Coronavirus- coronavirus symptoms,coronavirus prevention,coronavirus origin,coronavirus treatment
Coronavirus disease
COVID-19 is a respiratory caused disease that was first reported in China in December 2019. Because this is a new disease, doctors are still learning about it. You can expect them, along with other health experts, to provide new information about it frequently. A coronavirus is a virus that is found in animals and, rarely, can be transmitted from animals to humans and then spread person to person. Coronavirus (COVID-19), the new name for the disease being caused by the recent coronavirus, SARS-CoV-2 is all over the news. You may hear one thing from one source, then hear the opposite thing from another source. That makes it hard to know what’s true.
The SARS virus, or severe acute respiratory syndrome, which first occurred in the Guangdong province in southern China.
Coronavirus Origin
Coronaviruses are common in certain species of animals, such as cattle and camels. Although the transmission of coronaviruses from animals to humans is rare, this new strain likely came from bats, though one study suggests pangolins may be the origin. However, it remains unclear exactly how the virus first spread to humans.
Some reports trace the earliest cases back to a seafood and animal market in Wuhan. It may have been from here that SARS-CoV-2 started to spread to humans.
The analysis of public genome sequence data from SARS-CoV-2 and related viruses found no evidence that the virus was made in a laboratory or otherwise engineered.
“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, Ph.D., 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 the 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).
On December 31 of last year, Chinese authorities alerted the World Health Organization of an outbreak of a novel strain of coronavirus causing severe illness, which was subsequently named SARS-CoV-2. As of February 20, 2020, nearly 167,500 COVID-19 cases have been documented, although many more mild cases have likely gone undiagnosed. The virus has killed over 6,600 people.
Shortly after the epidemic began, Chinese scientists sequenced the genome of SARS-CoV-2 and made the data available to researchers worldwide. The resulting genomic sequence data has shown that Chinese authorities rapidly detected the epidemic and that the number of COVID-19 cases has been increasing because of human to human transmission after a single introduction into the human population. Andersen and collaborators at several other research institutions used this sequencing data to explore the origins and evolution of SARS-CoV-2 by focusing on several tell-tale features of the virus.
The scientists analyzed the genetic template for spike proteins, armatures on the outside of the virus that it uses to grab and penetrate the outer walls of human and animal cells. More specifically, they 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 the natural evolution of Coronavirus
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 form 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, rule out laboratory manipulation as a potential origin for SARS-CoV-2,” said Andersen.
Josie Golding, Ph.D., 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. For instance, some coronaviruses from pangolins, armadillo-like mammals found in Asia and Africa, have an RBD structure very similar to that of SARS-CoV-2. A coronavirus from a pangolin could possibly have been transmitted to a human, either directly or through an intermediary host such as civets or ferrets.
Then the other distinct spike protein characteristic of SARS-CoV-2, the cleavage site, could have evolved within a human host, possibly via limited undetected circulation in the human population prior to the beginning of the epidemic. The researchers found that the SARS-CoV-2 cleavage site appears similar to the cleavage sites of strains of bird flu that have been shown to transmit easily between people. SARS-CoV-2 could have evolved such a virulent cleavage site in human cells and soon kicked off the current epidemic, as the coronavirus would possibly have become far more capable of spreading between people.
Study co-author Andrew Rambaut cautioned that it is difficult if not impossible to know at this point which of the scenarios is most likely. If the SARS-CoV-2 entered humans in its current pathogenic form from an animal source, it raises the probability of future outbreaks, as the illness-causing strain of the virus could still be circulating in the animal population and might once again jump into humans. The chances are lower of a non-pathogenic coronavirus entering the human population and then evolving properties similar to SARS-CoV-2.
Coronavirus symptoms
Common symptoms of COVID-19 include a fever, cough, and shortness of breath. The Centers for Disease Control and Prevention considers a person to have a fever when he or she has a measured temperature of at least 100.4 °F [38 °C]. These symptoms may occur 2 to 14 days after being exposed to the virus. Most people who come down with COVID-19 have mild symptoms. These symptoms can make you feel like you have the flu. However, some people have more severe symptoms. In these cases, the virus may lead to pneumonia.
Around the world, more than 100,000 people (as of the date of this article) so far have had Coronavirus (COVID-19). In comparison, at least 22 million people in the United States have had influenza this season.
If you or someone in your family begins to feel sick, stay home. Don’t go to work or school. Call your doctor. He or she will advise what you should do next. If you or someone in your family develops a fever, cough, and has trouble breathing, call your doctor right away or go to the emergency room.
Coronavirus Treatment
A drug used in Japan to treat influenza seems to be effective at treating the novel coronavirus that causes COVID-19, according to news reports.
The antiviral drug, called Favipiravir or Avigan, showed positive outcomes in clinical trials involving 340 individuals in Wuhan and Shenzhen, said Zhang Xinmin, of China’s science and technology ministry.
Developed by Fujifilm Toyama Chemical, the antiviral drug is being manufactured by Zhejiang Hisun Pharmaceutical for treating influenza viruses. Last month, the drug reportedly received approval as an experimental treatment for COVID-19 infections, Pharmaceutical Technology reported.
Patients in Shenzhen who had tested positive for COVID-19 and who were given the drug got a negative virus test back four days later, as a median (half showed a negative test earlier and half later than four days). That was compared with a negative test about 11 days later, as a median, for patients not on the drug, according to news reports. In that same trial, lung conditions (as shown in X-rays) improved in about 91% of patients taking Favipiravir, compared with just 62% who weren’t taking the antiviral drug.
In the Wuhan trial, the drug also seemed to shorten the duration of a patient’s fever from an average of 4.2 days to 2.5 days, according to Pharmaceutical Technology.
The drug is specifically made to treat RNA viruses like SARS-CoV-2; these are viruses whose main genetic material is RNA, rather than DNA. The drug stops some viruses from replicating by crippling the enzyme (a substance that gets chemical reactions going) called RNA polymerase, which builds RNA. Without that enzyme intact, the virus can’t duplicate its genetic material efficiently once inside a host cell, according to an article describing the drug that was published in 2017 in the journal Proceedings of the Japan Academy, Ser. B, Physical, and Biological Sciences.
However, the drug seems less effective in patients with severe symptoms. “We’ve given Avigan to 70 to 80 people, but it doesn’t seem to work that well when the virus has already multiplied,” a source from the Japanese Health Ministry told the Mainichi Shimbun newspaper, according to The Guardian.
Doctors are using the same drug in Japan to treat coronavirus patients with mild to moderate symptoms, The Guardian reported. In addition, results from these trials have not been published in a peer-reviewed scientific journal and seem to be just preliminary findings.
To date, there is no approved or known drug to treat SARS-CoV-2. However, antiviral drugs developed to treat other illnesses are being tested for their use in treating the coronavirus. For instance, Remdesivir was developed to treat Ebola but it has shown promise in treating monkeys infected with another coronavirus, the Middle East respiratory syndrome (MERS); that drug is currently being tested in China and the U.S., according to NBC News.
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