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“[The coronavirus] can attack almost anything in the body with devastating consequences” cardiologist Harlan Krumholz of Yale University.The coronavirus wreaked extensive damage (yellow) on the lungs of a 59-year-old man who died at George Washington University Hospital, as seen in a 3D model based on computerized tomography scans.Share from ScienceHow does coronavirus kill? Clinicians trace a ferocious rampage through the body, from brain to toesBy Meredith Wadman, Jennifer Couzin-Frankel, Jocelyn Kaiser, Catherine MatacicApr. 17, 2020 , 6:45 PMScience’s COVID-19 reporting is supported by the Pulitzer Center.On rounds in a 20-bed intensive care unit (ICU) one recent day, physician Joshua Denson assessed two patients with seizures, many with respiratory failure and others whose kidneys were on a dangerous downhill slide. Days earlier, his rounds had been interrupted as his team tried, and failed, to resuscitate a young woman whose heart had stopped. All shared one thing, says Denson, a pulmonary and critical care physician at the Tulane University School of Medicine. “They are all COVID positive.”As the number of confirmed cases of COVID-19 surges past 2.2 million globally and deaths surpass 150,000, clinicians and pathologists are struggling to understand the damage wrought by the coronavirus as it tears through the body. They are realizing that although the lungs are ground zero, its reach can extend to many organs including the heart and blood vessels, kidneys, gut, and brain.“[The disease] can attack almost anything in the body with devastating consequences,” says cardiologist Harlan Krumholz of Yale University and Yale-New Haven Hospital, who is leading multiple efforts to gather clinical data on COVID-19. “Its ferocity is breathtaking and humbling.”Understanding the rampage could help the doctors on the front lines treat the fraction of infected people who become desperately and sometimes mysteriously ill. Does a dangerous, newly observed tendency to blood clotting transform some mild cases into life-threatening emergencies? Is an overzealous immune response behind the worst cases, suggesting treatment with immune-suppressing drugs could help? What explains the startlingly low blood oxygen that some physicians are reporting in patients who nonetheless are not gasping for breath? “Taking a systems approach may be beneficial as we start thinking about therapies,” says Nilam Mangalmurti, a pulmonary intensivist at the Hospital of the University of Pennsylvania (HUP).What follows is a snapshot of the fast-evolving understanding of how the virus attacks cells around the body, especially in the roughly 5% of patients who become critically ill. Despite the more than 1000 papers now spilling into journals and onto preprint servers every week, a clear picture is elusive, as the virus acts like no microbe humanity has ever seen. Without larger, prospective controlled studies that are only now being launched, scientists must pull information from small studies and case reports, often published at warp speed and not yet peer reviewed. “We need to keep a very open mind as this phenomenon goes forward,” says Nancy Reau, a liver transplant physician who has been treating COVID-19 patients at Rush University Medical Center. “We are still learning.”The infection beginsWhen an infected person expels virus-laden droplets and someone else inhales them, the novel coronavirus, called SARS-CoV-2, enters the nose and throat. It finds a welcome home in the lining of the nose, according to a preprint from scientists at the Wellcome Sanger Institute and elsewhere. They found that cells there are rich in a cell-surface receptor called angiotensin-converting enzyme 2 (ACE2). Throughout the body, the presence of ACE2, which normally helps regulate blood pressure, marks tissues vulnerable to infection, because the virus requires that receptor to enter a cell. Once inside, the virus hijacks the cell’s machinery, making myriad copies of itself and invading new cells.As the virus multiplies, an infected person may shed copious amounts of it, especially during the first week or so. Symptoms may be absent at this point. Or the virus’ new victim may develop a fever, dry cough, sore throat, loss of smell and taste, or head and body aches.If the immune system doesn’t beat back SARS-CoV-2 during this initial phase, the virus then marches down the windpipe to attack the lungs, where it can turn deadly. The thinner, distant branches of the lung’s respiratory tree end in tiny air sacs called alveoli, each lined by a single layer of cells that are also rich in ACE2 receptors.Normally, oxygen crosses the alveoli into the capillaries, tiny blood vessels that lie beside the air sacs; the oxygen is then carried to