Topline: New York City Mayor Bill de Blasio said during a Sunday CNN appearance that “if we don’t get more ventilators in the next 10 days, people will die who don’t have to die” as the city—now the epicenter of the U.S. coronavirus epidemic—faces a possible shortage of medical supplies.
“We’re about 10 days from seeing widespread shortages,” de Blasio said, adding, “We have seen next to nothing from the federal government at this point.”
De Blasio also said that the military hasn’t been mobilized by the Trump administration, and that the Defense Production Act, which the president invoked by executive order Wednesday, has not been put into motion.
“It feels like we’re on our own at this point,” de Blasio said, adding that April would be worse for New York City than March has been, and he fears May could be even worse.
CNN also reported Sunday that Federal Emergency Management Agency head Peter Gaynor could not provide a number of how many medical masks were in the federal stockpile or how many have been shipped to state and local governments.
In a sign of demand on medical supplies, a Friday letter from a New York-Presbyterian Hospital department head said each employee would only be given one N95 mask (when it typically uses 4,000 per day).
Big number: 300 million. That’s how many masks could be needed for healthcare workers versus the current stockpile of 30 million, as testified to Congress by Health and Human Services Secretary Alex Azar at the end of February.
Key background: The Defense Production Act is intended to be used by Trump to obtain “health and medical resources needed to respond to the spread of Covid-19, including personal protective equipment and ventilators.” Trump faced questions Thursday around his reticence to use the Defense Production Act to compel companies to produce healthcare items to combat the coronavirus, one day after he said he’d be invoking its powers. The New York Times reported Thursday that both the U.S. and countries abroad are facing a shortage of ventilators, with manufacturers saying that they can’t increase production to meet the demand.
I’m a New York-based journalist covering breaking news at Forbes. I hold a master’s degree from Columbia University’s Graduate School of Journalism. Previous bylines: Gotham Gazette, Bklyner, Thrillist, Task & Purpose and xoJane.
A sequel to a movie that you didn’t want to see in the first place is one thing, like Ghost Rider 2 after Ghost Rider. A sequel to having a COVID-19 infection would be something completely different.
You may think that the one “positive” of testing positive for the COVID-19 causing coronavirus (SARS-CoV2) and surviving would be that you won’t get infected by that virus again. At least not during this pandemic. Ah, but is this assumption really true? Will you indeed be immune to the SARS-CoV2 after you’ve recovered from a COVID-19 infection? Some reports out of Japan and China seem to suggest otherwise.
Does this case actually prove that re-infection with the virus is possible? Or was this just a mistake in the testing? Or did the person have a particularly weak immune system so that she couldn’t generate immunity? After all, one case can be an accident, an aberration, an anomaly, an aardvark in a sea of anemone.
Well, oops something like this happened again, according to a more recent NHK-World Japan report. This time it was a man in his 70’s, who first tested positive for SARS-CoV2 on February 14 while on a Diamond Princess cruise ship. After being transferred to a medical facility in Tokyo, he stayed there until testing negative for the virus. On March 2, he left the facility and traveled home via public transportation. However, the man eventually began feeling sick with a fever, which prompted him to go to a hospital on March 13. The following day he tested positive for the virus again.
Then there’s the February 14 article from Caixin, a Beijing, China-based media group, that was entitled “14% of Recovered Covid-19 Patients in Guangdong Tested Positive Again.” Umm, 14% would seem more like an “ooop” than an “ooops.” This CGTN news warned of such reinfection possibilities:
Remember though, these are news reports and not scientific studies yet. While the reappearance of Nicholas Cage with a flaming skull riding a motorcycle may not call for additional scientific studies, all of these cases certainly do. First, scientists need to confirm whether the test results were indeed accurate. Remember, no test is perfect. If people can screw up a drink order, they can certainly mess up a medical test. Even if a test is performed properly, you could still get a positive result when you don’t actually have an infection. On the flip side, just because you test negative doesn’t necessarily mean that there is no way that you are carrying the virus. That’s why a doctor may test you multiple times to be sure of a result.
