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Physiology

American Scientists Found COVID-19 Patients Who Have Recovered and Re-acquired Coronavirus Would Most Likely N – Science Times

As coronavirus continues to push scientists and medical experts, to find a cure, numerous new studies are being regularly birthed towards immunity. In America, two new studies emerged: an immune response experiment and a DNA vaccine protection study, both evaluating in rhesus macaques.

From Oregon Health and Science University, scientists tested 9 adult rhesus macaques with SARS-CoV-2 antibodies, and evaluated re-exposure the following month.

These primates have the closest physiology and immune systems to humans and therefore hold promising results in all kinds of vaccine testing against COVID-19.

However, Jacob Estes, one of the study's authors said that 'while these monkeys are a very good approximation of humans, they're not humans.' He goes on to explain that the genetic structure of humans contains more variables when it comes to severe diseases.

Studying the infection, the medical experts assessed immunity as well as pathology and virology.

All 9 subjects were evident with viral pneumonia, neutropenia, and lymphopenia with symptoms such as decreased appetite. However, they did not seem to experience respiratory distress, weight loss, nor mortality.

After 35 days of initial infection, the macaques were re-challenged with the same doses of SARS-CoV-2.

Evidence in their RNA showed lower rates of infection, as well as 'little or no clinical disease, was observed in the animals following rechallenge,' the study notes.

For humans, it could mean that patients who have recovered and re-acquire the virus would most likely not infect others and have low levels of COVID-19 antibodies.

The conclusion to the experiments records that individuals who have recovered from coronavirus typically develop antibody responses specific to the virus which provides 'robust protective immunity against re-exposure.'

Read Also:Canadian Nurse Tests Positive for COVID-19 8 Times Since March but Doctors Couldn't Explain Why

Despite hopeful progress, the researchers still noted that 'additional research will be required to define the durability of natural immunity.'

Sarah Henrickson from theChildren's Hospital of Pediatrics, Division of Allergy Immunologyin Pennsylvania conducted a study about human immunology history.

Henrickson states that 20 years ago when SARS-CoV caused its first worldwide epidemic, public health strategies contained the spread of the virus, 'without a successful vaccine or targeted therapy.'

She goes into depth of focusing on the behavioral patterns between the virus and its host during infection. However, the general focus of her study contains limitations on necessary data to understand how coronavirus affects human immunity,

There had also been other studies attempting to answer the question if re-infection is possible. Last week, a study challenged the timeline of immunity.

This is especially challenging since many people remain asymptomatic to the virus.

A study of reinfection on 10 male subjects from older forms of coronavirus was also conducted.

For 3 years, frequent reinfection would occur as early as 6 months after the previous infection, according to the study at the University of Amsterdam.

Reliable antibody testing is still necessary to help prevent the continuous spread of COVID-19.

Efforts include Oxford's new portable antibody testing device and their movements toward human trials for vaccines.

What remains uncertain is that without additional research, the rest of the world continues to wait for a definite answer to the question - when will humans have lasting immunity against coronavirus?

Read Also:Coronavirus Results in More Male Deaths, Yet Affect Women with Other Consequences

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American Scientists Found COVID-19 Patients Who Have Recovered and Re-acquired Coronavirus Would Most Likely N - Science Times

Physiology

Largest Scandals Ever Involving The Nobel Prize – World Atlas

The history of the Nobel Prize dates back to 1895, when Swedish industrialistand inventor Alfred Nobel created his will. Nobel set aside the largest part of his fortune to fund an annual award of five prizes for those who, during the preceding year, shall have conferred the greatest benefit on mankind.

Considered as the most prestigious intellectualachievement awards on the planet, Nobel Prizes were originally given for achievements in chemistry, literature, physiology or medicine, physics, and peace. In 1969, an additional Nobel Prize was added; the Sveriges Riksbank Prize inEconomicScience.

Though the Nobel Prize is an illustrious honor, not all of the circumstances surrounding its recipients have been completely honorable. There have been scandals associated with the award, and here are some of the most notable.

Fritz Haber was awarded the Nobel Prize in Chemistry in 1919 for creating the Haber-Bosch process. This invention allowed ammonia to be produced on a mass scale and helped create fertilizer, which supported agriculture and helped feed billions. However, this Polish inventor also helped developed chlorine gas into a chemical weapon, which was used in World War I.