the rest of the body. But as the immune system wars with the invader, the battle itself disrupts this healthy oxygen transfer. Front-line white blood cells release inflammatory molecules called chemokines, which in turn summon more immune cells that target and kill virus-infected cells, leaving a stew of fluid and dead cells—pus—behind. This is the underlying pathology of pneumonia, with its corresponding symptoms: coughing; fever; and rapid, shallow respiration. Some COVID-19 patients recover, sometimes with no more support than oxygen breathed in through nasal prongs.But others deteriorate, often quite suddenly, developing a condition called acute respiratory distress syndrome (ARDS). Oxygen levels in their blood plummet and they struggle ever harder to breathe. On x-rays and computerized tomography scans, their lungs are riddled with white opacities where black space—air—should be. Commonly, these patients end up on ventilators. Many die. Autopsies show their alveoli became stuffed with fluid, white blood cells, mucus, and the detritus of destroyed lung cells (see graphic).An invader’s impactIn serious cases, SARS-CoV-2 lands in the lungs and can do deep damage there. But the virus, or the body’s response to it, can injure many other organs. Scientists are just beginning to probe the scope and nature of that harm.V. ALTOUNIAN/SCIENCESome clinicians suspect the driving force in many gravely ill patients’ downhill trajectories is a disastrous overreaction of the immune system known as a “cytokine storm,” which other viral infections are known to trigger. Cytokines are chemical signaling molecules that guide a healthy immune response; but in a cytokine storm, levels of certain cytokines soar far beyond what’s needed, and immune cells start to attack healthy tissues. Blood vessels leak, blood pressure drops, clots form, and catastrophic organ failure can ensue.Some studies have shown elevated levels of these inflammation-inducing cytokines in the blood of hospitalized COVID-19 patients. “The real morbidity and mortality of this disease is probably driven by this out of proportion inflammatory response to the virus,” says Jamie Garfield, a pulmonologist who cares for COVID-19 patients at Temple University Hospital.But others aren’t convinced. “There seems to have been a quick move to associate COVID-19 with these hyperinflammatory states. I haven’t really seen convincing data that that is the case,” says Joseph Levitt, a pulmonary critical care physician at the Stanford University School of Medicine.He’s also worried that efforts to dampen a cytokine response could backfire. Several drugs targeting specific cytokines are in clinical trials in COVID-19 patients. But Levitt fears those drugs may suppress the immune response that the body needs to fight off the virus. “There’s a real risk that we allow more viral replication,” Levitt says.Meanwhile, other scientists are zeroing in on an entirely different organ system that they say is driving some patients’ rapid deterioration: the heart and blood vessels.Striking the heartIn Brescia, Italy, a 53-year-old woman walked into the emergency room of her local hospital with all the classic symptoms of a heart attack, including telltale signs in her electrocardiogram and high levels of a blood marker suggesting damaged cardiac muscles. Further tests showed cardiac swelling and scarring, and a left ventricle—normally the powerhouse chamber of the heart—so weak that it could only pump one-third its normal amount of blood. But when doctors injected dye in the coronary arteries, looking for the blockage that signifies a heart attack, they found none. Another test revealed why: The woman had COVID-19.How the virus attacks the heart and blood vessels is a mystery, but dozens of preprints and papers attest that such damage is common. A 25 March paper in JAMA Cardiology documented heart damage in nearly 20% of patients out of 416 hospitalized for COVID-19 in Wuhan, China. In another Wuhan study, 44% of 138 hospitalized patients had arrhythmias.The disruption seems to extend to the blood itself. Among 184 COVID-19 patients in a Dutch ICU, 38% had blood that clotted abnormally, and almost one-third already had clots, according to a 10 April paper in Thrombosis Research. Blood clots can break apart and land in the lungs, blocking vital arteries—a condition known as pulmonary embolism, which has reportedly killed COVID-19 patients. Clots from arteries can also lodge in the brain, causing stroke. Many patients have “dramatically” high levels of D-dimer, a byproduct of blood clots, says Behnood Bikdeli, a cardiovascular medicine fellow at Columbia University Medical Center.