Secondly, doctors and other scientists need to double-check or triple-check that each of these patients actually got re-infected with the virus rather than had an infection that simply lasted a long time. What if, for example, the cruise passenger and the tour bus guide each had fairly long infections and just happened to have intervening false negative test results? The tests could have simply been like commercial breaks in the middle of a single long episode of a television show.
Third of all, the amount of immunity that you build up after being exposed to any virus depends on not only virus itself but surprise, surprise your immune system and its response. When your immune system sees a particular virus for the first time, it can essentially get caught with its pants down, not ready to defend your body against this new invader. However, exposure to the virus either through a vaccine or getting infected may train your immune system so that, borrowing the words of former President George W. Bush, “fool me once, shame on — shame on you. Fool me — you can’t get fooled again.” If strong enough, your immune system then may be ready with proper defenses next time the virus comes calling. Could the cases of reinfection then be examples of people who happened to have weaker immune systems?
Or are these cases any indication that our immune systems may not be able to consistently build up enough protection against SARS-CoV2? Well, a review article published in January 2020 in the Journal of Medical Virology summarizes much of what is known about your immune system’s response to various types of coronavirus. As you can see, this involves a complex orchestra of different cells and chemicals. Therefore, the immune response to one virus won’t necessarily be the same as to another virus, even if both viruses were different types of coronaviruses. All of this also depends on how strong your immune system may be and how well your immune system recognizes an invader like SARS-CoV2.
Plus, your immune system has got to remember the virus. Over time, immunity may fade, allowing the virus to reinfect you. It’s like when you get back together with an ex after you have forgotten how terrible you are for each other. The question then is how long can your immune system remember SARS-CoV2?
With SARS-CoV2 having emerged so quickly, there just haven’t been enough studies yet on how your immune system may react specifically to SARS-CoV2 and how this may differ from person to person. Therefore, we have to rely on studies of other coronaviruses for now. The closest approximation is probably the even more evil cousin of SARS-CoV2, the original SARS virus that caused the outbreak of 2002-2003.
In a study published in a 2007 issue of Emerging Infectious Diseases, a research team from the Shanxi Provincial Center for Disease Control and Prevention in Taiyuan, China, followed 176 patients who had had severe acute respiratory syndrome (SARS). On average, SARS-specific antibodies remained at the same level in a patient’s blood for about two years. Then, during the third year after infection, antibody levels tended to drop precipitously. This suggests that immunity to the SARS virus may remain for two to three years with reinfection possible after three years.
Keep in mind though that antibody levels do not always correlate with immunity. They can be like selfies on Instagram, only indirect measures of what’s really going on at a deeper level. Some people may have immunity against a virus without detectable antibody levels, and some people may be very susceptible to infection even though antibodies are present. The only way to have determined if the patients actually had immunity against the SARS virus would have been to have re-exposed them to the virus and checked what happened. And that would have been a horrible experiment to do.
The other question is how many different versions of SARS-CoV2 may be running around, or rather spreading around since viruses don’t have little feet and little sneakers. It’s difficult to answer this question for sure without more thorough and widespread testing. According to a study published in the journal National Science Review, an analysis of samples from 103 COVID-19 cases suggests that at least two different versions of SARS-CoV2 are circulating. This doesn’t necessarily mean that these versions are so different that immunity to one version doesn’t mean immunity to another. Regardless, things may evolve in the near future. Viruses can be like the characters in Game of Thrones or an actor in a Broadway show, changing rapidly. Over time, the new coronavirus could possibly mutate to the point that new versions are no longer as recognizable by your immune system as the original version. After all, mutations are probably what allowed the virus to jump from another animal to humans.