German inventor Harald zur Hausen, received the 2008 Nobel physiology or medicine award for his discovery of human papilloma virus (HPV) as well as its link to cervical cancer. It was soon learned that the pharmaceutical giant AstraZeneca sponsored the Nobel Prize website, and also produced HPV vaccines.

Adolf Hitler was involved in two Nobel scandals. He was nominated for a Nobel peace prize in 1939, and although it was done by a Swedish legislator as a joke, it backfired. The nomination was withdrawn after it had created quite an uproar.

The other scandal occurred in 1935 when German journalistCarl von Ossietzky was awarded the Nobel Peace Prize. Von Ossietzky had openly criticized Hitler, which angered the Nazi leader. Hitler then barred Germans from accepting any Nobel Prizes, and created the countrys own German National Prize for Art and Science.

Critics feel that former U.S. President Barack Obama was awarded his Nobel Peace Prize too early. He was just nine months into his first term when he received it in 2009. Some felt it was too premature; Brian Becker, national coordinator of Act Now To Stop War and End Racism, said that the award equaled giving Obama the you are not George W. Bush award. Geir Lundestad, former director of the Nobel Institute, wrote in his 2015 autobiography that the Nobel committee felt that the award would strengthen the president, yet this did not seem to happen.

This revered Indian political activist battled racial discrimination in South Africa, was instrumental in pushing through the 1914 Indian Relief Act, and was the main person responsible for India achieving their independence. Nonetheless, Gandhi was shortlisted five times for a Nobel Prize but was never awarded one. Some believe that this was because the committee had a Euro-centric viewpoint and did not appreciate Indias struggles for its freedom.

The Palestine Liberation Organizations (PLO) leaderYasser Arafat won the Nobel Peace Prize in 1994, sharing it with Israeli leaders Yitzhak Rabin and Shimon Peres. This was given for their achievements on the Oslo Accords, which was a main component of the Palestine and Israel peace process. It was controversial because Arafat was also head of Fatah, the PLO group that was involved in acts of terrorism.

From 1901 to2019, theNobel Prizesand thePrizesin Economic Sciences have been awardedto 597 times to 950 people and organizations. Out of these, only 54 women have won, with Marie Curie being honored twice. One example of this gender discrepancy is the omission of Jocelyn Bell Burnell. She discovered pulsars back in 1967, and published a paper with Antony Hewish, her advisor. In 1974, Hewish and one other colleague, Martin Ryle, received the 1974 Nobel Prize for Physics. Bell Burnell was left out.

Alfred Nobel may have founded the awards, but he also invented explosives, including dynamite. This sullied his reputation, and he was once referred to as The merchant of death by a French newspaper, which had mistakenly printed his obituary. The article also stated that he became wealthy by finding ways to kill more people faster than ever before. This story could have been the impetus that led him to create the awards, as a way to return honor to his name.

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Largest Scandals Ever Involving The Nobel Prize - World Atlas

Physiology

Social determinants of health and survival in humans and other animals – Science Magazine

Social animals need connection

Much research over the past decade or so has revealed that health and lifespan in humans, highly social animals, are reduced with social adversity. We humans are not the only animals that are social, however, and similar research has shown that other social mammals are similarly influenced by isolation and adversity. Snyder-Mackler et al. reviewed the relationships between social environment and many aspects of health and well-being across nonhuman mammals and investigated the similarities between these and patterns in humans. They found many of the same threats and responses across social mammals.

Science, this issue p. eaax9553

The social environment shapes human health, producing strong relationships between social factors, disease risk, and survival. The strength of these links has drawn attention from researchers in both the social and natural sciences, who share common interests in the biological processes that link the social environment to disease outcomes and mortality risk. Social scientists are motivated by an interest in contributing to policy that improves human health. Evolutionary biologists are interested in the origins of sociality and the determinants of Darwinian fitness. These research agendas have now converged to demonstrate strong parallels between the consequences of social adversity in human populations and in other social mammals, at least for the social processes that are most analogous between species. At the same time, recent studies in experimental animal models confirm that socially induced stress is, by itself, sufficient to negatively affect health and shorten life span. These findings suggest that some aspects of the social determinants of healthespecially those that can be modeled through studies of direct social interaction in nonhuman animalshave deep evolutionary roots. They also present new opportunities for studying the emergence of social disparities in health and mortality risk.

