A Team Of Scientist identifies four possible drugs to treat COVID-19

The team- Dr. Kamlendra Singh, an Associate Prof. at the Uni. of Missouri and his colleagues have    identified 4 antiviral drugs-including remdesivir that was originally developed to treat Ebola- which may be effective in inhibiting the replication of the novel coronavirus that causes COVID-19.

The researchers used computer-aided drug design to examine the effectiveness of remdesivir, 5-fluorouracil, ribavirin and favipiravir in treating COVID-19.

The study found that all 4 drugs were effective in inhibiting or blocking, the coronavirus' RNA proteins from making genomic copies of the novel coronavirus.

As researchers, we've an obligation to search for possible treatments given that so many people are dying from this virus, the researcher said.

These antiviral drugs, if they turn out to be effective, all have some limitations. But in the midst of a global pandemic, they're worth taking a deeper look at because based on our research, we've reason to believe that all of these drugs could potentially be effective in treating Covid-19, he said.

The researchers noted that SARS-Cov2 that causes Covid-19, like all viruses, can mutate and develop resistance to antiviral drugs.

Further testing in a lab setting and in patients is needed to better evaluate how the proposed treatments interact with the virus' RNA polymerase, they said.

Our goal is to help doctors by providing the options for possible treatments of Covid-19, and to ultimately contribute in improving the health outcomes of patients suffering from the infectious disease, he said.

As researchers, we're simply playing our part in the fight against the pandemic, he said.

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Illama-derived antibodies may block coronavirus entry into host cells

Molecules derived from the immune system of the South American mammals illamas may block the entry of the novel coronavirus into host cells, according to a study which could lead to a potential avenue for COVID-19 treatment. Researchers, including those from The University of Texas at Austin in the US, have linked two copies of a special kind of antibody molecules produced by the llama immune system to create a new type that binds tightly to a key protein on the novel coronavirus, SARS-CoV-2.

According to the study, published in the journal Cell, this protein, called the spike protein, allows the coronavirus to break into host cells. The findings, according to the researchers, indicate that the Illama-derived antibody may block viruses with this spike protein from infecting cells cultured in the lab. "This is one of the first antibodies known to neutralise SARS-CoV-2," said study co-author Jason McLellan from UT Austin.

The scientists said they are preparing to conduct preclinical studies in animals such as hamsters or nonhuman primates, with the goal of developing a treatment that would help people soon after infection with the virus. While vaccines have to be given a month or two before infection to provide protection, the researchers said antibody therapies can achieve this immediately.

"With antibody therapies, you're directly giving somebody the protective antibodies and so, immediately after treatment, they should be protected," McLellan said. "The antibodies could also be used to treat somebody who is already sick to lessen the severity of the disease," he added. According to the researchers, this would be especially helpful for vulnerable groups such as elderly people, who mount a modest response to vaccines, meaning that their protection may be incomplete.

The scientists explained that the strategy can be made to work since the immune system of illamas produce antibodies similar to that of humans. When llamas' immune systems detect foreign invaders such as bacteria and viruses, these animals produce two types of antibodies. One of these is similar to human antibodies, and another that's only about a quarter of the size, the researchers said.

They added that the smaller ones, called single-domain antibodies or nanobodies, can be nebulised and used in an inhaler. "That makes them potentially really interesting as a drug for a respiratory pathogen because you're delivering it right to the site of infection," said Daniel Wrapp, study co-author from UT Austin.

The scientists extracted the antibodies for the study from a 4-year-old illama, Winter, living on a farm in the Belgian countryside along with approximately 130 other llamas and alpacas. In 2016, when Winter was about 9 months old, the researchers were studying two earlier coronaviruses -- SARS-CoV-1 and MERS-CoV. In a process similar to humans getting shots to immunise them against a virus, the researchers injected the illama with stabilised spike proteins from the coronaviruses over the course of about six weeks.

They then collected a blood sample and isolated the antibodies bound to each version of the spike protein. According to the researchers, one of these antibodies, VHH-72, showed promise in stopping a virus with spike proteins from SARS-CoV-1 from infecting cells cultured in the lab. "There wasn't a big need for a coronavirus treatment then. This was just basic research. Now, this can potentially have some translational implications, too," Wrapp said.