“The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19,” Bikdeli says.Infection may also lead to blood vessel constriction. Reports are emerging of ischemia in the fingers and toes—a reduction in blood flow that can lead to swollen, painful digits and tissue death.The more we look, the more likely it becomes that blood clots are a major player in the disease severity and mortality from COVID-19.Behnood Bikdeli, Columbia University Irving Medical CenterIn the lungs, blood vessel constriction might help explain anecdotal reports of a perplexing phenomenon seen in pneumonia caused by COVID-19: Some patients have extremely low blood-oxygen levels and yet are not gasping for breath. It’s possible that at some stages of disease, the virus alters the delicate balance of hormones that help regulate blood pressure and constricts blood vessels going to the lungs. So oxygen uptake is impeded by constricted blood vessels, rather than by clogged alveoli. “One theory is that the virus affects the vascular biology and that’s why we see these really low oxygen levels,” Levitt says.If COVID-19 targets blood vessels, that could also help explain why patients with pre-existing damage to those vessels, for example from diabetes and high blood pressure, face higher risk of serious disease. Recent Centers for Disease Control and Prevention (CDC) data on hospitalized patients in 14 U.S. states found that about one-third had chronic lung disease—but nearly as many had diabetes, and fully half had pre-existing high blood pressure.Mangalmurti says she has been “shocked by the fact that we don’t have a huge number of asthmatics” or patients with other respiratory diseases in HUP’s ICU. “It’s very striking to us that risk factors seem to be vascular: diabetes, obesity, age, hypertension.”Scientists are struggling to understand exactly what causes the cardiovascular damage. The virus may directly attack the lining of the heart and blood vessels, which, like the nose and alveoli, are rich in ACE2 receptors. Or perhaps lack of oxygen, due to the chaos in the lungs, damages blood vessels. Or a cytokine storm could ravage the heart as it does other organs.“We’re still at the beginning,” Krumholz says. “We really don’t understand who is vulnerable, why some people are affected so severely, why it comes on so rapidly … and why it is so hard [for some] to recover.”Multiple battlefieldsThe worldwide fears of ventilator shortages for failing lungs have received plenty of attention. Not so a scramble for another type of equipment: dialysis machines. “If these folks are not dying of lung failure, they’re dying of renal failure,” says neurologist Jennifer Frontera of New York University’s Langone Medical Center, which has treated thousands of COVID-19 patients. Her hospital is developing a dialysis protocol with different machines to support additional patients. The need for dialysis may be because the kidneys, abundantly endowed with ACE2 receptors, present another viral target.According to one preprint, 27% of 85 hospitalized patients in Wuhan had kidney failure. Another reported that 59% of nearly 200 hospitalized COVID-19 patients in and near Wuhan had protein and blood in their urine, suggesting kidney damage. Those with acute kidney injury (AKI), were more than five times as likely to die as COVID-19 patients without it, the same Chinese preprint reported.Medical staff work to help a COVID-19 patient in an intensive care unit in Italy.Antonio Masiello/Getty Images“The lung is the primary battle zone. But a fraction of the virus possibly attacks the kidney. And as on the real battlefield, if two places are being attacked at the same time, each place gets worse,” says Hongbo Jia, a neuroscientist at the Chinese Academy of Sciences’s Suzhou Institute of Biomedical Engineering and Technology and a co-author of that study.Viral particles were identified in electron micrographs of kidneys from autopsies in one study, suggesting a direct viral attack. But kidney injury may also be collateral damage. Ventilators boost the risk of kidney damage, as do antiviral drugs including remdesivir, which is being deployed experimentally in COVID-19 patients. Cytokine storms also can dramatically reduce blood flow to the kidney, causing often-fatal damage. And pre-existing diseases like diabetes can boost the risk of AKI. “There is a whole bucket of people who already have some chronic kidney disease who are at higher risk for acute kidney injury,” says Suzanne Watnick, chief medical officer at Northwest Kidney Centers.Buffeting the brainAnother striking set of symptoms in COVID-19 patients centers on the brain and central nervous system. Frontera says neurologists are needed to assess 5% to 10% of coronavirus patients at her hospital. But she says that “is probably a gross underestimate” of the number whose brains are struggling, especially because many are sedated and on ventilators.Frontera has