{"id":23070,"date":"2020-08-02T17:18:14","date_gmt":"2020-08-02T21:18:14","guid":{"rendered":"http:\/\/stateofthenation.co\/?p=23070"},"modified":"2020-08-02T17:19:54","modified_gmt":"2020-08-02T21:19:54","slug":"it-looks-like-the-novel-coronavirus-is-more-than-a-respiratory-virus","status":"publish","type":"post","link":"http:\/\/stateofthenation.co\/?p=23070","title":{"rendered":"It looks like the novel coronavirus is much more than a respiratory virus."},"content":{"rendered":"<p><!--more--><a href=\"http:\/\/thehealthcoach1.com\/wp-content\/uploads\/2020\/08\/coronavirus-does-to-body-balbusso-twins-illustration.png\"><img loading=\"lazy\" decoding=\"async\" class=\"alignleft size-full wp-image-7755\" src=\"http:\/\/thehealthcoach1.com\/wp-content\/uploads\/2020\/08\/coronavirus-does-to-body-balbusso-twins-illustration.png\" alt=\"\" width=\"720\" height=\"780\" \/><\/a><\/p>\n<h1>We Thought It Was Just a Respiratory Virus<\/h1>\n<p>We were wrong.<\/p>\n<p>By Ariel Bleicher and Katherine Conrad<br \/>\nUCSF Magazine<\/p>\n<div class=\"page_narrow\">\n<p class=\"feature-text\">In late January, when hospitals in the United States confirmed the presence of the novel coronavirus, health workers knew to watch for precisely three symptoms: <span class=\"covid-mag-teal-callout\">fever<\/span>, <span class=\"covid-mag-teal-callout\">cough<\/span>, and <span class=\"covid-mag-teal-callout\">shortness of breath<\/span>. But as the number of infections climbed, the symptom list began to grow. Some patients <span class=\"covid-mag-red-callout\">lost their sense of smell<\/span> and <span class=\"covid-mag-red-callout\">taste<\/span>. Some had <span class=\"covid-mag-red-callout\">nausea<\/span> or <span class=\"covid-mag-red-callout\">diarrhea<\/span>. Some had <span class=\"covid-mag-red-callout\">arrhythmias<\/span> or even <span class=\"covid-mag-red-callout\">heart attacks<\/span>. Some had <span class=\"covid-mag-red-callout\">damaged kidneys<\/span> or <span class=\"covid-mag-red-callout\">livers<\/span>. Some had <span class=\"covid-mag-red-callout\">headaches<\/span>, <span class=\"covid-mag-red-callout\">blood clots<\/span>, <span class=\"covid-mag-red-callout\">rashes<\/span>, <span class=\"covid-mag-red-callout\">swelling<\/span>, or <span class=\"covid-mag-red-callout\">strokes<\/span>. Many had <span class=\"covid-mag-blue-callout\">no symptoms at all<\/span>.<\/p>\n<p>By June, clinicians were swapping journal papers, news stories, and tweets describing more than three dozen ways that COVID-19, the disease the coronavirus causes, appears to manifest itself. Now researchers at UC San Francisco and around the world have begun taking a closer look at this dizzying array of symptoms to get at the disease\u2019s root causes. They are learning from people inside the hospital and out; people on the brink of death and only mildly sick; people newly exposed and recovered; people young and old, Black, brown, and white. And they are beginning to piece together the story of a virus unlike any known before.<\/p>\n<h2 class=\"covid-mag-red-callout\">How infection sets in<\/h2>\n<p>Viruses lead a curious purgatorial existence of being neither fully alive nor dead. Enveloped in a protein cloak, a virus consists almost entirely of genetic material \u2013 DNA or RNA, the blueprints for all of life. But it can\u2019t reproduce on its own. To survive, it must break into a cell and co-opt the cell\u2019s gene-copying machinery.<\/p>\n<p>The novel coronavirus, an RNA virus named SARS-CoV-2, has become notorious for its skill at breaking and entering human cells. Its tools of choice are the protein spikes protruding from its surface \u2013 a feature that distinguishes all coronaviruses. The spikes of SARS-CoV-2 are the cr\u00e8me de la cr\u00e8me: By the luck of the evolutionary draw, they are able to easily grab hold of protein gates on human cells known as ACE2 receptors and, like jackknives, pry these gates open.<\/p>\n<aside class=\"ucsfcallout mag-body-callout callout-right in-viewport\" data-image=\"1\">\n<div class=\"callout__image\">\n<div>\n<figure class=\"embedded-entity\"><picture><img loading=\"lazy\" decoding=\"async\" class=\"element-fade lazyloaded element-fade--in-viewport\" src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/quarter\/public\/2020-07\/covid-symbol.png\" alt=\"Illustration of a coronavirus symbol.\" width=\"330\" height=\"330\" data-src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/quarter\/public\/2020-07\/covid-symbol.png\" \/><\/picture><\/figure>\n<\/div>\n<\/div>\n<div class=\"callout__content\">\n<p class=\"small-text covid-mag-red-callout\">Spikes on the virus\u2019s surface act like jackknives to break and enter human cells.<\/p>\n<\/div>\n<\/aside>\n<p>\u201cYou can think of an ACE2 receptor like a docking site,\u201d says <a href=\"https:\/\/fattahilab.ucsf.edu\/lab-members\" target=\"_blank\" rel=\"noopener noreferrer\">Faranak Fattahi, PhD<\/a>, a <a href=\"https:\/\/fellows.ucsf.edu\/current-fellows\" target=\"_blank\" rel=\"noopener noreferrer\">UCSF Sandler Fellow<\/a>. When the coronavirus pandemic hit San Francisco, Fattahi repurposed her laboratory to study this key receptor, which normally plays a role in regulating blood pressure. \u201cWhen the virus lands on it,\u201d she says, \u201cit initiates a molecular process that brings the virus inside the cell.