The scientists then engineered a new antibody that showed promise for treating the current SARS-CoV-2. According to the researchers, the engineered antibody involved linking two copies of VHH-72 that bound more effectively to the novel coronavirus spike protein. They said the engineered protein can bind strongly to viruses displaying spike proteins from SARS-CoV-2 in cell cultures, adding that this is the first known antibody that neutralise both SARS-CoV-1 and SARS-CoV-2. 

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Newly discovered antibiotics kill bacteria differently

Antibiotic resistance is a growing public health problem across the globe, with many diseases becoming harder to treat. Now, a newly discovered antibiotic group shows promise in the fight against superbugs as it has a unique way of killing bacteria.

A team of scientists at McMaster University has found a new group of antibiotics that can fight infections in a new and unique way. These antibiotics fight infections in a way researchers have never seen before, according to the findings of the study described in the journal Nature.
Holy grail' of antibiotics

The newly found group of antibiotics, consisting of corbomycin and complestatin, can kill bacteria by blocking the function of the bacterial cell wall. These drugs come from a family of antibiotics known as glycopeptides, which are produced by soil bacteria.

The two antibiotics attack peptidoglycan, the main component of the bacterial cell wall that is vital to the growth and survival of almost all bacteria. They inhibit the action of autolysins, which are important for cell division and growth.

Other antibiotics, such as penicillin, work by preventing the bacteria from building its wall, which is the source of its strength. In killing the bacteria, removing its wall will make it vulnerable and easier to kill.

These new antibiotics work by doing the opposite. Instead of preventing building the wall, it halts the wall ll from being broken down. As a result, blocking the breakdown of the wall would make it impossible for them to divide and expand – just like being trapped in prison.

Unique bacteria killer
The two new antibiotics are known as glycopeptides. The team studied the genes of the group to see if they lack resistance mechanisms. The team believes that if the genes that made these drugs different, perhaps the way they kill will also be different.

In collaboration with scientists from the Université de Montréal, including Yves Brun, they found that the drugs act on the bacterial cell wall to prevent it from dividing and proliferating. 

"Knowing the detailed structure at the atomic level of this connection between the surface layer and the surface of the cell offers enormous potential to then develop molecules that can target this attachment and make the cell more sensitive to antibacterials," Yves Brun, study co-author, said.

"Combined with the discovery of the new mode of action of two antibiotics, this development opens up prospects for weakening the action of bacteria and making them more vulnerable," he added.

The researchers believe the group of drugs is a promising clinical candidate in the hopes of stemming bacteria from becoming resistant to antibiotics.

Fight against antibiotic resistance

Antibiotic resistance is one of the greatest threats to global health, according to the World Health Organization (WHO). Though it happens naturally, the misuse of antibiotics is hastening the process, making it easy to treat infections in the past harder to curb now.

Further, antibiotic resistance increase hospital stays and medical costs. For instance, diseases in the past that were responsive to certain antibiotics may become resistant and difficult to stem, such as tuberculosis, pneumonia, gonorrhea, and other infections. Now, as the diseases become stronger and more resilient, outbreaks may become inevitable, unless new drugs are discovered.

In the United States alone, at least 2.8 million people become infected with antibiotic-resistant bacteria each year, while more than 35,000 people die.

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Neuroscientists Reveal How the Brain Selectively Remembers New Places

When you enter a room, your brain is bombarded with sensory information. If the room is a place you know well, most of this information is already stored in long-term memory. However, if the room is unfamiliar to you, your brain creates a new memory of it almost immediately.

MIT neuroscientists have now discovered how this occurs. A small region of the brainstem, known as the locus coeruleus, is activated in response to novel sensory stimuli, and this activity triggers the release of a flood of dopamine into a certain region of the hippocampus to store a memory of the new location.

“We have the remarkable ability to memorize some specific features of an experience in an entirely new environment, and such ability is crucial for our adaptation to the constantly changing world,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience and director of the RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory.