The relationship between the social environment and mortality risk has been known in humans for some time, but studies in other social mammals have only recently been able to test for the same general phenomenon. These studies reveal that measures of social integration, social support, and, to a lesser extent, social status independently predict life span in at least four different mammalian orders. Despite key differences in the factors that structure the social environment in humans and other animals, the effect sizes that relate social status and social integration to natural life span in other mammals align with those estimated for social environmental effects in humans. Also like humans, multiple distinct measures of social integration have predictive value, and in the taxa examined thus far, social adversity in early life is particularly tightly linked to later-life survival.

Animal models have also been key to advancing our understanding of the causal links between social processes and health. Studies in laboratory animals indicate that socially induced stress has direct effects on immune function, disease susceptibility, and life span. Animal models have revealed pervasive changes in the response to social adversity that are detectable at the molecular level. Recent work in mice has also shown that socially induced stress shortens natural life spans owing to multiple causes, including atherosclerosis. This result echoes those in humans, in which social adversity predicts increased mortality risk from almost all major causes of death.

Although not all facets of the social determinants of health in humans can be effectively modeled in other social mammals, the strong evidence that some of these determinants are shared argues that comparative studies should play a frontline role in the effort to understand them. Expanding the set of species studied in nature, as well as the range of human populations in which the social environment is well characterized, should be a priority. Such studies have high potential to shed light on the pathways that connect social experience to life course outcomes as well as the evolutionary logic that accounts for these effects. Studies that draw on the power and tools afforded by laboratory model organisms are also crucial because of their potential for identifying causal links. Important research directions include understanding the predictors of interindividual and intersocietal differences in response to social adversity, testing the efficacy of potential interventions, and extending research on the physiological signatures of social gradients to the brain and other tissues. Path-breaking studies in this area will not only integrate results from different disciplines but also involve cross-disciplinary efforts that begin at study conception and design.

Social adversity is closely linked to health and mortality outcomes in humans, across the life course. These observations have recently been extended to other social mammals, in which social integration, social status, and early-life adversity have been shown to predict natural life spans in wild populations and molecular, physiological, and disease outcomes in experimental animal models.

The social environment, both in early life and adulthood, is one of the strongest predictors of morbidity and mortality risk in humans. Evidence from long-term studies of other social mammals indicates that this relationship is similar across many species. In addition, experimental studies show that social interactions can causally alter animal physiology, disease risk, and life span itself. These findings highlight the importance of the social environment to health and mortality as well as Darwinian fitnessoutcomes of interest to social scientists and biologists alike. They thus emphasize the utility of cross-species analysis for understanding the predictors of, and mechanisms underlying, social gradients in health.

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Social determinants of health and survival in humans and other animals - Science Magazine

Genetics

Did you have COVID-19? 23andMe wants you for a study – KENS5.com

The biotech company 23andMe is launching a massive study to see if there is a connection.

SAN ANTONIO Scientists around the world are racing to understand coronavirus and why most people who are infected show mild to moderate symptoms or sometimes no symptoms at all and others develop a severe form of the disease, in some cases resulting in death.

23andMe has provided personalized genetic reports for years. But now he biotechnology company is switching gears to help battle coronavirus with a new study, and they're looking for those with a positive diagnosis to take part.

"Given that COVID-19 has taken a turn of turning our lives upside down so very, very quickly, at this stage we just don't know to what extent genetics plays a role in determining the severity of outcomes," said Adam Auton, the principal scientist of statistical genetics at 23andMe.

To participate in the study, you must be over 18 years of age and live in the U.S., be willing to provide a saliva sample for DNA testing, complete an online survey, have a positive coronavirus diagnosis, and you must have been hospitalized due to coronavirus-related symptoms. The stronger your symptoms, the likelier you could play a big part in the research.

"In order to maximize our abilities to make a discovery, we would really like to provide people with severe outcomes (the opportunity) to come into the study and participate in the study," Auton said.

This study could even shed some light on a phenomenon known as the COVID cliff when patients who seem to be improving suddenly get worse and whether or not genetics play a role. Dr. Diego Maselli, the Medical Director of respiratory therapy at University Hospital told us,

"Unfortunately, some of these patients, when this happens or this phenomenon starts to happen, then they get sicker and they end up in the ICU and sometimes on a ventilator," said Diego Maselli, the medical director of respiratory therapy at University Hospital.

"The hope (is) that our study can help provide information that will provide some answers to those sorts of questions," Auton said.

So far, 600,000 Americans have agreed to participate, but only 9,000 say they had COVID-19. 23andMe is looking for thousands more.