\u201d<\/p>\n<p>If you\u2019re exposed to SARS-CoV-2 \u2013 say, from a cough or sneeze \u2013 the virus will likely first encounter ACE2 receptors on cells in your nose or throat. But these receptors also populate your heart, gut, and other organs. Fattahi\u2019s team has found evidence suggesting that male sex hormones such as testosterone may increase the number of ACE2 receptors that cells produce, which could help explain <a href=\"https:\/\/www.ucsf.edu\/magazine\/frontliner-fattahi\">why SARS-CoV-2 seems to wreak greater havoc on men than on women<\/a>and why kids rarely get sick. \u201cThe fewer ACE2 receptors, the less risk of infection \u2013 that\u2019s the idea,\u201d she says, adding that this hypothesis for the disease\u2019s gender gap is only one of several.<\/p>\n<p>Once inside a few initial host cells, the virus sets them to work churning out copies of itself. Within hours, thousands of new virus particles begin bursting forth, ready to infect more cells. Although SARS-CoV-2 is less deadly than the original SARS virus, which emerged in 2002, it replicates more rapidly. Also unlike SARS, which primarily infects the lungs, SARS-CoV-2 replicates throughout the airway, including in the nose and throat, making it highly contagious \u2013 like the common cold.<\/p>\n<figure class=\"caption caption-drupal-entity align-center\">\n<figure class=\"embedded-entity\"><picture><img loading=\"lazy\" decoding=\"async\" class=\"element-fade lazyloaded element-fade--in-viewport\" src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/w\/public\/2020-07\/coronavirus-head-throat-balbusso-twins-illustration.png\" alt=\"Illustration of the inside of a head, with coronavirus cells throughout the airways.\" width=\"850\" height=\"916\" data-src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/w\/public\/2020-07\/coronavirus-head-throat-balbusso-twins-illustration.png\" \/><\/picture><\/figure><figcaption>SARS-CoV-2 replicates throughout the airway, making it highly contagious, like the common cold.<\/figcaption><\/figure>\n<\/div>\n<div class=\"paragraph-text-block\">\n<p>However, infection with SARS-CoV-2 usually doesn\u2019t feel like a cold. Fewer than 20% of infected people who eventually show up at a hospital report having had a sore throat or runny nose. During the first few days of being infected, you\u2019re more likely to have a fever, dry cough or, peculiarly, lose your sense of smell or taste.<\/p>\n<p>Most likely, though, you won\u2019t feel sick at all. When UCSF researchers tested people for SARS-CoV-2 in San Francisco\u2019s Mission District, <a href=\"https:\/\/www.ucsf.edu\/news\/2020\/05\/417356\/initial-results-mission-district-covid-19-testing-announced\">53% of those infected never had any symptoms<\/a>. \u201cThat\u2019s much higher than expected,\u201d says <a href=\"https:\/\/profiles.ucsf.edu\/monica.gandhi\" target=\"_blank\" rel=\"noopener noreferrer\">Monica Gandhi, MD, MPH<\/a>, a UCSF professor of medicine with expertise in HIV. Surveys of outbreaks in nursing homes and prisons show similar or even higher numbers. \u201cIf we did a mass testing campaign on 300 million Americans right now, I think the rate of asymptomatic infection would be somewhere between 50% and 80% of cases,\u201d Gandhi says. Millions of people may be spreading the virus without knowing it, she points out, making asymptomatic transmission the <a href=\"https:\/\/www.nejm.org\/doi\/full\/10.1056\/NEJMe2009758\" target=\"_blank\" rel=\"noopener noreferrer\">Achilles\u2019 heel<\/a>of efforts to control the pandemic \u2013 and highlighting the <a href=\"https:\/\/academic.oup.com\/ofid\/article\/7\/4\/ofaa131\/5820544\" target=\"_blank\" rel=\"noopener noreferrer\">importance of universal masking<\/a>.<\/p>\n<p>\u201cThe majority of people who have COVID-19 are out in the community, and they are either asymptomatic or only mildly ill,\u201d says <a href=\"https:\/\/profiles.ucsf.edu\/sulggi.lee\" target=\"_blank\" rel=\"noopener noreferrer\">Sulggi Lee, MD, PhD<\/a>, a UCSF assistant professor of medicine. When the coronavirus pandemic hit San Francisco in early March, Lee conceived a study to investigate why. She scrambled to assemble a team and <a href=\"https:\/\/pbbr.ucsf.edu\/awards\/awardees\" target=\"_blank\" rel=\"noopener noreferrer\">procure funding<\/a> and equipment. She borrowed a colleague\u2019s <a href=\"https:\/\/twitter.com\/ucsfdelivercare?lang=en\" target=\"_blank\" rel=\"noopener noreferrer\">mobile clinic<\/a> \u2013 a van outfitted with an exam table and a phlebotomy chair \u2013 so that her team could drive around the city, collecting samples from infected people. Lee hopes data from the study, called CHIRP (COVID-19 Host Immune Response Pathogenesis), will show how people\u2019s immune systems respond as SARS-CoV-2 starts to gain a foothold in their bodies.