“This study opens an exciting avenue of research into the circuit mechanism by which behaviorally relevant stimuli are specifically encoded into long-term memory, ensuring that important stimuli are stored preferentially over incidental ones,” adds Tonegawa, the senior author of the study.

Akiko Wagatsuma, a former MIT research scientist, is the lead author of the study. 

New places
In a study published about 15 years ago, Tonegawa’s lab found that a part of the hippocampus called the CA3 is responsible for forming memories of novel environments. They hypothesized that the CA3 receives a signal from another part of the brain when a novel place is encountered, stimulating memory formation.

They believed this signal to be carried by chemicals known as neuromodulators, which influence neuronal activity. The CA3 receives neuromodulators from both the locus coeruleus (LC) and a region called the ventral tegmental area (VTA), which is a key part of the brain’s reward circuitry. The researchers decided to focus on the LC because it has been shown to project to the CA3 extensively and to respond to novelty, among many other functions.

The LC responds to an array of sensory input, including visual information as well as sound and odor, then sends information on to other brain areas, including the CA3. To uncover the role of LC-CA3 communication, the researchers genetically engineered mice so that they could block the neuronal activity between those regions by shining light on neurons that form the connection.

To test the mice’s ability to form new memories, the researchers placed the mice in a large open space that they had never seen before. The next day, they placed them in the same space again. Mice whose LC-CA3 connections were not disrupted spent much less time exploring the space on the second day, because the environment was already familiar to them. However, when the researchers interfered with the LC-CA3 connection during the first exposure to the space, the mice explored the area on the second day just as much as they had on the first. This suggests that they were unable to form a memory of the new environment.

The LC appears to exert this effect by releasing the neuromodulator dopamine into the CA3 region, which was surprising because the LC is known to be a major source of norepinephrine to the hippocampus. The researchers believe that this influx of dopamine helps to boost CA3’s ability to strengthen synapses and form a memory of the new location.

They found that this mechanism was not required for other types of memory, such as memories of fearful events, but appears to be specific to memory of new environments. The connections between the LC and CA3 are necessary for long-term spatial memories to form in CA3.

“The selectivity of successful memory formation has long been a puzzle,” says Richard Morris, a professor of neuroscience at the University of Edinburgh, who was not involved in the research. 

“This study goes a long way toward identifying the brain mechanisms of this process. Activity in the pathway between the locus coeruleus and CA3 occurs most strongly during novelty, and it seems that activity fixes the representations of everyday experience, helping to register and retain what’s been happening and where we’ve been.”

Choosing to remember
This mechanism likely evolved as a way to help animals survive, allowing them to remember new environments without wasting brainpower on recording places that are already familiar, the researchers say.

“When we are exposed to sensory information, we unconsciously choose what to memorize. For an animal’s survival, certain things are necessary to be remembered, and other things, familiar things, probably can be forgotten,” Wagatsuma says.

Still unknown is how the LC recognizes that an environment is new. The researchers hypothesize that some part of the brain is able to compare new environments with stored memories or with expectations of the environment, but more studies are needed to explore how this might happen.

“That’s the next big question,” Tonegawa says. “Hopefully new technology will help to resolve that.”

The research was funded by the RIKEN Brain Science Institute, the Howard Hughes Medical Institute, and the JPB Foundation.
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Newly Identified Memory Pathway Could Prevent PTSD

In a newly published study, a team of researchers show that blocking amygdala cells’ interactions with serotonin after trauma may prevent post-traumatic stress disorder.

About 8 million Americans suffer from nightmares and flashbacks to a traumatic event. This condition, known as post-traumatic stress disorder (PTSD), is particularly common among soldiers who have been in combat, though it can also be triggered by physical attack or natural disaster.

Studies have shown that trauma victims are more likely to develop PTSD if they have previously experienced chronic stress, and a new study from MIT may explain why. The researchers found that animals who underwent chronic stress prior to a traumatic experience engaged a distinctive brain pathway that encodes traumatic memories more strongly than in unstressed animals.

Blocking this type of memory formation may offer a new way to prevent PTSD, says Ki Goosens, the senior author of the study.

