What is the symptom when you are infected the COVID-19 virus.
Signs and symptoms of COVID-19 may appear 2 to 14 days after exposure and can include:
- Shortness of breath or difficulty breathing
Other symptoms can include:
- Runny nose
- Sore throat
- Some people have experienced the loss of smell or taste.
The severity of COVID-19 symptoms can range from very mild to severe. Some people may have no symptoms at all. People who are older or who have existing chronic medical conditions, such as heart disease, lung disease or diabetes, or who have compromised immune systems may be at higher risk of serious illness. This is similar to what is seen with other respiratory illnesses, such as influenza.
Infection with the new coronavirus (severe acute respiratory syndrome coronavirus 2, or SARS-CoV-2) causes coronavirus disease 2019 (COVID-19).
It's unclear exactly how contagious the new coronavirus is. Data has shown that it spreads from person to person among those in close contact (within about 6 feet, or 2 meters). The virus spreads by respiratory droplets released when someone with the virus coughs, sneezes or talks.
It can also spread if a person touches a surface with the virus on it and then touches his or her mouth, nose or eyes.
Risk factors for COVID-19 appear to include:
Recent travel from or residence in an area with ongoing community spread of COVID-19 as determined by CDC or WHO
Close contact with someone who has COVID-19 — such as when a family member or health care worker takes care of an infected person
Although most people with COVID-19 have mild to moderate symptoms, the disease can cause severe medical complications and lead to death in some people. Older adults or people with existing chronic medical conditions are at greater risk of becoming seriously ill with COVID-19.
Complications can include:
Pneumonia in both lungs
Organ failure in several organs
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, 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).
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 have 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 in 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 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. 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 has 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.
Funding for the research was provided by the US National Institutes of Health, the Pew Charitable Trusts, the Wellcome Trust, the European Research Council, and an ARC Australian Laureate Fellowship.
Claim: ‘It is mutating into a more deadly strain’
All viruses accumulate mutations over time and the virus that causes Covid-19 is no different. How widespread different strains of a virus become depends on natural selection – the versions that can propagate quickest and replicate effectively in the body will be the most “successful”. This doesn’t necessarily mean most dangerous for people though, as viruses that kill people rapidly or make them so sick that they are incapacitated may be less likely to be transmitted.
Genetic analysis by Chinese scientists of 103 samples of the virus, taken from patients in Wuhan and other cities, suggests that early on two main strains emerged, designated L and S. Although the L strain appeared to be more prevalent than the S strain (about 70% of the samples belonged to the former), the S branch of the virus was found to be the ancestral version.
The team behind this research suggested that this may indicate the L strain is more “aggressive”, either transmitting more easily or replicating faster inside the body. However, this theory is speculative at this stage – there haven’t yet been direct comparisons to see whether people who catch one version of the virus are more likely to pass it on or suffer more severe symptoms.
Claim: ‘It is no more dangerous than winter flu’
Many individuals who get coronavirus will experience nothing worse than seasonal flu symptoms, but the overall profile of the disease, including its mortality rate, looks more serious. At the start of an outbreak the apparent mortality rate can be an overestimate if a lot of mild cases are being missed. But Bruce Aylward, a WHO expert, who led an international mission to China to learn about the virus and the country’s response, said this has not been the case with Covid-19. The evidence did not suggest that we were only seeing the tip of the iceberg. If borne out by further testing, this could mean that current estimates of a roughly 1% fatality rate are accurate. This would make Covid-19 about 10 times more deadly than seasonal flu, which is estimated to kill between 290,000 and 650,000 people a year globally.
Claim: ‘It only kills the elderly, so younger people can relax’
Most people who are not elderly and do not have underlying health conditions will not become critically ill from Covid-19. But the illness still has a higher chance of leading to serious respiratory symptoms than seasonal flu and there are other at-risk groups – health workers, for instance, are more vulnerable because they are likely to have higher exposure to the virus. The actions that young, healthy people take, including reporting symptoms and following quarantine instructions, will have an important role in protecting the most vulnerable in society and in shaping the overall trajectory of the outbreak.
Claim: ‘You need to be with an infected person for 10 minutes’
For flu, some hospital guidelines define exposure as being within six feet of an infected person who sneezes or coughs for 10 minutes or longer. However, it is to be infected with shorter interactions or even by picking the virus up from contaminated surfaces, although this is thought to be a less common route of transmission.
Claim: ‘A vaccine could be ready within a few months’
Scientists were quick out of the gates in beginning development of a vaccine for the new coronavirus, helped by the early release of the genetic sequence by Chinese researchers. The development of a viable vaccine continues apace, with several teams now testing candidates in animal experiments. However, the incremental trials required before a commercial vaccine could be rolled out are still a lengthy undertaking – and an essential one to ensure that even rare side-effects are spotted. A commercially available vaccine within a year would be quick.’