seen patients with the brain inflammation encephalitis, with seizures, and with a “sympathetic storm,” an immune response that’s the brain’s version of a cytokine storm. Some people with COVID-19 briefly lose consciousness. Others have strokes. Many report losing their sense of smell. And Frontera and others wonder whether in some cases, infection depresses the brain stem reflex that senses oxygen starvation. This is another explanation for anecdotal observations that some patients aren’t gasping for air, despite dangerously low blood oxygen levels.ACE2 receptors are present in the neural cortex and brain stem, says Robert Stevens, an intensive care physician at Johns Hopkins Medicine. But it’s not known under what circumstances the virus penetrates the brain and interacts with these receptors. That said, the coronavirus behind the 2003 severe acute respiratory syndrome (SARS) epidemic—a close cousin of today’s culprit—could infiltrate neurons and sometimes caused encephalitis. On 3 April, a case study in the International Journal of Infectious Diseases, from a team in Japan, reported traces of new coronavirus in the cerebrospinal fluid of a COVID-19 patient who developed meningitis and encephalitis, suggesting it, too, can penetrate the central nervous system.A 58-year-old woman with COVID-19 developed encephalitis, resulting in tissue damage in the brain (arrows).N. Poyiadji et al., Radiology, (2020) doi.org/10.1148/radiol.2020201187But other factors could be damaging the brain. For example, a cytokine storm could cause brain swelling, and the blood’s exaggerated tendency to clot could trigger strokes. The challenge now is to shift from conjecture to confidence, at a time when staff are focused on saving lives, and even neurologic assessments like inducing the gag reflex or transporting patients for brain scans risk spreading the virus.Last month, Sherry Chou, a neurologist at the University of Pittsburgh Medical Center, began to organize a worldwide consortium that now includes 50 centers to draw neurological data from care patients already receive. The early goals are simple: Identify the prevalence of neurologic complications in hospitalized patients and document how they fare. Longer term, Chou and her colleagues hope to gather scans, lab tests, and other data to better understand the virus’ impact on the nervous system, including the brain.Chou speculates about a possible invasion route: through the nose, then upward and through the olfactory bulb—explaining reports of a loss of smell—which connects to the brain. “It’s a nice sounding theory,” she says. “We really have to go and prove that.”Most neurological symptoms “are reported from colleague to colleague by word of mouth,” Chou adds. “I don’t think anybody, and certainly not me, can say we’re experts.”Reaching the gutIn early March, a 71-year-old Michigan woman returned from a Nile River cruise with bloody diarrhea, vomiting, and abdominal pain. Initially doctors suspected she had a common stomach bug, such as Salmonella. But after she developed a cough, doctors took a nasal swab and found her positive for the novel coronavirus. A stool sample positive for viral RNA, as well as signs of colon injury seen in an endoscopy, pointed to a gastrointestinal (GI) infection with the coronavirus, according to a paper posted online on in The American Journal of Gastroenterology (AJG).Her case adds to a growing body of evidence suggesting the new coronavirus, like its cousin SARS, can infect the lining of the lower digestive tract, where the crucial ACE2 receptors are abundant. Viral RNA has been found in as many as 53% of sampled patients’ stool samples. And in a paper in press at Gastroenterology, a Chinese team reported finding the virus’ protein shell in gastric, duodenal, and rectal cells in biopsies from a COVID-19 patient. “I think it probably does replicate in the gastrointestinal tract,” says Mary Estes, a virologist at Baylor College of Medicine.Recent reports suggest up to half of patients, averaging about 20% across studies, experience diarrhea, says Brennan Spiegel of Cedars-Sinai Medical Center in Los Angeles, co–editor-in-chief of AJG. GI symptoms aren’t on CDC’s list of COVID-19 symptoms, which could cause some COVID-19 cases to go undetected, Spiegel and others say. “If you mainly have fever and diarrhea, you won’t be tested for COVID,” says Douglas Corley of Kaiser Permanente, Northern California, co-editor of Gastroenterology.The presence of virus in the GI tract raises the unsettling possibility that it could be passed on through feces. But it’s not yet clear whether stool contains live, infectious virus, not just RNA and proteins. To date, “We have no evidence” that fecal transmission is important, says coronavirus expert Stanley Perlman of the University