Not knowing exactly how immunity against SARS-CoV2 works and how long it may last throws a gigantic wrench into public health planning. Many trying to predict the course of the pandemic have been assuming that once a high enough proportion of the overall population has been infected and has become immune, the pandemic will subside. Herd immunity is the percentage of the overall population that is immune to a given pathogen. When this percentage gets high enough, the virus will struggle to find more susceptible people to infect, sort of like trying to sell Justin Bieber T-shirts in a crowd when most of the people are already wearing such shirts. The belief is that when around 70% of the population is immune to the virus, SARS-CoV2 will struggle to continue transmitting.
However, things could change substantially if people can actually get re-infected with the virus or different enough versions of the virus end up circulating. Such possibilities would be yet more reasons to question the “herd immunity” approach to controlling the pandemic that’s currently being discussed in the U.K. and described by Sarah Boseley for The Guardian. Since there is no vaccine available against SARS-CoV2, there is actually talk of allowing those with stronger immune systems to get infected to achieve the 70% or so herd immunity threshold. Huh?
This strategy would make sense except for the fact that it doesn’t. First of all, those who get infected could end up having serious consequences such as death, which is typically a very serious consequence. This would be reminiscent of the saying that “the operation was successful, but the patient died.” Allowing people to become infected by a potentially deadly virus is always a risky proposition, sort of like playing roulette when your lungs are on the betting table. So far, the COVID-19 case-fatality rate seems to be somewhere between 1% and 3.4%. This isn’t as high as the rate for SARS but nonetheless significantly higher than that of a bad flu season.
Secondly, this herd immunity strategy depends on people not getting re-infected with the virus. But with the aforementioned reports from Japan and China, you have to wonder if the strategy is not a “herd immunity” strategy but rather a “herd immunity maybe” strategy to borrow the words of Carly Rae Jepsen. “Maybe” may work to some degree with flirting and dating but not when lives are at stake.
Third of all, this strategy assumes that people will not leave or enter the U.K. That may work only if you want to completely eliminate travel to and from the country.
Finally, such a strategy would run counter to other mitigation strategies such as social distancing as indicated by the following tweet:
Uh, U.K., would this really be O.K.?
All of this is a reminder that scientists do not yet know enough about this new coronavirus. What percentage of people become immune to the virus if exposed? How strong is the immunity? Will it actually prevent reinfection? How long would this immunity last? Is it two years as the SARS study hints at or could it be much shorter than that? How does all of this vary from person to person? How many different versions of the virus may end up circulating? As the Internet meme goes, I and many other scientists have so many questions.
Therefore, if you do get exposed to the virus and recover, don’t view it as a free pass to start hugging strangers, digging your fingers deep into your nose like you are looking for pocket change, and licking door knobs. Keep doing what everyone else should be doing such as social distancing, washing your hands frequently and thoroughly, keeping your filthy fingers from gravitating towards your gigantic face, and actively disinfecting surfaces, objects, and that enormous BTS statue that you have in your living room. Just because you survived the first infection, doesn’t necessarily mean that future exposures and possible infections will end up OK. As you know, sequels don’t always have the same endings.