<\/p>\n<p>\u201cA lot is riding on that initial response,\u201d she says. If Lee and her collaborators can figure out the biological processes that allow some infected people to stay relatively well, they can perhaps use that knowledge to prevent others from falling severely ill.<\/p>\n<h2 class=\"covid-mag-orange-callout\">Battling in the lungs<\/h2>\n<p>True to its name, SARS-CoV-2 (which stands for severe acute respiratory syndrome coronavirus 2) is first and foremost a bad respiratory virus. If your immune system doesn\u2019t defeat it at its landing site in your nose or throat, it will advance down your windpipe, infiltrating the cells lining your lungs\u2019 branching air tubes. At the tubes\u2019 ends, tiny air sacs called alveoli pass oxygen to your blood. As the virus multiplies, the alveoli may fill with fluid, shutting down this critical gas exchange. Your blood-oxygen level may drop and, typically about six days into an infection, you may start feeling short of breath.<\/p>\n<p>What causes this mayhem? \u201cSome of it is definitely caused by the virus itself,\u201d says <a href=\"https:\/\/profiles.ucsf.edu\/michael.matthay\" target=\"_blank\" rel=\"noopener noreferrer\">Michael Matthay, MD<\/a>, a UCSF professor of medicine who has studied acute respiratory diseases for more than 30 years. Inevitably, a fast-replicating virus will kill or injure many of the lung cells it infects; the more cells it infects, the more ruin it will leave in its wake.<\/p>\n<aside class=\"ucsfcallout mag-body-callout callout-left in-viewport\" data-image=\"1\">\n<div class=\"callout__image\">\n<div>\n<figure class=\"embedded-entity\"><picture><img loading=\"lazy\" decoding=\"async\" class=\"element-fade lazyloaded element-fade--in-viewport\" src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/quarter\/public\/2020-07\/covid-symbol.png\" alt=\"Illustration of a coronavirus symbol.\" width=\"330\" height=\"330\" data-src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/quarter\/public\/2020-07\/covid-symbol.png\" \/><\/picture><\/figure>\n<\/div>\n<\/div>\n<div class=\"callout__content\">\n<p class=\"small-text covid-mag-red-callout\">The virus\u2019s fatality rate seems to be roughly 10 times that of the flu.<\/p>\n<\/div>\n<\/aside>\n<p>But SARS-CoV-2 doesn\u2019t appear to be a savage destroyer of cells. Although it\u2019s too early to know for sure, the virus\u2019s fatality rate seems to be roughly 10 times that of the flu. \u201cYou would think that\u2019s because it\u2019s just a killing machine,\u201d says <a href=\"https:\/\/profiles.ucsf.edu\/max.krummel\" target=\"_blank\" rel=\"noopener noreferrer\">Max Krummel, PhD<\/a>, UCSF\u2019s Smith Professor of Experimental Pathology and chair of the Bakar ImmunoX initiative. So far, however, the science suggests otherwise.<\/p>\n<p>\u201cOne of the weirder things about this new coronavirus is it doesn\u2019t seem to be incredibly cytopathic, by which we mean cell-killing,\u201d Krummel says. \u201cFlu is really cytopathic; if you add it to human cells in a petri dish, the cells burst within 18 hours.\u201d But when UCSF researchers subjected human cells to SARS-CoV-2, many of the infected cells never perished. \u201cIt\u2019s pretty compelling data that maybe we\u2019re not dealing with a hugely aggressive virus,\u201d Krummel says.<\/p>\n<p>The bigger provocation, he suspects, may be your own immune system. Like any pathogen, SARS-CoV-2 will trigger an immune attack within minutes of entering your body. This counterstrike is extraordinarily complex, involving many tactics, cells, and molecules. In a <a href=\"https:\/\/www.comet-study.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">UCSF study called COMET<\/a> (COVID-19 Multi-Phenotyping for Effective Therapies), Krummel and other scientists have been observing this immune warfare in more than 30 people admitted to UCSF hospitals with COVID-19 and other respiratory infections. \u201cWhat we\u2019re doing is looking at patients\u2019 blood, their genes, and the secretions from their noses and lungs, and we\u2019re asking, \u2018What\u2019s your army? What\u2019s your response strategy?\u2019\u201d<\/p>\n<blockquote class=\"blockquote blockquote--half-right in-viewport\">\n<p class=\"blockquote-content__text\">It\u2019s pretty compelling data that maybe we\u2019re not dealing with a hugely aggressive virus.\u201d<\/p>\n<footer>\n<p class=\"blockquote-content__cite\">MAX KRUMMEL, PHD<\/p>\n<\/footer>\n<\/blockquote>\n<p>An early analysis of COMET data, Krummel says, suggests that the immune systems of many hospitalized patients mobilize differently \u2013 and more aggressively \u2013 against SARS-CoV-2 than against influenza viruses, which cause the flu. Their lungs are ravaged, these data suggest, not by the virus alone but by the detritus of an immunological battle gone awry. This rogue immune response could explain why, around day 11 of a COVID-19 infection, patients often develop a severe pneumonia known as acute respiratory distress syndrome, or ARDS.