“The idea is not to make people amnesic but to reduce the impact of the trauma in the brain by making the traumatic memory more like a ‘normal,’ unintrusive memory,” says Goosens, an assistant professor of neuroscience and investigator in MIT’s McGovern Institute for Brain Research.

The paper’s lead author is former MIT postdoc Michael Baratta.

Strong memories
Goosens’ lab has sought for several years to find out why chronic stress is so strongly linked with PTSD. “It’s a very potent risk factor, so it must have a profound change on the underlying biology of the brain,” she says.

To investigate this, the researchers focused on the amygdala, an almond-sized brain structure whose functions include encoding fearful memories. They found that in animals that developed PTSD symptoms following chronic stress and a traumatic event, serotonin promotes the process of memory consolidation. When the researchers blocked amygdala cells’ interactions with serotonin after trauma, the stressed animals did not develop PTSD symptoms. Blocking serotonin in unstressed animals after trauma had no effect.

“That was really surprising to us,” Baratta says. “It seems like stress is enabling a serotonergic memory consolidation process that is not present in an unstressed animal.”

Memory consolidation is the process by which short-term memories are converted into long-term memories and stored in the brain. Some memories are consolidated more strongly than others. For example, “flashbulb” memories, formed in response to a highly emotional experience, are usually much more vivid and easier to recall than typical memories.

Goosens and colleagues further discovered that chronic stress causes cells in the amygdala to express many more 5-HT2C receptors, which bind to serotonin. Then, when a traumatic experience occurs, this heightened sensitivity to serotonin causes the memory to be encoded more strongly, which Goosens believes contributes to the strong flashbacks that often occur in patients with PTSD.

“It’s strengthening the consolidation process so the memory that’s generated from a traumatic or fearful event is stronger than it would be if you don’t have this serotonergic consolidation engaged,” Baratta says.

“This study is a very nice dissection of the mechanism by which chronic stress seems to activate new pathways not seen in unstressed animals,” says Mireya Nadal-Vicens, medical director of the Center for Anxiety and Traumatic Stress Disorders at Massachusetts General Hospital, who was not part of the research team.

Drug intervention
This memory consolidation process can take hours to days to complete, but once a memory is consolidated, it is very difficult to erase. However, the findings suggest that it may be possible to either prevent traumatic memories from forming so strongly in the first place, or to weaken them after consolidation, using drugs that interfere with serotonin.

“The consolidation process gives us a window in which we can possibly intervene and prevent the development of PTSD. If you give a drug or intervention that can block fear memory consolidation, that’s a great way to think about treating PTSD,” Goosens says. “Such an intervention won’t cause people to forget the experience of the trauma, but they might not have the intrusive memory that is ultimately going to cause them to have nightmares or be afraid of things that are similar to the traumatic experience.”

The Food and Drug Administration has already approved a drug called agomelatine that blocks this type of serotonin receptor and is used as an antidepressant.

Such a drug might also be useful to treat patients who already suffer from PTSD. These patients’ traumatic memories are already consolidated, but some research has shown that when memories are recalled, there is a window of time during which they can be altered and reconsolidated. It may be possible to weaken these memories by using serotonin-blocking drugs to interfere with the reconsolidation process, says Goosens, who plans to begin testing that possibility in animals.

The findings also suggest that the antidepressant Prozac and other selective serotonin reuptake inhibitors (SSRIs), which are commonly given to PTSD patients, likely do not help and may actually worsen their symptoms. Prozac enhances the effects of serotonin by prolonging its exposure to brain cells. While this often helps those suffering from depression, “There’s no biological evidence to support the use of SSRIs for PTSD,” Goosens says.

“The consolidation of traumatic memories requires this serotonergic cascade and we want to block it, not enhance it,” she adds. “This study suggests we should rethink the use of SSRIs in PTSD and also be very careful about how they are used, particularly when somebody is recently traumatized and their memories are still being consolidated, or when a patient is undergoing cognitive behavior therapy where they’re recalling the memory of the trauma and the memory is going through the process of reconsolidation.”

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