"It's the nature of genetic studies that we really need very large numbers of people to participate," Auton said.

If you would like more information about the study or to participate, click here.

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Did you have COVID-19? 23andMe wants you for a study - KENS5.com

Genetics

COVID-19 study looks at genetics of healthy people who develop severe illness – Washington University School of Medicine in St. Louis

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Researchers seek answers to viruss mysteries, clues to possible treatments

Washington University School of Medicine in St. Louis is one of more than 30 genome sequencing hubs worldwide participating in a study to sequence the DNA of young, healthy adults and children who develop severe COVID-19 despite having no underlying medical problems. The researchers also will study people who never become infected despite repeated exposures to coronavirus. Knowledge gained from understanding COVID-19s extremes could lead to new therapeutic strategies for the illness.

To help unravel the mysteries of COVID-19, scientists are sequencing the DNA of young, healthy adults and children who develop severe illness despite having no underlying medical problems. The researchers are looking for genetic defects that could put certain individuals at high risk of becoming severely ill from the novel coronavirus.

The McDonnell Genome Institute at Washington University School of Medicine in St. Louis is one of more than 30 genome sequencing hubs worldwide participating in the study. Rheumatologist Megan A. Cooper, MD, PhD, an associate professor of pediatrics, is leading the research at Washington University. Called the COVID Human Genetic Effort, the international project is co-led by the National Institute of Allergy and Infectious Diseases of the National Institutes of Health (NIH), and Rockefeller University.

The researchers also plan to study people who never become infected with SARS-CoV-2, the virus that causes COVID-19, despite repeated exposures. Such individuals may have genetic variations that protect against infection. For example, certain rare genetic variants are known to thwart some types of viral infections, including HIV and norovirus. Knowledge gained from understanding COVID-19s extremes unusual susceptibility and resistance could lead to new therapeutic strategies for the illness.

The first focus of our study will be patients with severe responses to SARS-CoV-2 infection severe enough to require intensive care who appear otherwise healthy and are younger than 50, said Cooper, who also leads the clinical immunology program and the Jeffrey Modell Diagnostic and Research Center for Primary Immunodeficiencies at St. Louis Childrens Hospital.

These patients dont have uncontrolled diabetes, heart disease, chronic lung disease or any other condition that we know increases the risk of severe complications from COVID-19, she said. For example, we sometimes see stories about, say, a marathon runner or a generally fit, healthy person who nevertheless got very sick from this virus, or the few healthy children who are getting very sick with COVID-19. These are the kinds of patients were interested in for this study. A small proportion of hospitalized patients will fit this category, likely less than 10%.

Cooper studies primary immunodeficiencies in children. Primary immunodeficiencies are a group of more than 450 genetic disorders of the immune system. They often are caused by mutations in single genes that affect different aspects of immunity.

With this pandemic, we can use our skills in gene hunting to search for genes that might be associated with severe COVID-19 in children and younger adults, she said. We can foresee a future ability to do a genetic sequencing test for individual patients hospitalized with SARS-CoV-2 and get an idea of whether they are likely to need more intensive care. In the meantime, we will be able to learn a great deal about how the immune system responds to this virus and what it needs to be able to respond effectively and in an appropriate manner.

These patients genetics could reveal the important immune pathways that the body needs to fight the virus. That knowledge could lead to therapies that also could help other patients who dont have a genetic susceptibility to the virus but perhaps have high-risk conditions, such as diabetes or heart disease.

Our immune systems have never seen this virus before, Cooper said. Were seeing severe COVID-19 complications play out across the world right now. It is going to take a global effort to investigate the genetic factors and the immune system factors that really control this infection.

Research related to COVID-19, including collecting and distributing of patient samples, is managed through Washington Universitys Institute of Clinical and Translational Sciences (ICTS), led by William G. Powderly, MD, who is also the Larry J. Shapiro Director of the Institute for Public Health, the J. William Campbell Professor of Medicine and co-director of the Division of Infectious Diseases.

This research is supported by funding from the St. Louis Childrens Hospital Foundation and the Jeffrey Modell Foundation.

Washington University School of Medicines 1,500 faculty physicians also are the medical staff of Barnes-Jewish and St. Louis Childrens hospitals. The School of Medicine is a leader in medical research, teaching and patient care, ranking among the top 10 medical schools in the nation by U.S. News & World Report. Through its affiliations with Barnes-Jewish and St. Louis Childrens hospitals, the School of Medicine is linked to BJC HealthCare.