<\/p>\n<p>Ultimately, COMET seeks to find COVID-19 therapies that can rein in an overeager immune system in order to prevent or treat ARDS. But that feat won\u2019t be easy, says <a href=\"https:\/\/profiles.ucsf.edu\/carolyn.calfee\" target=\"_blank\" rel=\"noopener noreferrer\">Carolyn Calfee, MD, MAS \u201909<\/a>, an ARDS expert, UCSF professor of medicine, and co-leader of the study. Too much or the wrong kind of intervention, she explains, could cripple a person\u2019s immune system to the point where it can\u2019t clear an infection. \u201cIt\u2019s a fine line between therapeutic and deleterious,\u201d Calfee says. \u201cWe\u2019re trying to find that balance.\u201d<\/p>\n<p>Typically, people who die from COVID-19 ARDS die around day 19. Reported rates of mortality have varied widely, with the highest rates being where the pandemic has hit hardest, overwhelming hospital resources and staff. At UCSF hospitals \u2013 likely due to the city\u2019s early shelter-in-place orders, which prevented an initial surge of COVID-19 cases \u2013 so far only 10 of 85\u00a0critically ill patients have died.<\/p>\n<p>\u201cThe good news is that we\u2019ve been doing clinical trials of best-care practices for ARDS since 1998,\u201d Matthay says. Thanks to <a href=\"https:\/\/petalnet.org\/general-public\" target=\"_blank\" rel=\"noopener noreferrer\">research by him and others<\/a>, for example, clinicians have long known which ventilator settings result in the fewest deaths and how to flip patients onto their stomachs \u2013 a technique known as proning \u2013 to best help them breathe. If public health measures can keep hospital admissions low so that frontline providers can make good use of the skills and knowledge they already have, we may find that we have less to fear from SARS-CoV-2 than we thought.<\/p>\n<p>On the other hand, the virus behaves in ways that are still mysterious.<\/p>\n<\/div>\n<div class=\"layout-columns__1 bg-white\">\n<div class=\"field field-content-wrapper-content field--type-entity-reference-revisions field--label-hidden field__items\">\n<div class=\"layout-column\">\n<div class=\"paragraph paragraph--type--column-content paragraph--view-mode--default\">\n<div class=\"field field-column-content-content field--type-entity-reference-revisions field--label-hidden field__items\">\n<div class=\"field__item\">\n<div class=\"paragraph-text-block\">\n<div>\n<div><iframe loading=\"lazy\" src=\"https:\/\/view.genial.ly\/5f136fec170c9c0d85d5f79e\" width=\"1280px\" height=\"1508px\" frameborder=\"0\" scrolling=\"yes\" allowfullscreen=\"allowfullscreen\" data-mce-fragment=\"1\"><\/iframe><\/div>\n<\/div>\n<p>Text upper left: From Head to \u201cCOVID Toes\u201d underlined. Text below underline: People with COVID-19 exhibit from none to many of these symptoms. Some symptoms (such as fever, cough, and loss of smell) are common, while others (such as sore throat, pink eye, and stroke) are rare. Middle of page: Illustration of human body. From the top: Brain with one plus sign that opens to text reading: Headaches, brain fog, dizziness, delirium, stroke, and another plus sign that opens to text reading: Pink eye. Throat area with plus sign that opens to text reading: Loss of smell or taste, runny nose, sneezing, sore throat. Heart with plus sign that opens to box reading: Arrhythmia, weakened cardiac muscle, heart attack. Lower left lung with plus sign that opens to text reading: Cough, shortness of breath, lung injury. Kidney with plus sign that opens to text reading: Kidney injury, elevated liver enzymes. Intestines with plus sign that opens to text reading: Nausea, stomachache, vomiting, diarrhea. Upper thigh with plus sign that opens to text reading: Fever, fatigue, muscle aches, inflammation, blood clots, vascular injury. Toe with with plus sign that opens to text reading: Skin rash, numbness or swelling in feet or hands. Bottom of illustration: rectangle filled with faded-back coronaviruses and text at far right reading: illustration Stephanie Koch. Left of body illustration: small illustration of coronavirus. Top and right of illustration: small illustration of coronavirus.<\/p>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<\/div>\n<div class=\"paragraph-text-block paragraph-responsive-areas\">\n<div class=\"clearfix text-formatted field field-desktop-area field--type-text-long field--label-hidden field__item\">\n<div>\n<div><iframe loading=\"lazy\" src=\"https:\/\/view.genial.ly\/5f136fec170c9c0d85d5f79e\" width=\"1280px\" height=\"1508px\" frameborder=\"0\" scrolling=\"yes\" allowfullscreen=\"allowfullscreen\" data-mce-fragment=\"1\"><\/iframe><\/div>\n<\/div>\n<p>Text upper left: From Head to \u201cCOVID Toes\u201d underlined. Text below underline: People with COVID-19 exhibit from none to many of these symptoms. Some symptoms (such as fever, cough, and loss of smell) are common, while others (such as sore throat, pink eye, and stroke) are rare. Middle of page: Illustration of human body. From the top: Brain with one plus sign that opens to text reading: Headaches, brain fog, dizziness, delirium, stroke, and another plus sign that opens to text reading: Pink eye. Throat area with plus sign that opens to text reading: Loss of smell or taste, runny nose, sneezing, sore throat. Heart with plus sign that opens to box reading: Arrhythmia, weakened cardiac muscle, heart