I am a writer, journalist, professor, systems modeler, computational and digital health expert, avocado-eater, and entrepreneur, not always in that order. Currently, I am a Professor of Health Policy and Management at the City University of New York (CUNY), Executive Director of PHICOR (@PHICORteam), Associate Professor at the Johns Hopkins Carey Business School, and founder and CEO of Symsilico. My previous positions include serving as Executive Director of the Global Obesity Prevention Center (GOPC) at Johns Hopkins University, Associate Professor of International Health at the Johns Hopkins Bloomberg School of Public Health, Associate Professor of Medicine and Biomedical Informatics at the University of Pittsburgh, and Senior Manager at Quintiles Transnational, working in biotechnology equity research at Montgomery Securities, and co-founding a biotechnology/bioinformatics company. My work involves developing computational approaches, models, and tools to help health and healthcare decision makers in all continents (except for Antarctica) and has been supported by a wide variety of sponsors such as the Bill and Melinda Gates Foundation, the NIH, AHRQ, CDC, UNICEF, USAID and the Global Fund. I have authored over 200 scientific publications and three books. Follow me on Twitter (@bruce_y_lee) but don’t ask me if I know martial arts
Coronaviruses (CoV) are a family of viruses that cause sicknesses like the common cold, as well as more severe diseases, such as Middle East Respiratory Syndrome and Severe Acute Respiratory Syndrome. A novel coronavirus (nCoV) is a new strain – one that hasn’t previously been recognized in humans. Coronaviruses cause diseases in mammals and birds. A zoonotic virus is one that is transmitted between animals and people. When a virus circulating in animal populations infects people, this is termed a “spillover event”. How does CoVID-19 affect the body? The virus is fitted with protein spikes sticking out of the envelope that forms the surface and houses a core of genetic material. Any virus that enters your body looks for cells with compatible receptors – ones that allow it to invade the cell. Once they find the right cell, they enter and use the cell’s replication machinery to create copies of themselves. It is likely that COVID-19 uses the same receptor as SARS – found in both lungs and small intestines. It is thought that CoVID-19 shares many similarities with SARS, which has three phases of attack: viral replication, hyper-reactivity of the immune system, and finally pulmonary destruction. Early on in infection, the coronavirus invades two types of cells in the lungs – mucus and cilia cells. Mucus keeps your lungs from drying out and protects them from pathogens. Cilia beat the mucus towards the exterior of your body, clearing debris – including viruses! – out of your lungs. Cilia cells were the preferred hosts of SARS-CoV, and are likely the preferred hosts of the new coronavirus. When these cells die, they slough off into your airways, filling them with debris and fluid. Symptoms include a fever, cough, and breathing difficulties. Many of those infected get pneumonia in both their lungs. Enter the immune system. Immune cells recognize the virus and flood into the lungs. The lung tissue becomes inflamed. During normal immune function, the inflammatory process is highly regulated and is confined to infected areas. However, sometimes the immune system overreacts, and this results in damage to healthy tissue. More cells die and slough off into the lungs, further clogging them and worsening the pneumonia. As damage to the lungs increases, stage three begins, potentially resulting in respiratory failure. Patients that reach this stage of infection can incur permanent lung damage or even die. We see the same lesions in the lungs of those infected by the novel coronavirus as those with SARS. SARS creates holes in the lungs, so they look honeycomb-like. This is probably due to the aforementioned over-reactive immune response, which affects tissue both infected and healthy and creates scars that stiffen the lungs. As such, some patients may require ventilators to aid breathing. The inflammation also results in more permeable alveoli. This is the location of the thin interface of gas exchange, where your lungs replace carbon dioxide in your blood with fresh oxygen you just inhaled. Increased permeability causes fluid to leak into the lungs. This decreases the lungs’ ability to oxygenate blood, and in severe cases, floods them so that you become unable to breathe. Sometimes, this can be fatal. The immune system’s over-reaction can also cause another kind of damage. Proteins called cytokines are the immune system’s alarm system, recruiting immune cells to the infection site. Over-production of cytokines can result in a cytokine storm, where there is large-scale inflammation in the body. Blood vessels become more permeable and fluid seeps out. This makes it difficult for blood and oxygen to reach the rest of the body and can result in multi-organ failure. This has happened in the most severe cases of CoVid-19. Although there are no specific treatments for coronaviruses, symptoms can be treated through supportive care. Also, vaccines are currently in development. What can you do to protect yourself from CoVid-19? Basic protocol comes down to regular hand washing, avoiding close contact with anyone coughing or sneezing, avoiding unnecessary contact with animals, washing hands after contact with animals, thoroughly cooking meat and eggs prior to consumption, and covering your mouth and nose while coughing or sneezing. Respiratory viruses are typically transmitted via droplets in sneezes or coughs of those infected, so preventing their travel stops the spread of disease. Alveoli model from: https://www.turbosquid.com/3d-models/…