of Iowa. CDC says that based on experiences with SARS and with the virus that causes Middle East respiratory syndrome, another dangerous cousin of the new coronavirus, the risk from fecal transmission is probably low.The intestines are not the end of the disease’s march through the body. For example, up to one-third of hospitalized patients develop conjunctivitis—pink, watery eyes—although it’s not clear that the virus directly invades the eye. Other reports suggest liver damage: More than half of COVID-19 patients hospitalized in two Chinese centers had elevated levels of enzymes indicating injury to the liver or bile ducts, according to two preprints. But several experts told Science that direct viral invasion isn’t likely the culprit. They say other events in a failing body, like drugs or an immune system in overdrive, are more likely driving the liver damage.This map of the devastation that COVID-19 can inflict on the body is still just a sketch. It will take years of painstaking research to sharpen the picture of its reach, and the cascade of cardiovascular and immune effects it might set in motion. As science races ahead, from probing tissues under microscopes to testing drugs on patients, the hope is for treatments more wily than the virus that has stopped the world in its tracks.Posted in:BiologyCoronavirusdoi:10.1126/science.abc3208

This was from a Chinese website that has been following the most recent events regarding the D614G mutation.北京新冠基因序列公布：具有D614G突变 - Beijing new crown gene sequence announced: with D614G mutation.6月18日晚，中国疾病预防控制中心通过“新型冠状病毒国家科技资源服务系统”正式发布2020年6月北京新发地新冠疫情及病毒基因组序列数据。该中心还同时向世界卫生组织及全球共享流感数据倡议组织（GISAID）提交了新冠疫情及病毒基因组序列数据，与国际社会共享这一数据。- On the evening of June 18, the Chinese Center for Disease Control and Prevention officially released the new coronavirus epidemic situation and viral genome sequence data in June 2020 in Beijing through the "New Coronavirus National Science and Technology Resource Service System". The center also submitted the new crown epidemic situation and viral genome sequence data to the World Health Organization and the Global Influenza Data Initiative (GISAID) to share this data with the international community.此次提交的3组病毒序列信息中，2组分别来源于53岁与25岁的男性患者（NMDC60013902-01、NMDC60013903-02），1组来源于环境样本（NMDC60013903-03），均采集于6月11日。根据上传的病毒序列信息，本次在北京流行的新冠病毒隶属于进化枝20B（图1），而该进化枝常见于欧洲，与该序列最接近的病毒来源于捷克、中国台湾、希腊以及葡萄牙。- Of the 3 sets of virus sequence information submitted this time, 2 sets were derived from male patients aged 53 and 25 (NMDC60013902-01, NMDC60013903-02), and 1 set was derived from environmental samples (NMDC60013903-03), they were collected on June 11th. According to the uploaded virus sequence information, the new coronavirus popular in Beijing this time belongs to clade 20B (Figure 1), and this clade is common in Europe. The viruses closest to this sequence are from the Czech Republic, Taiwan, Greece, and Portugal.3组病毒序列均携带D614G突变 - The three groups of virus sequences all carry the D614G mutation.This announcement coincided with a ban on importing pork, specifically from Germany where there was an outbreak of COVID-19 in Tönnies, largest German pork plant. "At the moment it's a local outbreak," said Ralf Reintjes, professor of epidemiology and surveillance at the Hamburg University of Applied Sciences. But if the approach fails in Gütersloh and in other towns such as Göttingen, where a tower block is in quarantine, he warned, Germany will "probably have a second wave."Via Global Times: Real-time update on coronavirus outbreak. Excerpt:4:48 pm July 1Since the outbreak connected to the Xinfadi market began on June 11, confirmed COVID-19 cases have been found in 11 districts and 47 streets of Beijing. Five and 39 streets were respectively classified as high- and medium-risk regions: Beijing CDC6:00 pm Jun 18Export of pork products from a German company have been suspended in China from Wed as a cluster of COVID-19 infections have been confirmed at the firm. The company’s export of products related to cutting and cold storage were also suspended.Sometime in the middle of January, a mutation (S-D614G) allowed the virus to become more infectious. According to a study in April the estimation by Los Alamos National Laboratory in New Mexico is that those who carried the coronavirus in Wuhan were passing it on to 5.7 people on average. The “Han strain” taken from a patient in Wuhan in December 2019 mutated into the European strain, by May, 70% of the world had the strain. It does make the virus more infectious as reported in another study which showed that the S-D614G clade (mostly found in Europe), had a viral load 19 times higher compared to other viral isolates. It was not the first study to suggest mutation of the spike (S) protein.Epidemiologists speak of Tipping points as the name given