attack. Lower left lung with plus sign that opens to text reading: Cough, shortness of breath, lung injury. Kidney with plus sign that opens to text reading: Kidney injury, elevated liver enzymes. Intestines with plus sign that opens to text reading: Nausea, stomachache, vomiting, diarrhea. Upper thigh with plus sign that opens to text reading: Fever, fatigue, muscle aches, inflammation, blood clots, vascular injury. Toe with with plus sign that opens to text reading: Skin rash, numbness or swelling in feet or hands. Bottom of illustration: rectangle filled with faded-back coronaviruses and text at far right reading: illustration Stephanie Koch. Left of body illustration: small illustration of coronavirus. Top and right of illustration: small illustration of coronavirus.<\/p>\n<\/div>\n<\/div>\n<div class=\"paragraph-text-block\">\n<p class=\"concept-credit\">Concept credit: Jennifer Babik, MD, PhD<\/p>\n<\/div>\n<div class=\"paragraph-text-block\">\n<h2 class=\"covid-mag-teal-callout\">Heart failure<\/h2>\n<p>In April, Susan Parson, MD, a Bay Area medical examiner, made a startling discovery. For nearly two months, officials had believed that the first people in the U.S. to die from COVID-19 had died of respiratory failure in Washington state in late February. At the time, the U.S. Centers for Disease Control and Prevention limited testing to people who had respiratory symptoms and had recently traveled to China or otherwise been exposed to the virus. Those restrictions, however, turned out to be misguided.<\/p>\n<p>As a medical examiner for California\u2019s Santa Clara County, Parson had done a routine autopsy on a 57-year-old woman named Patricia Dowd, who had died suddenly at home on February 6. In Dowd\u2019s tissues, Parson found the cause of her death: SARS-CoV-2. But the virus hadn\u2019t wrecked Dowd\u2019s lungs. In fact, she had only mild pneumonia. Instead, SARS-CoV-2 had ruptured her heart.<\/p>\n<p>Meanwhile, epidemiologists began learning that preexisting heart disease and related conditions put people at greater risk of suffering and dying from COVID-19. \u201cWe\u2019re finding that many patients who have more severe forms of the illness are obese, they are diabetic, they are hypertensive,\u201d says cardiologist <a href=\"https:\/\/profiles.ucsf.edu\/nisha.parikh\" target=\"_blank\" rel=\"noopener noreferrer\">Nisha Parikh, MD<\/a>, a UCSF associate professor who specializes in population health research. Such risk factors, she says, are unusual. \u201cThey\u2019re not ones that really stood out in prior epidemics.\u201d<\/p>\n<p>Clinicians, too, were seeing surprising numbers of COVID-19 patients develop heart problems \u2013 muscle weakness, inflammation, arrhythmias, even heart attacks. \u201cWe\u2019re not used to respiratory viruses having such dire consequences on the heart in such apparently high numbers,\u201d says cardiologist <a href=\"https:\/\/profiles.ucsf.edu\/gregory.marcus\" target=\"_blank\" rel=\"noopener noreferrer\">Gregory Marcus, MD, MAS \u201908<\/a>, UCSF\u2019s Endowed Professor of Atrial Fibrillation Research. Many patients whose hearts acted up also had failing lungs. But others had no other symptoms or, like Dowd, only mild ones.<\/p>\n<p>Since March, Marcus has co-led one of the largest community surveys to better understand the spread of SARS-CoV-2 and its myriad effects. The study, dubbed COVID-19 Citizen Science, has so far enrolled more than 27,000 people; anyone with a smartphone <a href=\"https:\/\/eureka.app.link\/covid19\" target=\"_blank\" rel=\"noopener noreferrer\">can participate<\/a>. Marcus plans to also start collecting data from wearable devices, including Fitbits and Zio patches, which wirelessly monitor heart rhythms. \u201cThere may be large numbers of people who are suffering from cardiovascular effects of COVID-19 in the absence of other symptoms,\u201d Marcus says. \u201cI\u2019m worried we\u2019re missing those cases.\u201d<\/p>\n<p>It stands to reason that SARS-CoV-2 affects the heart. After all, heart cells are flush with ACE2 receptors, the virus\u2019s vital port of entry. And, indeed, laboratory experiments suggest that the virus can enter and replicate in cultured human heart cells, says <a href=\"https:\/\/profiles.ucsf.edu\/bruce.conklin\" target=\"_blank\" rel=\"noopener noreferrer\">Bruce Conklin, MD<\/a>, a professor of medicine and an expert in heart-disease genetics at UCSF and the Gladstone Institutes.<\/p>\n<p>But Conklin doesn\u2019t think SARS-CoV-2 necessarily kills heart cells outright. Rather, in the process of copying itself, the virus steals pieces of the genetic instructions that tell the heart cells how to do their job. \u201cIt\u2019s hauling away and hijacking stuff that\u2019s necessary for the heart to beat,\u201d he says. He is currently testing this hypothesis using human heart cells grown in cup-sized vessels\u00a0in the lab of <a href=\"https:\/\/profiles.ucsf.edu\/todd.mcdevitt\" target=\"_blank\" rel=\"noopener noreferrer\">Todd McDevitt, PhD<\/a>, a bioengineer at UCSF and the Gladstone Institutes.