for example, it “instructs” the protein synthesis machinery in our cells, which normally generates proteins from the mRNAs that derive from our genes, to produce a piece of the SARS-CoV-2 virus spike protein. Since the SARS-CoV-2 virus spike protein is foreign to our bodies, our bodies will then make antibodies that inactivate the protein.
“Should the virus enter our body from an infected person, these antibodies will bind to and inactivate the virus by binding to its spike proteins, which coat the outside of the viral capsule,” Maquat says.
An RNA-based vaccine therefore acts as a code to instruct our human cells to make many copies of the virus protein which, as a consequence, creates antibodies resulting in an immune response.
Unlike more traditional vaccines, RNA-based vaccines are also beneficial in that they eliminate the need to work with the actual virus.
“Working with a live virus is costly and very involved, requiring that researchers use special biosafety laboratories and wear bulky personal protective equipment so that the virus is ‘biocontained,’ and no one gets infected,” Maquat says.
Developing a vaccine from a live virus additionally takes much longer than generating an mRNA-based vaccine, but “no one should think the process is simple,” Maquat says of the Pfizer/BioNTech vaccine. “Since it is the first of its kind, a lot had to be worked out.”
What does RNA stand for?
RNA stands for ribonucleic acid.
What is RNA?
RNA delivers the genetic instructions contained in DNA to the rest of the cell.
What does Covid stand for?
Covid-19 stands for “coronavirus disease 2019.”
How is Rochester’s RNA research applicable to COVID-19?
Researchers Douglas Anderson, Dragony Fu, and Lynne Maquat are among the scientists at the University of Rochester who study the RNA of viruses to better understand how RNAs work and how they are involved in diseases. (University of Rochester photos / Matt Wittmeyer / J. Adam Fenster)
Maquat has been studying RNA since 1972 and was part of the earliest wave of scientists to realize the important role RNA plays in human health and disease.
Our cells have a number of ways to combat viruses in what can be viewed as an “arms race” between host and virus. One of the weapons in our cells’ arsenal is an RNA surveillance mechanism Maquat discovered called nonsense-mediated mRNA decay (NMD).
“Nonsense-mediated mRNA decay protects us from many genetic mutations that could cause disease if NMD were not active to destroy the RNA harbouring the mutation,” she says.
Maquat’s discovery has contributed to the development of drug therapies for genetic disorders such as cystic fibrosis, and may be useful in developing treatments for coronavirus.
“NMD also helps us combat viral infections, which is why many viruses either inhibit or evade NMD,” she adds. “The genome of the virus COVID-19 is a positive-sense, single-stranded RNA. It is well known that other positive-sense, single-stranded RNA viruses evade NMD by having RNA structures that prevent NMD from degrading viral RNAs.”
Maquat’s lab has been collaborating with a lab at Harvard University to test how viral proteins can inhibit the NMD machinery.
Their recent work is focused on the SARS-CoV-2 structural protein called N. Lab experiments and data sets from infected human cells indicate this virus is unusual because it does not inhibit the NMD pathway that regulates many of our genes and some of the virus’s genes. Instead, the virus N protein seems to promote the pathway.
“SARS-CoV-2 reproduces its RNA genome with much higher efficiency than other pathogenic human viruses,” Maquat says. “Maybe there is a connection there; time will tell.”
In the Department of Biology, Fu and Jack Werren, the Nathaniel and Helen Wisch Professor of Biology, received expedited funding awards from the National Science Foundation to apply their expertise in cellular and evolutionary biology to research proteins involved in infections from COVID-19. The funding was part of the NSF’s Rapid Response Research (RAPID) program to mobilize funding for high priority projects.
Werren’s research will be important in ameliorating some of the potential side effects of COVID-19 infections, including blood clots and heart diseases, while Fu’s research will provide insight into the potential effects of viral infection on human cell metabolism.
“Our research will provide insight into the potential effects of viral infection on host cellular processes,” Fu says. “Identifying which cell functions are affected by the virus could help lessen some of the negative effects caused by COVID-19.”
Douglas Anderson, an assistant professor of medicine in the Aab Cardiovascular Research Institute and a member of the Center for RNA Biology, studies how RNA mutations can give rise to human disease and has found that alternative therapeutics, such as the gene-editing technology CRISPR, may additionally “usher in a new approach to how we target and combat infectious diseases,” he says.
For the past few years, Anderson’s lab has developed tools and delivery systems that use the RNA-targeting CRISPR-Cas13 to treat human genetic diseases that affect muscle function. CRISPR-Cas13 is like a molecular pair of scissors that can target specific RNAs for degradation, using small, programmable guide RNAs.
When the health crisis first became apparent in Wuhan, China, researchers in Anderson’s lab turned their focus toward developing a CRISPR-Cas13 therapeutic aimed at SARS-CoV-2. Applying the knowledge already available about coronavirus RNA replication, they designed single CRISPR guide RNAs capable of targeting every viral RNA that is made within a SARS-CoV-2 infected cell. Using a novel cloning method developed in Anderson’s lab, multiple CRISPR guide-RNAs could be packaged into a single therapeutic vector (a genetically engineered carrier) to target numerous viral RNA sites simultaneously. The multi-pronged targeting strategy could be used as a therapy to safeguard against virus-induced cell toxicity and prevent ‘escape’ of viruses which may have undergone mutation.
“Infectious viruses and pandemics seemingly come out of nowhere, which has made it hard to rapidly develop and screen traditional small molecule therapeutics or vaccines,” Anderson says. “There is a clear need to develop alternative targeted therapeutics, such as CRISPR-Cas13, which have the ability to be rapidly reprogrammed to target new emerging pandemics.”
While many new treatments for the novel coronavirus are being considered, there is one thing that is certain, Maquat says: “Targeting RNA, or the proteins it produces, is essential for therapeutically combatting this disease.”
What role will RNA play in the future of vaccines and disease treatments?
Most people living in the United States today have only read about the 1918 flu pandemic and the relatively recent RNA viruses, such as Ebola or Zika, that are seen largely in other countries.
“RNA treatments will most likely be a wave of the future for these and other emerging diseases,” Maquat says. “Epidemiologists know new infectious pathogens are coming given how small the world has become with international travel, including to and from places where humans and animals are in close contact.”
Bats, in particular, are reservoirs for viruses. Many bat species are able to live with viruses without experiencing ill effects, given the bats’ unusual physiology. If these bat viruses mutate so they become capable of infecting humans, however, there will be new diseases, Maquat says.
“It is just a matter of when this will happen and what the virus will be. The hope is that we will be ready and able to develop vaccines against these new viruses with the new pipelines that have been put in place for COVID-19.”
This story was originally published on April 28, 2020, and updated on December 14, 2020.
Read more
FDA votes to approve emergency use of Pfizer coronavirus vaccine
Researchers and volunteers in Rochester have been involved in the testing of the Pfizer/BioNTech vaccine since May, and technologies used in the development of the vaccine can trace their origins to decades of infectious disease research conducted at Rochester.
Bats carry many viruses, including the one behind COVID-19, without becoming ill. University of Rochester biologists are studying the immune system of bats to find potential ways to “mimic” that system in humans.
Rochester biologists selected for ‘rapid research’ on COVID-19Rochester biologists are exploring how coronavirus interacts with cellular proteins to cause COVID-19 under a priority NSF program.
Category: Science & Technology
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