to that moment in an epidemic when a virus reaches critical mass. It’s the moment on the graph when the line starts to shoot straight upwards. In an Ebola article in 2014 it was called the moment of escape velocity, viruses exhibit non-linear and exponential characteristics.Currently, the virus is in an exponential growth phase, so it makes sense that it’s become more infectious, about 10X more. It is estimated the reproductive number of SARS-CoV-2 is likely to be within (95% CI 3.8–8.9), with a median R0 of 5.7 (Sanche et al. July,2020).Note: I am using the word isolate and strain interchangeably, although most virologists agree when SARS-CoV-2 is isolated from a COVID-19 patient, that virus is called an isolate. The origin of the term is clear: the virus has been isolated from a patient.Another study, conducted by Kristian Andersen from the Scripps Research Institute in California, Andrew Rambaut from the University of Edinburgh in Scotland, Ian Lipkin from Columbia University in New York, Edward Holmes from the University of Sydney, and Robert Garry from Tulane University in New Orleans, was published in the scientific journal Nature Medicine on March 17.The Scripp Institute in Florida detected the S-D614G mutation more recently, the data in the study of D614G mutation raises interesting questions about the natural history of SARS-CoV-2 as it moved presumably from horseshoe bats to humans. At some point in this process, the virus acquired a furin-cleavage site, allowing its S1/S2 boundary to be cleaved in virus producing cells. In contrast, the S1/S2 boundary of SARS-CoV-1, and indeed all SARS like viruses isolated from bats, lack this polybasic site and are cleaved by TMPRSS2 or endosomal cathepsins in the target cells.Therefore, the D614G mutation may have emerged to compensate for this newly acquired furin site. In summary, the study shows that an S protein mutation results in more transmissible SARS-CoV-2 also limits shedding of the S1 domain and increases S-protein incorporation into the virion.Some human viruses including HIV and Ebola have the same furin-like cleavage site, which makes them contagious. Bats are also notorious for carrying Ebola and Marburg viruses, members of the family of filoviruses known to cause pandemics.I think this mutation has significance, considering you have the European strain raging in China right now, with Beijing under lockdown. Recently there was an article on G4 EA H1N1 having the potential to become a pandemic, the timeline is self-evident that all this happened around the time that Tönnies closed the largest German pork plant in Gütersloh which is having the worst outbreak. If it can’t be controlled than Germany and Europe will have a second wave. I honestly think they should come out and say it’s the pigs that are infecting the workers, instead of making excuses of poor ventilation and air quality.Measures to control this virus in pigs and closely monitor workers in pig farms and pork processing plants should be swiftly implemented.During a Senate committee hearing on progress toward reopening workplaces and schools, Anthony Fauci, MD, director of the National Institutes of Allergy and Infectious Diseases (NIAID), when asked about the G4 strain, said US officials need to keep an eye its emergence in China. He added, however, that it isn't an immediate threat, The Hill reported.I was left scratching my head, “keep an eye out” while it’s raging in China, there is confirmed human to human transmission, Beijing is under lockdown, why would you downplay the whole thing?The Washington post takes note: The coronavirus is mutating. Excerpt:When the first coronavirus cases in Chicago appeared in January, they bore the same genetic signatures as a germ that emerged in China weeks before.But as Egon Ozer, an infectious-disease specialist at the Northwestern University Feinberg School of Medicine, examined the genetic structure of virus samples from local patients, he noticed something different.A change in the virus was appearing again and again. This mutation, associated with outbreaks in Europe and New York, eventually took over the city. By May, it was found in 95 percent of all the genomes Ozer sequenced.At a glance, the mutation seemed trivial. About 1,300 amino acids serve as building blocks for a protein on the surface of the virus. In the mutant virus, the genetic instructions for just one of those amino acids — number 614 — switched in the new variant from a “D” (shorthand for aspartic acid) to a “G” (short for glycine).But the location was significant, because the switch occurred in the part of the genome that codes for the all-important “spike protein” — the protruding structure that gives the coronavirus its crownlike profile and allows it to enter human cells the way a burglar picks a lock.And its ubiquity is undeniable. Of the approximately 50,000 genomes of the new virus that researchers worldwide have uploaded to a shared database, about 70 percent carry the mutation, officially designated D614G but known more familiarly to scientists as “G.”