<\/p>\n<p>It\u2019s also possible, however, that an infected person\u2019s own immune system may do the majority of the damage in the heart, as it appears to do in the lungs. \u201cThe heart probably gets infected by a lot of other viruses, and they don\u2019t have a lethal effect,\u201d Conklin says. \u201cWhat makes this one different?\u201d<\/p>\n<div>\n<div><iframe loading=\"lazy\" src=\"https:\/\/view.genial.ly\/5f15e3e21bf1030d9265f948\" width=\"1363.2px\" height=\"852px\" frameborder=\"0\" scrolling=\"yes\" allowfullscreen=\"allowfullscreen\" data-mce-fragment=\"1\"><\/iframe><\/div>\n<\/div>\n<p>Graph with three bars. Bar at left has 80% at top and Non-Severe at bottom. Bar in middle has 15% at top and Severe at bottom Bar at right has 5% at top and Critical at bottom. Text below graph reads: Most symptomatic cases of COVID-19 are mild. To left of graph, small circle with the letter \u201ci\u201d in the middle opens to text reading: Graph Data: Wu et al., JAMA 2020. Livingston et al., JAMA 2020. Garg et al, MMWR 2020. Stoke et al., MMWR 2020. Left of graph: illustration of a coronavirus.<\/p>\n<p class=\"text-align-center\">Most symptomatic cases of COVID-19 are mild.<\/p>\n<p>&nbsp;<\/p>\n<h2 class=\"covid-mag-blue-callout\">Stranger things<\/h2>\n<p>Toward the end of March, as San Francisco began to warm up, Sonia got cold feet. She put on wool socks and turned up her heater. Still, her feet felt frozen. Three days later, her soles turned splotchy purple. Red dots appeared on her toes. At night, her cold feet itched and burned. Walking hurt. And she was exhausted, napping through afternoon Zoom meetings. \u201cIt was so bizarre,\u201d says Sonia, a San Francisco resident. A week later, her symptoms were gone.<\/p>\n<p>\u201cYes, COVID,\u201d wrote <a href=\"https:\/\/profiles.ucsf.edu\/lindy.fox\" target=\"_blank\" rel=\"noopener noreferrer\">Lindy Fox, MD<\/a>, a UCSF professor of dermatology, replying to an email describing Sonia\u2019s case. Sonia wasn\u2019t surprised. Anyone, like her, who\u2019s been following news of the pandemic has probably heard about \u201cCOVID toes,\u201d a painful or itchy skin rash that sometimes pops up in young adults with otherwise mild or asymptomatic cases of COVID-19. \u201cIt looks like what we call pernio, or chilblains,\u201d Fox says, \u201cwhich is a pretty common phenomenon when somebody goes out in cold weather \u2013 they start to get purple or pink bumps on their fingers or toes.\u201d<\/p>\n<p>Many people with rashes like Sonia\u2019s don\u2019t test positive for COVID-19, Fox says, which has made some clinicians skeptical of the connection; when patients have both, it\u2019s just a coincidence, they believe. But Fox doesn\u2019t think so. For one thing, \u201cthe time of year is wrong,\u201d she says. \u201cPernio usually shows up in the dead of winter.\u201d Even more compelling, dermatologists around the world are \u201cgetting crazy numbers of calls about it,\u201d Fox says. \u201cIn the last three weeks, I\u2019ve had somewhere between 10 and 12 patients.<br \/>\nNormally, I have four a year.\u201d<\/p>\n<aside class=\"ucsfcallout mag-body-callout callout-right in-viewport\" data-image=\"1\">\n<div class=\"callout__image\">\n<div>\n<figure class=\"embedded-entity\"><picture><img loading=\"lazy\" decoding=\"async\" class=\"element-fade lazyloaded element-fade--in-viewport\" src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/quarter\/public\/2020-07\/covid-symbol.png\" alt=\"Illustration of a coronavirus symbol.\" width=\"330\" height=\"330\" data-src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/quarter\/public\/2020-07\/covid-symbol.png\" \/><\/picture><\/figure>\n<\/div>\n<\/div>\n<div class=\"callout__content\">\n<p class=\"small-text covid-mag-red-callout\">20%-40% of people with COVID-19 experience diarrhea, nausea, or vomiting before other symptoms.<\/p>\n<\/div>\n<\/aside>\n<p>And it\u2019s not just dermatologists who are adding their observations to COVID-19\u2019s ever-expanding symptom list. Gut specialists are finding that 20% to 40% of people with the disease experience diarrhea, nausea, or vomiting before other symptoms, says gastroenterologist <a href=\"https:\/\/profiles.ucsf.edu\/michael.kattah\" target=\"_blank\" rel=\"noopener noreferrer\">Michael Kattah, MD, PhD<\/a>, a UCSF assistant professor. If you swallow virus particles, he says, there\u2019s a good chance they will infect cells lining your stomach, small intestine, or colon. As in the lungs and heart, these cells are studded with vulnerable ACE2 portals.<\/p>\n<p>Especially disconcerting, Kattah says, is how long the virus seems to persist in the gut. About 50% of patients with COVID-19 have virus particles in their stools, often for weeks after their nose swabs test negative, he points out. Laboratory studies show that these particles are often still alive and can infect cells in a petri dish. Whether fecal transmission occurs between people, however, is an open question. If the answer is yes, people recovering from COVID-19 may need to stay quarantined even after they feel well, and the rest of us will need to be as meticulous about bathroom hygiene as we\u2019ve become about handwashing and mask-wearing.