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COVID-19 study looks at genetics of healthy people who develop severe illness - Washington University School of Medicine in St. Louis

Genetics

What the genetics of COVID-19 mean for the survival of wild great apes – Landscape News

In 1994, researchers found two chimpanzees dead in Cte dIvoires Ta National Park, which holds West Africas largest rainforest. Autopsies of the chimpanzees revealed signs of hemorrhage resembling those found in humans during outbreaks of ebolavirus that occurred decades earlier in Zaire and Sudan. Indeed, further studies led to the designation of Ta Forest ebolavirus, one of five known strains of the virus that can lead to the ebolavirus disease. One researcher in the park contracted the disease during this time.

This is one of many stories of a zoonotic disease, also referred to as a zoonosis, which is a disease transmitted to humans by animals. Zoonoses are transmitted via direct or indirect contact with an infected individual, consuming contaminated food or water, or through vectors for example, being bitten by a mosquito carrying the disease.

The focus on transmission to humans dominates the global narrative of zoonoses, which include West Nile, rabies, Lyme and others. But certain pockets of the zoological research community focus on the reverse: humans transmitting zoonoses to wildlife, known as zooanthroponosis or anthroponosis.

In the current case of COVID-19, researchers of non-human primates have sounded alarm bells for the risks humans pose for transmitting SARS-CoV-2, the viral pathogen that causes the COVID-19 or coronavirus disease, to species of primates, including monkeys and apes. Being among some of the worlds most endangered species, of particular concern are wild great apes, including bonobos, eastern and western gorillas, orangutans and chimpanzees.

These types of outbreaks can have really devastating effects on primate populations, says says Amanda Melin, a biological anthropologist who runs the Primate Genomics and Ecology lab at the University of Calgary. This is a great example of the risks that we pose to other animals in the earth.

So far, there have been no positive tests of COVID-19 in wild great apes but the deadliness of the disease, should transmission occur, is likely high.

Its the quickest study Ive ever been involved in, says Melin of a study she co-led with Mareike Janiak, a postdoctoral scholar in molecular anthropology, and James Higham, a primate evolutionary biologist at New York University, that helps dispel the guesswork of which non-human primate species are at greatest risk. The study was conducted within about seven days in early April and posted to a preprint server shortly thereafter because of the urgency of its findings, which examine the genetics behind how the SARS-CoV-2 pathogen triggers the COVID-19 disease itself.

In order for a viral pathogen to take hold in a host, the proteins on its surface must bind with certain proteins on the surfaces of a hosts cells. Once the pathogens protein has found its cellular protein match, known as a receptor, the pathogen can enter the cell and trigger the disease. Coronavirus pathogens not just of COVID-19, but of other coronaviruses as well express spike proteins on their surfaces.

If the viruss protein cant find anywhere to bind, then its not going to become infectious, Melin puts simply.

Genes determine which proteins are formed on which cells. Melins study examines the coding sequence of the ACE2gene, which codes the cellular protein (the ACE2 receptor) for the SARS-CoV-2 pathogen. These receptors are found in endothelial tissues throughout the body, including in the lungs, hence the diseases respiratory effects.

As is the case concerning most forms of life, less diversity means less resilience to threat, and so too does it go for genetic predisposition to COVID-19.

Proteins are made of amino acids. Genes can vary in the sequences of their comprising DNA, and the variants of a gene will code protein receptors with different structures of their amino acids. Receptors with a range of structures make it more difficult for a pathogen to find its match.

With that context, consider this statement from Melins study: Here, we show that all apes, including chimpanzees, bonobos, gorillas, and orangutans, and all African and Asian monkeys, exhibit the same set of twelve key amino acid residues as human ACE2.

In other words, we and many of our primate cousins are in the same boat of being highly susceptible because we have highly similar ACE2 genes and receptors, making it easier for the SARS-CoV-2 pathogen to find its binding match on our cells.

Interestingly, the study found that monkeys in the Americas, and some tarsiers, lemurs and lorisoids, had more ACE2 genetic variation, indicating that many species are likely less susceptible. However, Melin warns, some lemur species are also likely to be highly susceptible, which is worrying as they are also among the most endangered primates.

(Bats, notorious for being hosts and spreaders of coronaviruses, have exceptionally high ACE2 genetic variation. Within just the handful of bat species that we looked at, we saw genetic variation equivalent to the variation we saw across the entire range of other mammals we included, says Melin.)

