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The novel SARS-CoV-2 coronavirus that emerged in the city of Wuhan, China, last year and has since caused a large scale COVID-19 epidemic and spread to more than 190 other countries is the product of natural evolution, according to findings published in the journal Nature Medicine.
“By comparing the available genome sequence data for known coronavirus strains, we can firmly determine that SARS-CoV-2 originated through natural processes,” said Kristian Andersen, PhD, an associate professor of immunology and microbiology at Scripps Research and corresponding author on the paper. In addition to Andersen, authors on the paper, “The proximal origin of SARS-CoV-2,” include Robert F. Garry, of Tulane University; Edward Holmes, of the University of Sydney; Andrew Rambaut, of University of Edinburgh; W. Ian Lipkin, of Columbia University.
Coronaviruses are a large family of viruses that can cause illnesses ranging widely in severity. The first known severe illness caused by a coronavirus emerged with the 2003 Severe Acute Respiratory Syndrome (SARS) epidemic in China. A second outbreak of severe illness began in 2012 in Saudi Arabia with the Middle East Respiratory Syndrome (MERS).
Shortly after the epidemic began, Chinese scientists sequenced the genome of SARS-CoV-2 and made the data available to researchers worldwide.
Andersen and collaborators focused on two important features of the spike protein: the receptor-binding domain (RBD), a kind of grappling hook that grips onto host cells, and the cleavage site, a molecular can opener that allows the virus to crack open and enter host cells.
Evidence for natural evolution
The scientists found that the RBD portion of the SARS-CoV-2 spike proteins had evolved to effectively target a molecular feature on the outside of human cells called ACE2, a receptor involved in regulating blood pressure. The SARS-CoV-2 spike protein was so effective at binding the human cells, in fact, that the scientists concluded it was the result of natural selection and not the product of genetic engineering.
This evidence for natural evolution was supported by data on SARS-CoV-2’s backbone — its overall molecular structure . If someone were seeking to engineer a new coronavirus as a pathogen, they would have constructed it from the backbone of a virus known to cause illness. But the scientists found that the SARS-CoV-2 backbone differed substantially from those of already known coronaviruses and mostly resembled related viruses found in bats and pangolins.
“These two features of the virus, the mutations in the RBD portion of the spike protein and its distinct backbone, rules out laboratory manipulation as a potential origin for SARS-CoV-2” said Andersen.
Josie Golding, PhD, epidemics lead at UK-based Wellcome Trust, said the findings by Andersen and his colleagues are “crucially important to bring an evidence-based view to the rumors that have been circulating about the origins of the virus (SARS-CoV-2) causing COVID-19.”
“They conclude that the virus is the product of natural evolution,” Goulding adds, “ending any speculation about deliberate genetic engineering.”
Possible origins of the virus
Based on their genomic sequencing analysis, Andersen and his collaborators concluded that the most likely origins for SARS-CoV-2 followed one of two possible scenarios.
In one scenario, the virus evolved to its current pathogenic state through natural selection in a non-human host and then jumped to humans. This is how previous coronavirus outbreaks have emerged, with humans contracting the virus after direct exposure to civets (SARS) and camels (MERS). The researchers proposed bats as the most likely reservoir for SARS-CoV-2 as it is very similar to a bat coronavirus. There are no documented cases of direct bat-human transmission, however, suggesting that an intermediate host was likely involved between bats and humans.
In this scenario, both of the distinctive features of SARS-CoV-2’s spike protein — the RBD portion that binds to cells and the cleavage site that opens the virus up — would have evolved to their current state prior to entering humans. In this case, the current epidemic would probably have emerged rapidly as soon as humans were infected, as the virus would have already evolved the features that make it pathogenic and able to spread between people.
In the other proposed scenario, a non-pathogenic version of the virus jumped from an animal host into humans and then evolved to its current pathogenic state within the human population.
How long does Covid-19 survive on surfaces?
As scientists around the globe work to understand the source of the pandemic, new research from the National Institutes of Health, CDC, UCLA and Princeton University scientists published in The New England Journal of Medicine where they attempted to mimic the virus being deposited from an infected person onto everyday surfaces in a household or hospital setting, such as through coughing or touching objects. The scientists then investigated how long the virus remained infectious on these surfaces.
The results provide key information about the stability of SARS-CoV-2, which causes COVID-19 disease, and suggests that people may acquire the virus through the air and after touching contaminated objects and it found:
- coronavirus 2 (SARS-CoV-2) was detectable in aerosols for up to three hours;
- up to four hours on copper;
- up to 24 hours on cardboard; and
- up to two to three days on plastic and stainless steel.
Can our bodies fight the virus?
Melbourne researchers have mapped immune responses from Australian infected patients, showing the body’s ability to fight the virus and recover from the infection.
Researchers at the Peter Doherty Institute for Infection and Immunity (Doherty Institute) — a joint venture between the University of Melbourne and the Royal Melbourne hospital — were able to test blood samples at four different time points in an otherwise healthy woman in her 40s, who presented with COVID-19 and had mild-to-moderate symptoms requiring hospital admission.
Published in Nature Medicine, one of the authors on the paper, research fellow Dr Oanh Nguyen said this was the first time that broad immune responses to COVID-19 have been reported.
“We looked at the whole breadth of the immune response in this patient using the knowledge we have built over many years of looking at immune responses in patients hospitalised with influenza,” Dr Nguyen said. “Three days after the patient was admitted, we saw large populations of several immune cells, which are often a tell-tale sign of recovery during seasonal influenza infection, so we predicted that the patient would recover in three days, which is what happened.”
The research team was able to do this research so rapidly thanks to SETREP-ID (Sentinel Travellers and Research Preparedness for Emerging Infectious Disease), led by Royal Melbourne Hospital Infectious Diseases Physician Dr Irani Thevarajan at the Doherty Institute.
SETREP-ID is a platform that enables a broad range of biological sampling to take place in returned travellers in the event of a new and unexpected infectious disease outbreak, which is exactly how COVID-19 started in Australia.
“When COVID-19 emerged, we already had ethics and protocols in place so we could rapidly start looking at the virus and immune system in great detail,” Dr Thevarajan said. “Already established at a number of Melbourne hospitals, we now plan to roll out SETREP-ID as a national study.”
Working together with University of Melbourne Professor Katherine Kedzierska, a laboratory head at the Doherty Institute and a world-leading influenza immunology researcher, the team were able to dissect the immune response leading to successful recovery from COVID-19, which might be the secret to finding an effective vaccine.
“We showed that even though COVID-19 is caused by a new virus, in an otherwise healthy person, a robust immune response across different cell types was associated with clinical recovery, similar to what we see in influenza,” Professor Kedzierska said. “This is an incredible step forward in understanding what drives recovery of COVID-19. People can use our methods to understand the immune responses in larger COVID-19 cohorts, and also understand what’s lacking in those who have fatal outcomes.”
Dr Thevarajan said that current estimates show more than 80% of COVID-19 cases are mild-to-moderate, and understanding the immune response in these mild cases is very important research.
“We hope to now expand our work nationally and internationally to understand why some people die from COVID-19, and build further knowledge to assist in the rapid response of COVID-19 and future emerging viruses,” she said.
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