“G” hasn’t just dominated the outbreak in Chicago — it has taken over the world. Now scientists are racing to figure out what it means.At least four laboratory experiments suggest that the mutation makes the virus more infectious, although none of that work has been peer-reviewed. Another unpublished study led by scientists at Los Alamos National Laboratory asserts that patients with the G variant actually have more virus in their bodies, making them more likely to spread it to others.The mutation doesn’t appear to make people sicker, but a growing number of scientists worry that it has made the virus more contagious.“The epidemiological study and our data together really explain why the [G variant’s] spread in Europe and the U.S. was really fast,” said Hyeryun Choe, a virologist at Scripps Research and a lead author of an unpublished study on the G variant’s enhanced infectiousness in laboratory cell cultures. “This is not just accidental.”But there may be other explanations for the G variant’s dominance: biases in where genetic data are being collected, quirks of timing that gave the mutated virus an early foothold in susceptible populations.“The bottom line is, we haven’t seen anything definitive yet,” said Jeremy Luban, a virologist at the University of Massachusetts at Amherst.The scramble to unravel this mutation mystery embodies the challenges of science during the coronavirus pandemic. With millions of people infected and thousands dying every day around the world, researchers must strike a high-stakes balance between getting information out quickly and making sure that it’s right.

All of them, cybersecurity experts are quick to emphasize. You may have heard smart home devices collectively referred to as the “Internet of Things” (IoT). Remembering the “I” in IoT can help you understand its vulnerabilities.“All of these smart devices are really networked computers in addition to what they traditionally are: refrigerators, light bulbs, televisions, cat litter boxes, dog feeders, cameras, garage door openers, door locks,” explains Professor Ralph Russo, Director of Information Technology Programs at Tulane University. “Many of these continually collect data from embedded sensors. Malicious actors could gain access to your home network through your device if they can exploit an IoT device vulnerability.”In other words, connected appliances can be hacked into like any other website or computer, and most of them are behind poorly secured consumer-grade home routers. Dr. Zahid Anwar of Fontbonne University gave us an overview of which smart devices are most at risk and why.Most vulnerable: Outdoor devices with embedded computers that support little or no security protocols. For example, garage door openers, wireless doorbells and smart sprinklers are all examples of devices that may be easily accessible to someone driving down the street with a computer or other Wi-Fi transmitter.Second most vulnerable: “Inside-the-home devices that can be controlled through an app from a smartphone or PC such as smart bulbs, smart switches, security cameras, baby monitors, smart door locks, smart thermostats, and personal home assistants,” says Dr. Anwar. “These devices rely on weak security tokens and may be hacked due to weaknesses in the communication protocols used, configuration settings or vulnerable entry-points left open by the vendor for maintenance.”Less likely to be attacked: Home appliances like refrigerators and ovens are the least likely to be attacked, but it can happen.Why would someone attack your refrigerator?Professor Russo anticipated this question. “Your home can be a gold mine to hackers, who are seeking to capture your banking password, your online accounts and your personally identifiable information, and entering and establishing a beach-head through an IoT device can be the low-hanging fruit.”Through the connected network, smart home devices give hackers much more information than the contents of your fridge. Once they have a way into your network, people with malicious intent might be able to turn off your security cameras, access your personal information or spy on you and your family. An insecure home network therefore opens the door to burglary, identity theft, privacy violations and more.The exact rate of security breaches is unknown. Manufacturers don’t disseminate this information and it doesn’t fall under the purview of any one regulatory body. What we do know is that anecdotal evidence is mounting. The FBI warned parents about the