Its easy to imagine that were closely related to other non-human primates, and so we should be careful with diseases. But knowing that they have the exact same sites and should be equally susceptible to us, and seeing what its doing to humans around the world its really concerning.

At the end of 2016 and into early 2017, chimpanzees in the Ta forest were seen with cold-like symptoms. While it did not prove deadly, the illness was found by researchers to have been a coronavirus passed to the chimpanzees from humans, likely poachers.

Similar to Gombe, disease is the leading challenge for conservation of chimpanzees at Ta, says Thomas Gillespie, whose work with wild great apes in Africa includes directing theGombe Ecosystem Health Project, in addition to running the Gillespie Lab at Emory University. Because of that, were always alert to the risk of disease exposure from people. The Ta team, 10 years ago or so, had a major respiratory outbreak that killed all the young chimpanzees

The tell-tale signs of COVID-19 are likely also the same for human and non-human primates, namely dry cough and fever.

We expect to see human-like symptoms, or more extreme versions of those. Laboratory-based infection of macaques resulted in similar disease progression to what were seeing in humans, says Gillespie.

Because best practices of wildlife conservation, and especially with wild great apes, demand limited human interaction, researchers rely on technology to check animals for symptoms from a safe and hidden distance. Laser thermometers are used to check fecal masses immediately after defecation to determine body temperatures. Blood meals from mosquitos are tested to keep track of pathogens circulating between them and animals. Carrion flies, which feast on dead animals, can give insights on mortality.

The Cross River gorillas, for example we never see them because theyre very cryptic, says Gillespie of the critically endangered species. Only an estimated 200 or 300 remain, residing at the border of Nigeria and Cameroon. But the flies are still going to find them. Flies are going to let us know if theres a spike in mortality. And then that can alert us to potential issues.

Should COVID-19 begin to be found in wild great apes, there is good and bad news. The bad is that quarantining isnt an option. Because of group dynamics, individual animals within most groups cannot be removed They dont respond well it tends to go quite badly, says Gillespie making the likelihood of virus spreading to the entire group of a single infected animal quite high.

And, once a wild animal has left the wild, he adds, there are tremendous threats involved with putting them back in the wild because we might have exposed them to additional pathogens in the sanctuary setting.

So we cant think about things like darting individuals, removing them from the group, quarantining them. We have to really focus on them not becoming infected. And thats the most important thing.

Gillespie nonetheless expects the virus to make its way into at least some populations of wild apes populations. The key now is to understand how it is likely to spread among species, based on exposure as well as the apes behavior and ecology. For example, in some places, habituated apes those accustomed to proximity to humans might be exposed to SARS-CoV-2, but will likely never come into contact with non-habituated apes. In other areas, this might not be the case.

And in yet other areas, monkeys that share habitats with apes baboons and vervet monkeys in Africa; macaques in Asia might spread the virus among great ape groups, or act as intermediaries, carrying the virus from humans to great apes.

This is something were actively working on, says Gillespie, who is leading a team focused on creating a model of sites across Africa and Asia to guide location-based best practices for ape conservation during the pandemic. Were modeling the different ape species, including variables like demographics, behavioral ecology, and proximity to humans and other susceptible species. This can all influence the dynamics of transmission to wild great apes.

Many protected areas inhabited by wild great apes have quickly developed lockdown measures of their own, such as shutting down tourism, logging and mining operations and extensively testing staff and researchers.

One of the major efforts currently addressing this is led by the Primate Specialist Group and the Wildlife Health Specialist Group, both of the International Union for Conservation of Nature. The two groups released a joint statement in early March, listing ways that humans can minimize risks to wild great apes, including disinfecting their footwear, wearing surgical masks, quarantining when coming from abroad, and immediately leaving an area when feeling the need to cough or sneeze and not returning.

But for local communities who depend on the use of certain forests, current measures might mean theyre left without a livelihood. To this end, the IUCN has created a task force, which includes Gillespie, focused on COVID-19s impacts on areas where wildlife and communities share and depend on the same ecosystems. One component of this effort has been distributing funds to communities that might otherwise be forced to resort to actions that could threaten wildlife.

Melins and Gillespies studies and others like them are proving crucial tools for these conservationists to know where and how to allocate resources to protect species highly vulnerable to the disease, as well as provide scientific backing to policy- and decision-makers about the vulnerability of these species.

