“Your Health Checkup” is our online column by Dr. Douglas Zipes, an internationally acclaimed cardiologist, professor, author, inventor, and authority on pacing and electrophysiology. Dr. Zipes is also a contributor to The Saturday Evening Post print magazine. Subscribe to receive thoughtful articles, new fiction, health and wellness advice, and gems from our archive.
Unless you have been living on another planet these past few weeks, you have been deluged with daily updates about the new coronavirus, 2019-nCoV, the seventh member of the family of coronaviruses that infect humans. The information, depending on its source, is at times reassuring and at other times frightening. At the very least, it is unsettling, especially as we read about the impact the virus has had in China, particularly in Wuhan where it began, perhaps transmitted by camels, bats or the pangolin, an animal used in traditional Chinese medicine. Infection has spread to over twenty countries, mostly in Japan, Singapore, Thailand, Hong Kong, and other Asian countries.
The purpose of this column is to provide readers with some facts as we know them today, and to offer reliable sources where readers can obtain valid information, such as from the Johns Hopkins website, the World Health Organization, or the American Medical Association that deliver expert information about the impact and extent of nCoV.
As I have written previously, due to deficiencies in worldwide health care, unfounded distrust of vaccinations and health services, and poor health infrastructure, our planet is ill- prepared to handle a pandemic of coronavirus proportion. At the time of this writing, there are around 40,000 confirmed cases of 2019-nCoV infection — the vast majority concentrated in China — and more than 900 deaths, for about a 2 percent mortality. One of the deaths included the unfortunate Chinese physician who first called attention to the new virus. Twelve cases of nCoV infection have occurred in the U.S. (nine people had been in Wuhan) with no deaths to date, although a 53-year-old American man has recently died in China. Thousands of people have been trapped on three cruise liners in Asia due to fears of contagion. Human-to-human transmission has been documented, leading the World Health Organization to declare a public health emergency on January 30, with a similar declaration by the U.S. a day later.
Coronavirus outbreaks are nothing new. The Severe Acute Respiratory Syndrome (SARS) virus was another coronavirus originating in China in 2003, not as contagious as nCoV, though more lethal. SARS infected over 8,000 people, killing almost 10 percent of infected people before it was contained. The Middle East Respiratory Syndrome coronavirus (MERS) was also a coronavirus stemming from animal reservoirs such as bats, perhaps with intermediate hosts. MERS infected 2,494 people and caused 858 deaths (34 percent mortality rate), the majority in Saudi Arabia.
In comparison, the influenza virus kills less than one person per thousand infected (0.1 percent), but about 200,000 people are hospitalized with the virus each year in the U.S., leading to about 35,000 deaths.
The SARS pandemic cost the global economy an estimated $30 billion to $100 billion. The full economic impact of nCoV is yet to be felt, and while the Chinese economy is likely most affected, the impact will be worldwide as it upends manufacturing, shipping, travel, education, and other activities.
Such respiratory viruses travel through the air in tiny droplets produced when an infected person breathes, talks, coughs or sneezes. This coronavirus is moderately contagious, harder to transmit than measles, chickenpox, and tuberculosis, but easier than H.I.V. or hepatitis, which are spread only through direct contact with bodily fluids. Face masks may help prevent its spread, though that has yet to be established.
The incubation period after being infected before symptoms manifest appears to be 2-14 days (more likely 5-6 days), raising the possibility of transmission before a person knows they are infected, though transmission by symptomatic persons is more probable due to a greater viral load at that time. Older men with other health issues seem more likely to become infected and young children less likely.
Symptoms can include fever, cough, shortness of breath, muscle ache, confusion and headache, sore throat, and GI problems such as diarrhea, nausea, and vomiting. Pneumonia has been documented in the majority of hospitalized patients and when severe, is probably the cause of most deaths. The median time from first symptoms to becoming short of breath is five days; to hospitalization, seven days; and to severe breathing trouble, eight days.
Additional information about 2019-nCoV is needed to better understand transmission, disease severity, and risk to the general population. Public health measures to quarantine infected individuals and prevent spread have been instituted worldwide.
Management of people with 2019-nCoV is largely supportive, although antiviral medications have been used, as have antibiotics in patients with superimposed bacterial infections. The effectiveness of antiviral medications is unproven, although they may have been effective in treating SARS. Interventions that will ultimately control nCoV are unclear because there is currently no vaccine available and one is not likely for a year or longer.
Staying home when ill, handwashing, and respiratory care including covering the mouth and nose during sneezing and coughing, were effective in controlling SARS and should be advocated for treating nCoV as well.
Presently, there is no reason for panic in Western countries. We need to follow updates and hope containment will eliminate the threat of this new nCoV pandemic over the next month or so. Remember that the virus is transmitted by humans during sneezing or coughing. Avoid such individuals or wear a face mask if in contact. The CDC does not recommend widespread use of masks for the healthy, general public at present.
If you sneeze or cough, do so into a disposable cloth or paper. A fist bump greeting rather than a handshake might be wise. For viral particles that have settled on the floor, table, and other objects, hand contact then brought to your face can transmit the infection. So, wash! wash! wash! your hands with antibacterial soap after contacting such surfaces and before touching your face. Alternatively, use an alcohol-based hand sanitizer containing at least 60 percent alcohol. Green leafy vegetables and other sources of vitamin C can help the immune system fight off disease.