<\/p>\n<p>Other specialists are also raising flags. Neurologists worry about reports of COVID-19 patients with headaches, \u201cbrain fog,\u201d loss of the sense of smell, dizziness, delirium, and, in rare cases, stroke. Nephrologists worry about kidney stress and failure. Hepatologists worry about liver injuries. Ophthalmologists worry about pink eye. Pediatricians, meanwhile, worry about a peculiar <a href=\"https:\/\/youtu.be\/ny4NivhjHAQ?t=5014\" target=\"_blank\" rel=\"noopener noreferrer\">COVID-related inflammatory syndrome that\u2019s showing up in kids<\/a> and young adults.<\/p>\n<blockquote class=\"blockquote blockquote--half-left in-viewport\">\n<p class=\"blockquote-content__text\">There\u2019s a lot of smoke. We need to figure out where the fire is coming from.\u201d<\/p>\n<footer>\n<p class=\"blockquote-content__cite\">MICHAEL WILSON, MD<\/p>\n<\/footer>\n<\/blockquote>\n<p>Researchers are still sorting out the causes for this constellation of effects. If you come down with a particular symptom, is it because the virus is attacking your cells? Because your immune system is overreacting? Or just because you\u2019re very sick? In any severe illness, for example, the kidneys must work extra hard to filter waste and control nutrients and fluid; if overtaxed, they may begin to fail. Similarly, cognitive problems can result from increased blood toxins due to stressed kidneys or from low oxygen due to respiratory distress. \u201cThere\u2019s a lot of smoke,\u201d says <a href=\"https:\/\/profiles.ucsf.edu\/michael.r.wilson\" target=\"_blank\" rel=\"noopener noreferrer\">Michael Wilson, MD \u201907, MAS \u201916<\/a>, the Rachleff Distinguished Professor at UCSF\u2019s Weill Institute for Neurosciences. \u201cWe need to figure out where the fire is coming from.\u201d<\/p>\n<p>Recently, there\u2019s been speculation that some of COVID-19\u2019s seemingly disparate symptoms may stem from trouble in the blood. Blood clots, for example, are showing up in cases of COVID-19 frequently enough for clinicians to take notice. \u201cThere\u2019s something unique about the coagulation system in these patients,\u201d says nephrologist <a href=\"https:\/\/profiles.ucsf.edu\/kathleen.liu\" target=\"_blank\" rel=\"noopener noreferrer\">Kathleen Liu, MD \u201999, PhD \u201997, MAS \u201907<\/a>, a UCSF professor of medicine. In caring for COVID-19 patients on dialysis machines, she\u2019s been surprised to see blood clots block dialysis tubes more than usual. Clotted tubes are common, she says, \u201cbut this is extreme.\u201d<\/p>\n<aside class=\"ucsfcallout mag-body-callout callout-right in-viewport\" data-image=\"1\">\n<div class=\"callout__image\">\n<div>\n<figure class=\"embedded-entity\"><picture><img loading=\"lazy\" decoding=\"async\" class=\"element-fade lazyloaded element-fade--in-viewport\" src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/quarter\/public\/2020-07\/covid-symbol.png\" alt=\"Illustration of a coronavirus symbol.\" width=\"330\" height=\"330\" data-src=\"https:\/\/www.ucsf.edu\/sites\/default\/files\/styles\/quarter\/public\/2020-07\/covid-symbol.png\" \/><\/picture><\/figure>\n<\/div>\n<\/div>\n<div class=\"callout__content\">\n<p class=\"small-text covid-mag-red-callout\">Evidence suggests SARS-CoV-2 can infect cells in the walls of blood vessels that help regulate clotting.<\/p>\n<\/div>\n<\/aside>\n<p>That may be because, as growing evidence suggests, SARS-CoV-2 can infect cells in the walls of blood vessels that help regulate blood flow and coagulation, or clotting. If true, this behavior could explain some of the virus\u2019s weirder (and rarer) manifestations, such as heart attacks, strokes, and even \u201cCOVID toes.\u201d<\/p>\n<p>\u201cOur vasculature is a contiguous system,\u201d says cardiologist Parikh. \u201cThus injury in one area, such as blood vessels in the lungs, can set off clotting cascades that affect multiple organs.\u201d Some of that trouble likely results from inflammation triggered by the immune system, she points out, although another culprit may be the body\u2019s RAAS, or renin-angiotensin-aldosterone system, a hormone system that controls blood pressure and fluid balance. Because RAAS involves ACE2 receptors, Parikh suspects it may become disrupted when the virus infects cells through these receptors, thus triggering coagulation and other downstream effects. Her lab is now studying this system in COVID-19 patients to better understand how SARS-CoV-2 infection affects it.<\/p>\n<p>Inevitably, some ailments may turn out to be red herrings. During a pandemic, when people are flocking to hospitals with infections, clinicians will also see a rise in other health problems, simply by the rules of statistics, points out <a href=\"https:\/\/profiles.ucsf.edu\/andy.josephson\" target=\"_blank\" rel=\"noopener noreferrer\">S. Andrew Josephson, MD<\/a>, the Francheschi-Mitchell Professor, chair of UCSF\u2019s neurology department, and a member of the Weill Institute for Neurosciences. \u201cIf the prevalence of infection is high, then almost any condition \u2013 a broken leg, if you will \u2013 you might conclude is associated with COVID-19.