Even after the heightened phase of the pandemic has lessened, changes must continue to be made, she says: For primate observational research, we need to continue to be really careful about quarantining ourselves and about our proximities, always using best practices when were interacting with non-human primates. More generally, I hope we can slow and then stop the illegal trade of wildlife, which might help prevent future, different outbreaks.

And then she broadens her thoughts: How will it feel collectively, as humans, if were responsible for the rapid extermination of these species from the Earth?

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What the genetics of COVID-19 mean for the survival of wild great apes - Landscape News

Genetics

Are genetics a factor in COVID-19 severity? – KOIN.com

PORTLAND, Ore. (KOIN) President Donald Trump announced Friday that his administration was declaring houses of worship as essential services. He said that the declaration would allow them to reopen in spite of local stay-home orders.

KOIN 6 News spoke to local religious leaders to see if this order changes things for them. So far, two have said no, they are going to opt to remain closed in the name of safety for their members and for the community. The senior minister at First Unitarian Church in Portland and a spokesperson for the Ahmadiyya Muslim Community both said they are keeping their doors closed for the time being.

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Are genetics a factor in COVID-19 severity? - KOIN.com

Genetics

mRNA vaccines could provide a breakthrough for coronavirus and other illness – Boston Herald

A new vaccine platform that harnesses the power of genetics has been thrust into the public eye as the success of Modernas coronavirus vaccine continues to grow, which if proven safe and effective, would be the first of its kind.

Theres never been a successful vaccine developed this way before, so it would be very, very novel, which is exciting, but potentially risky, said Dr. Helen Boucher, chief of the division of geographic medicine and infectious diseases at Tufts Medical Center.

Messenger ribonucleic acid, or mRNA, is a chemical readout of DNA that can be transferred into cells to make proteins.

Dr. Mark Poznansky, director of the Vaccine and Immunotherapy Center at Massachusetts General Hospital, compared DNA to delivery of information to the immune system from a book about coronavirus, and RNA to a chapter or two about it.

You are fundamentally engineering the cells in your body to make a foreign protein from the virus that your immune system can then react to, said Poznansky.

The mRNA vaccine encodes proteins of a virus, which are inserted into a cell to trigger an immune response.

Cambridge-based company Modernas mRNA coronavirus vaccine is highly regarded by health experts and was created at lightning speed after the virus sequence was released.

The companys stock has soared and the vaccine attracted the attention of the public and top health officials alike.

The vaccine has shown positive results in early participants of its Phase 1 study and after two doses, all participants showed binding antibody levels and neutralizing antibody levels that were at or above those who have recovered from coronavirus, according to Moderna.

There are several other mRNA coronavirus vaccines in development, such as one from Pfizer and German company BioNTech and another developed by PharmaJet and Tawainese company Abnova that uses needle-free technology.

If any make it past Phase 3 studies and onto consumers, it would be a major breakthrough, not just for the coronavirus pandemic, but for accelerated vaccine development in general, said Poznansky.

We always need more platforms that generate effective vaccines and having an additional one based on mRNA would be a great advantage, said Poznansky.

He added, If it turned out to be safe and effective in Phase 3 studies, that would be enormous success.

But making it to Phase 3 is pretty rare, said Poznansky, and safety is key in vaccine development.

In many ways we are very, very early on in this very accelerated process of multiple platforms going after a target and I think thats our biggest advantage at this point, there are lots of horses in the race, said Poznansky.

A report published in Nature Research Journal said the mRNA vaccine field is developing quickly and the technology offers a lot of positives.

mRNA is non-infectious, can be administered repeatedly and modifications can make it stable and highly translatable, the report states.

The vaccines have potential for rapid, cheap scalability, as well, the paper said.

Many drugs, therapies and interventions are being developed to combat the coronavirus crisis, but a vaccine will make the ultimate impact.

To really impact disease on a global level we are going to need a vaccine, said Boucher.

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mRNA vaccines could provide a breakthrough for coronavirus and other illness - Boston Herald

Genetics

Enhancing food diversity in the midst of a climate crisis: How plant genetic material ensures future food security – Kenya – ReliefWeb

Throughout history 6 000 -- 7 000 plant species have been cultivated for food. Yet today 40 percent of our daily calories come from just three crops: rice, wheat and maize. Humans depend on little more than 30 plant species, many of which are struggling in the face of today's environmental changes. With biodiversity and entire ecosystems in serious decline, the International Treaty on Plant Genetic Resources for Food and Agriculture plays an increasingly important role in promoting farmers and their essential contribution to diversifying the crops that feed the world. The Treaty was negotiated by FAO and the Commission on Genetic Resources for Food and Agriculture (CGRFA) and adopted in 2001 to create a global system that provides farmers, plant breeders and scientists with access to plant genetic materials.