If we all pay attention to these simple measures, we will help contain the virus and it will eventually die out, particularly as warmer weather approaches.
Featured image: Shutterstock
Flu, AIDS, meningitis, Ebola, polio, herpes, measles, rabies—the list of diseases caused by viruses is a litany of woe ranging from the merely annoying to the deadly. Every year almost two million people are killed by the human immunodeficiency virus (HIV), and around half that many people succumb to viral hepatitis infections. The economic toll of viral illnesses is nearly as staggering as the human one; flu costs the United States an estimated $25 billion a year, and HIV costs $36 billion. To make matters worse, new viruses continue to appear (see “Virus Hunter” below), often after hiding in animal populations for centuries before moving into humans—as did HIV, avian flu, and severe acute respiratory syndrome (SARS). But while public health officials and physicians focus on the threat of emerging viruses, little-noticed research is implicating these primitive microbes in diseases long thought to have nothing to do with them: mental illnesses.
The notion that “insanity is infectious,” as virologist Ian Lipkin of Columbia University’s Mailman School of Public Health bluntly puts it, goes back to antiquity. As late as the 1800s, the mentally ill were locked away because, among other reasons, they were thought to be contagious. The notion wasn’t completely misguided. Until the discovery of penicillin ushered in the age of antibiotics, a major cause of mental illness was syphilis. But biomedicine is subject to fads and fashion no less than skirts are, and over the last 40 years disease detectives seeking the cause of mental conditions such as schizophrenia, bipolar disorder, autism, and obsessive-compulsive disorder have turned from microbes to genes as the cause. And now, a parade of discoveries suggests that viruses may be the culprit rather than your family tree. The new research indicates that viral infection can affect the developing brain and contribute to mental illnesses even before birth.
At first the evidence for a viral link to mental illness was spotty and inconsistent. Early studies piggy-backed on observations that when mothers suffered an infection during pregnancy, the children who were in utero at the time had an elevated risk of developing schizophrenia. But rigorous studies of whether that link was real produced contradictory results: Some found that maternal infection with influenza increased the risk of a child developing schizophrenia 20 years later, but others did not. Only in the last few years have scientists sorted it out. Instead of assuming that every child who had been in utero at the time of a flu outbreak had been infected, researchers began examining mothers’ blood for the telltale antibodies that indicate a past infection. With that advance, the link became clear: As researcher Alan Brown of Columbia University calculated in a 2010 paper, more than 30 percent of the risk of developing schizophrenia comes from prenatal exposure to the flu virus.
The flu virus is not the only culprit. In 2000, Brown and colleagues produced the first watertight evidence that young adults who had been exposed to the rubella virus (aka “German measles”) while they were fetuses less than three months old had a five-times-greater risk of developing psychosis—including schizophrenia—than their peers who had not been exposed to the virus.
Contrary to expectations, however, it is not rubella or other viruses, per se, that harm the developing brain. That became clear as scientists documented a veritable menagerie of maternal infections able to cause psychiatric and neurodevelopmental illnesses—not only flu and rubella but also toxoplasmosis and genitourinary infections. To their shock, scientists began to find that, although mothers had antibodies to flu in their blood (showing that the mother had been infected), the kids—in utero at the time—often did not: They were not infected with the virus.
So what was happening? It’s not that the fetus becomes infected. Instead, the infection triggers the mother’s innate immune system, the army of molecules that prime other cells to kill the invaders. “It is the reaction of the mother’s immune system to the infection, not the infection itself, that affects the developing brain,” says Lipkin. Specifically, a flood of antibodies and other immune-system chemicals with names like chemokines and cytokines surges through the placenta and into the fetus. “The result may be compromised fetal brain development,” explains Dr. Robert Freedman, a psychiatrist at the University of Colorado Denver Health Sciences Center.
Researchers put the final piece into the puzzle when they exposed pregnant mice to a molecular mimic of viral RNA (viral genes are often made of RNA instead of the closely related DNA). That exposure put the brakes on special stem cells that give rise to new nerve cells (neurons)—not just in the embryo but on into adulthood. Most egregiously, it blocked the growth of a specialized kind of neuron destined for the neocortex, the most advanced region of the brain.
How bad was the damage? The offspring of the virus-exposed mice could not even walk normally, reported epidemiologist Mady Hornig of Columbia and colleagues last year. And, after the mice grew to adulthood, they had other neurological abnormalities as well.
Because the mother’s immune system’s response to infection causes the harm to the fetus, almost any virus is a potential threat to the developing fetus. “The damage to neurons and neural stem cells might not be evident right away,” says Hornig, “but manifests later as cognitive and behavioral problems.”