risks of connected toys, an Internet-connected fish tank helped hackers steal data from a Las Vegas casino, and there are even free live streams of hacked security cameras broadcasting for free on the web and smartphone apps. We also know that there is no shortage of sophisticated scammers and identity thieves, and that they continually refine their methods alongside changing culture and technology.It’s also possible for IoT devices to be hacked and operating maliciously without you even knowing it. “The most common reason for taking over smart home devices is to use them to build a botnet network,” explains Maciej Markiewicz, Security CoP Coordinator & Sr. Android Developer at Netguru, a digital consultancy and software company. “These devices can be easily used to conduct more complex attacks. Very often, the management of such botnet networks consisting of smart home devices are sold on the darknet to be used in crimes.” These “botnets” are typically programmed to orchestrate the large-scale capture of personal data for identity theft and other financial exploitation.Help Hackproof Your Devices: Smart Home Safety TipsMany homeowners don’t want to go through the hassle of advanced electronics configurations. Don’t worry – we’ve compiled the easiest-to-follow tech tips that dramatically lower your smart devices’ susceptibility to hackers.Weigh the vulnerabilities vs. the benefits.“Unfortunately, it is always worth remembering that there is no IT infrastructure that can be 100% secured. The only thing we can do is seek to reduce the risk. Therefore, when designing a smart home system, it is worth analyzing what is important to us and what the risk is,” says Markiewicz.Before you add to your home network, ask yourself: Is the convenience this device offers worth the potential risk of a hack? If not, don’t buy one. Research every device and brand you buy.Create a secure Wi-Fi network.Purchase a router from a reputable brand and follow the manufacturer’s instructions to change the name of the network and default password. Choose a network name that doesn’t automatically give away your location or personal details. Consider also hiding your network from view, an option which can usually be found in the router’s settings menu.It’s also possible to create a second Wi-Fi network specifically for your smart home devices. Many routers allow you to create multiple networks, each with their own name and password. This way, hacking your IoT device will confine an attacker to that network and keeping it segregated from where you do your banking and store your sensitive information. It’s also a good idea to set up a Guest network for visitors’ smartphones and computers, where they can’t see or access your IoT devices.Don’t underestimate the importance of your passwords.It’s incredible that the humble, old-fashioned password system is the main line of defense protecting our most high-tech devices. Take your passwords seriously! Whenever you get a new device, change the default password immediately. Otherwise, the password to your Wi-Fi router or security camera might be just a Google search away. Use unique, hard to guess passwords with several characters, numbers and letters on all of your devices. A password manager like LastPass can help you remember them all more conveniently.Register every new device with the manufacturer and keep them up to date.Registration is important because companies frequently push out software updates that address newfound bugs and security concerns. If a vulnerability has been discovered, you’ll need the company’s software updates to patch it up. Also, when you install the associated apps, be cognizant of what permissions you’re granting. Don’t allow access to anything that isn’t necessary.Consider professional installation.If the previous tips are making your head spin, remember that the leading home security providers offer professional installation with great built-in smart home integration. Technicians can handle any necessary hardwiring for you and answer all of your questions about more advanced security measures.Unplug devices that aren’t in use.When you leave town, unplug any appliances that won’t be active. Not only will it save on your energy bill, it will also make them inaccessible to hackers. You’ll probably want to leave important appliances like the security camera, video doorbell and the thermostat on, but you can unplug extra smart speakers, vacuums, etc.Factory reset devices before getting rid of them.If you decide to sell, throw out or give away one of your smart electronics, follow the manufacturer’s instructions to remove all of your data. Otherwise, the next person who gets their hands on it may automatically access all of your information or communicate with other devices on your network.