The genetic material in each variety of species is unique and precious. Derived from human and natural selection for many decades, these genetics are fundamental to our future of food. Genetic material ensures agricultural biodiversity and gives different species the ability to cope with changes, whether it be climate change, new pests and diseases, drought and even flooding. The Treaty's Benefit-sharing Fund invests in projects that conserve and develop crop genetic resources to improve food security in cooperation with farmers.

Here are three examples of how this Treaty has helped farming communities in developing countries cope with climate change and other environmental threats.

1. Exchanging and developing biodiverse potato varieties in Peru, Nepal and Bhutan

There are over 4 000 native varieties of potato growing in the Andean highlands. These varieties are well-adapted to harsh conditions and a changing climate. In contrast, Nepal and Bhutan have only two locally adapted potato varieties but face similar conditions and environmental threats as the Andes. With this in mind, the project sought to reduce the vulnerability of these mountain communities by introducing potatoes that are more resilient to extreme temperatures and offer better nutritional quality. Working closely with the International Potato Centre in Peru, farmers in Nepal and Bhutan became directly involved in selecting new, high-yielding, resilient and biodiverse varieties of potato. The genetic material from these potatoes has since been conserved, multiplied and used by national agricultural research systems in all three countries.

** 2. Conserving plant genetic resources to improve food and nutrition in Zimbabwe, Malawi and Zambia

Being heavily reliant on the success of the maize crop, communities in Zimbabwe, Malawi and Zambia have in recent years faced a severe food shortage because maize crops have been unable to withstand the effects of climate change, such as higher temperatures and torrential rains. "Because of the changing climate, our farm was producing less food, and most crops have not been doing so well apart from millet and sorghum," explained Lovemore Tachokere, a smallholder farmer from Malawi. Through the Benefit-sharing fund and the introduction of 159 Farmer Field Schools across the three countries, farmers were given support and a voice. They started introducinglost varieties of different crops, creating diversity in their fields that also ensured more varied and nutritious diets. As part of the project a total of 300 lost or forgotten small grain crop varieties were retrieved from national, regional and international gene banks as part of the Treaty's Multilateral System. These seeds are now available to farmers and scientists for further study and the development of new climate-smart varieties.

3. Ensuring a resilient cassava crop in Tanzania and Kenya

Cassava is the third largest source of carbohydrates in the world, playing a particularly important role in agriculture in sub-Saharan Africa because it does well in poor soils and with low rainfall. Additionally, because it is a perennial, cassava acts as a famine reserve. In recent years, however, extreme temperatures, drought, flooding and a new virus, provoking 'brown streak disease', have affected cassava cultivation in the region. In Tanzaniaand Kenya, a project implemented through the Benefit-sharing Fund has led to new, more resistant and tolerant cassava breeding lines, including 30 that are heat and disease tolerant. While the farmers are now experimenting with planting new cassava varieties and using improved agricultural practices, breeders and scientists have access to improved plant material from which to select essential genetic material for future use. Community seed banks have been established through the Benefit-sharing Fund in conjunction with Farmer Field Schools and are an important initiative to collect and conserve local crop varieties. They function as a platform for farmers to control and make informed decisions on the conservation of agrobiodiversity and the cultivation of a variety of crops with nutritional value.

In the 15 years since it came into force, the International Treaty hosted by FAO has created the largest global gene pool for sharing plant material for food and agriculture, the Multilateral System of Access and Benefit-sharing (MLS). The Benefit-sharing Fund has supported over one million people through 80 agricultural development projects in 67 developing countries. These projects are clear examples of how effective the sharing of skills and knowledge across continents can be and they are crucial in the race to meet the Sustainable Development Goals (SDGs), in particular SDG 15 (Life on Land) and SDG2 (Zero Hunger). Projects under the Benefit-sharing Fund are an indication that FAO's Strategy on mainstreaming biodiversity across agricultural sectors is already taking shape and showing positive results, demonstrating that the greater the diversification of crops, the more food secure a community can become and the more resilient they find themselves in the face of current threats like climate change, pests and disease.

Original post:
Enhancing food diversity in the midst of a climate crisis: How plant genetic material ensures future food security - Kenya - ReliefWeb