How bad will those problems become? “The specific result depends on the timing,” says Lipkin. He explains that if neural stem cells are killed by the flood of immune-system molecules (the chemokines and cytokines) before they mature, they will not take their rightful place in the brain’s neural networks. Circuits that are forming at the time of the infection will be most vulnerable, while those already hooked up are spared. In schizophrenia, for instance, there are abnormally low numbers of neurons and incomplete clustering in a particular area of the brain, hinting that something went wrong when these regions were being constructed. The effect of the viral infection may be delayed even into adulthood if a circuit damaged by the cytokine flood is not recruited until that time.
The apparent link between prenatal viral infection and later brain disorders led Johns Hopkins Children’s Hospital to establish in 1998 the nation’s first pediatric research center to investigate links between severe mental illness and prenatal or early childhood viral infections. Last year, Robert Yolken, who heads the Stanley Division of Developmental Neurovirology at Johns Hopkins Medical School, and colleagues reported that in their study of all children born in Denmark since 1981, mothers who had been infected with herpes simplex 2 had a 56 percent greater risk of having a child who later developed schizophrenia.
Although current thinking holds that the mother’s immune response, not the virus itself, is the culprit behind viral causes of mental illness and neurodevelopmental disorders, there may be exceptions. Yolken, for instance, suspects that herpes and influenza viruses (as well as the Toxoplasma gondii parasite carried by cats and other warm-blooded animals) might invade the brain and lie dormant for years before triggering schizophrenia or bipolar illness.
The evidence that viruses can cause psychiatric illnesses and neurodevelopmental disorders does not mean they are the only causes. For example, bacteria can also trigger an immune response, which may explain why strep infection can damage the developing brain, leading to the constellation of tics, obsessive-compulsive disorder, and other symptoms called Pediatric Autoimmune Neuropsychiatric Disorders Associated with Streptococcal infections (PANDAS). Additionally, many mental illnesses are more likely to arise in people with a family history of them, indicating that they are at least partly heritable. But the failure of geneticists to find genes that have a strong effect on the likelihood of developing schizophrenia, depression, bipolar disorder, or autism suggests that genes do not cause these complex disorders the way a single gene directly causes, say, sickle-cell disease. More likely, says Lipkin, genes make people more or less susceptible to other causes of these diseases—including viruses.
Although the research is still new, scientists believe that it is not too early for obstetricians to take the emerging findings into account. The most obvious step is to monitor pregnant women closely for infections—even those that seem mild—because what may be a minor inconvenience to the mother could be devastating to the unborn child. Women should be educated to be aware of when they might have contracted a viral infection and to tell their obstetrician, who may need to treat them more aggressively than is current practice. In animal studies, after pregnant females were exposed to virus genes, the damage to their unborn pups was prevented when the mothers were given nonsteroidal anti-inﬂammatory drugs (NSAIDs) such as ibuprofen. That provides a rationale for using these drugs when a pregnant woman contracts an infection, says Hornig. Currently, obstetricians prescribe acetaminophen (Tylenol) for pain relief in pregnant women, but that compound does not have the anti-inflammatory effects needed to turn off the cytokine flood.
The old expression “take two aspirin—or ibuprofen—and call me in the morning” never had so much meaning.
It is no coincidence that the most widespread and dangerous viruses began infecting humans some 11,000 years ago, says virologist Nathan Wolfe, CEO of Global Virus Forecasting (GVF) Initiative. When animals and people live in close proximity, as they began to do with the advent of agriculture and animal husbandry, viruses from the former can jump the species barrier—as did HIV/AIDS, Ebola, Marburg, and more kinds of flu than you can count.
Wolfe, who founded GVF in 2008 and has been nicknamed the “Indiana Jones of virus hunters,” warns that our fellow mammals aren’t done with this problematic sharing. Some 60 percent of emerging viruses—that is, those new to medical science—come from animals. And as the world becomes smaller and more connected, allowing a traveler to get from the deepest jungles of Africa to London or New York or Tokyo in less than a day, the chance of a virus jumping from a monkey to a bush meat hunter to a western tourist and the entire developed world has soared. In his upcoming book The Viral Storm: The Dawn of a New Pandemic Age (to be published in October), Wolfe argues that this has made us sitting ducks for another global epidemic.
The greatest threats come from two sources: completely new viruses (such as HIV/AIDS) and viruses that mutate. Primates are the most likely reservoirs of the former because the closer the evolutionary relationship, the more likely a virus is to cross over. (For example, there are no cases of viruses jumping to humans from fish or insects, says Wolfe.) But viruses from mammals other than primates can also spread through the human population like wildfire. The H1N1 virus from pigs was so highly transmissible that it went from infecting zero percent of the human population to 10 percent in only a year, notes Wolfe, killing some 20,000 to 30,000 people. The only reason its toll has not been greater is that transmissibility and lethality are inversely related; that’s why Ebola, though deadly, is not highly transmissible.
An even greater threat is mutation of existing human viruses. If one that is deadly but not very transmissible or very transmissible but not deadly acquires genes for that second trait, the results could be catastrophic. That is most likely to happen when viruses from widely separated regions come into contact—as is more and more likely in what Wolfe calls “this viral mixing vessel” caused by global travel.
“Viruses aren’t static,” he says. “They change over time; they exchange genes with other viruses, which can make them more likely to develop deadly recombinants. The greatest threat is probably something we don’t even know is out there.”