\u201d<\/p>\n<p>\u201cAs clinicians, we want to get information to our medical community and to the public as quickly as possible,\u201d Josephson says, \u201cbut we have to be cautious about not making too big a deal of a little blip.\u201d<\/p>\n<h2 class=\"covid-mag-teal-callout\">The long tail<\/h2>\n<p>As with any infection, how long a bout of COVID-19 lasts <a href=\"https:\/\/www.sfchronicle.com\/bayarea\/article\/The-curious-case-of-the-SF-doctor-who-s-been-15304660.php\" target=\"_blank\" rel=\"noopener noreferrer\">varies from person to person<\/a>. If you\u2019re ill enough to need critical care, you can expect the disease to take at least a few weeks to run its course. In some cases, symptoms persist for months. For a typical milder case, though, you should feel better within a couple weeks.<\/p>\n<p>At that point, the question foremost on your mind will be: Am I immune? There are now more than a dozen antibody tests on the market, but most are unreliable, <a href=\"https:\/\/www.nytimes.com\/2020\/04\/24\/health\/coronavirus-antibody-tests.html\" target=\"_blank\" rel=\"noopener noreferrer\">according to UCSF research<\/a>. And even the best tests can\u2019t tell you whether you have enough of the right kinds of antibodies to protect you against reinfection. \u201cThere is a lot of hope and belief that we\u2019ll have an antibody test that actually informs us of immunity, but we\u2019re not quite there yet,\u201d says <a href=\"https:\/\/profiles.ucsf.edu\/charles.langelier\" target=\"_blank\" rel=\"noopener noreferrer\">Chaz Langelier, MD, PhD<\/a>, a UCSF assistant professor of medicine who is working to improve diagnostic tools for COVID-19.<\/p>\n<p>What we have in the meantime are a lot of unknowns: If you do become immune to SARS-CoV-2, when and how does that occur? Will you gain immunity from a mild or asymptomatic case, as well as a severe one? How long will that immunity last?<\/p>\n<p>\u201cThe answers will have huge implications for social distancing and masking and for getting the economy back up and running,\u201d says <a href=\"https:\/\/profiles.ucsf.edu\/michael.peluso\" target=\"_blank\" rel=\"noopener noreferrer\">Michael Peluso, MD<\/a>, a clinical fellow who came to UCSF three years ago to help fight HIV. Now he\u2019s co-leading <a href=\"https:\/\/www.liincstudy.org\/\" target=\"_blank\" rel=\"noopener noreferrer\">a new study called LIINC<\/a>(Long-term Impact of Infection with Novel Coronavirus), which is enrolling people who have been infected with SARS-CoV-2 and will follow them for two years. Besides illuminating changes in immunity over time, LIINC is investigating chronic effects of infection on the immune system, lungs, heart, brain, blood, and other parts of the body.<\/p>\n<p>\u201cI hope people will recover and immunity will be protective and long-lasting, and that will be that,\u201d Peluso says.<\/p>\n<p>It\u2019s what we all hope. We hope we will beat an infection swiftly \u2013 or, better yet, avoid the virus until there is a vaccine. We hope that if we do fall gravely ill, we will be cared for by the best providers and tended to by people we love. The reality, as we already know, is more complicated. And even if COVID-19 doesn\u2019t batter our bodies, the pandemic will surely leave scars \u2013 on our psyches, our livelihoods, our institutions, and our health \u2013 that we are only beginning to fathom. In truth, we don\u2019t know how our cards will fall, as individuals or as a people. Only time \u2013 and data \u2013 will tell.<\/p>\n<p>___<br \/>\n<a href=\"https:\/\/www.ucsf.edu\/magazine\/covid-body?fbclid=IwAR0XVCzF-QC9WZOW_Rc3Wutx3p16QBxhtW-c3s0Xb7yfVW0n8TR35ruiXno\">https:\/\/www.ucsf.edu\/magazine\/covid-body?fbclid=IwAR0XVCzF-QC9WZOW_Rc3Wutx3p16QBxhtW-c3s0Xb7yfVW0n8TR35ruiXno<\/a><\/p>\n<\/div>\n","protected":false},"excerpt":{"rendered":"","protected":false},"author":1,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[1],"tags":[],"class_list":["post-23070","post","type-post","status-publish","format-standard","hentry","category-uncategorized"],"_links":{"self":[{"href":"http:\/\/stateofthenation.co\/index.php?rest_route=\/wp\/v2\/posts\/23070","targetHints":{"allow":["GET"]}}],"collection":[{"href":"http:\/\/stateofthenation.co\/index.php?rest_route=\/wp\/v2\/posts"}],"about":[{"href":"http:\/\/stateofthenation.co\/index.php?rest_route=\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"http:\/\/stateofthenation.co\/index.php?rest_route=\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"http:\/\/stateofthenation.co\/index.php?rest_route=%2Fwp%2Fv2%2Fcomments&post=23070"}],"version-history":[{"count":0,"href":"http:\/\/stateofthenation.co\/index.php?rest_route=\/wp\/v2\/posts\/23070\/revisions"}],"wp:attachment":[{"href":"http:\/\/stateofthenation.co\/index.php?rest_route=%2Fwp%2Fv2%2Fmedia&parent=23070"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"http:\/\/stateofthenation.co\/index.php?rest_route=%2Fwp%2Fv2%2Fcategories&post=23070"},{"taxonomy":"post_tag","embeddable":true,"href":"http:\/\/stateofthenation.co\/index.php?rest_route=%2Fwp%2Fv2%2Ftags&post=23070"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}