Its not just your neck of the woods that the spread of the coronavirus is increasing. Its everywhere in New Jersey.
For a second straight week, all 21 counties saw increases in coronavirus cases. Every countys number of new cases for the week of Nov. 5-11 was at least 24% higher than the week prior, and 11 counties increased their caseloads by 50% or more.
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Passaic County saw the most severe spread, adding 32.8 cases per 10,000 residents, a 73% increase over the week prior. Essex County also cleared 30 new cases per 10,000, landing at 30.2.
Eight counties added more than 20 cases per 10,000 residents. The state as a whole added 20.5 cases per 10,000 residents, a 49% jump from the week prior. The U.S. added 25.5 cases per 10,000, up 35% from last week.
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Just three counties Cape May, Salem and Sussex managed to keep their new caseload under 10 per 10,000 residents. All were over 9.
The biggest spike from last week came in Warren County. After sitting at 8.7 new cases per 10,000 residents last week, the county jumped to 18.8 a 117% increase.
In an effort to curb the spread of the virus, Gov. Phil Murphy signed a new rule Thursday that will allow New Jersey counties and municipalities to order nonessential businesses to close at 8 p.m.
It came on the same day that new restrictions on bars and restaurants limiting hours and indoor dining went into effect.
Thursday brought 3,517 new cases of the coronavirus in N.J., the fourth time in six days that number has eclipsed 3,000.
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Nick Devlin is a reporter on the data & investigations team. He can be reached at ndevlin@njadvancemedia.com.
Even in normal times, mass-vaccination campaigns involve many moving parts within a vast network of suppliers, transporters and middlemen.
The particulars of Pfizers vaccine will make this effort even more complex. The vaccine, developed with the German company BioNTech, has to be stored at around minus 70 degrees Celsius (minus 94 Fahrenheit) until shortly before it is injected. That is about the temperature of the South Pole on a winter day and colder than any of the other leading vaccines in development.
Pending results from other front-runners in the vaccine race could change the stakes. Moderna Therapeutics said on Wednesday that it had seen enough Covid-19 cases in its late-stage study to do an early analysis of its vaccine, which uses the same messenger RNA technology that Pfizers does. The technology has never produced an approved vaccine.
Nine other candidates are also in the final stage of testing. If any of those win approval from the F.D.A., that will reduce the importance of Pfizers vaccine but also introduce new questions, such as which hospitals and people get the different vaccines.
For now, though, Pfizer is in the spotlight.
If an analysis planned for next week confirms the vaccines safety, the company is likely to ask the F.D.A. this month for emergency authorization to distribute its vaccine. In that case, limited doses will most likely be shipped to large hospitals and pharmacies to be provided to health care workers and other vulnerable groups.
But the specifics of how that will work are hazy at best.
Pfizer does not yet know where the government wants the vaccine sent or who will be first in line to receive it, said Ms. Alcorn, the supply-chain executive.
Were working very closely, in the U.S., in particular, with Operation Warp Speed to identify those distribution points, Ms. Alcorn said, referring to the federal initiative to produce and distribute Covid-19 vaccines. We dont have them today.
The announcement that a coronavirus vaccine developed by Pfizer with the German drugmaker BioNTech is more than 90 percent effective at preventing Covid-19 cases much better than many anticipated is cause for celebration. With a vaccine of this efficacy, suppression of the disease is entirely realistic.
Unfortunately, this development doesnt mean we can all relax and start doing more things. It means we need to tighten up even further until the vaccine becomes available.
The goal is now no longer to learn to live indefinitely with the virus. Its to get as many people through the winter as possible without getting sick. Keeping the infection rate low is important, because thats what will allow us to push the virus into the ground as quickly as possible once we have the vaccine in hand.
A death avoided this winter is a life saved. We are no longer delaying the inevitable.
Its always been hard to convince people to make good choices when considering sacrifices. Uncertainty around when wed get an effective vaccine made it even harder. Cutting off in-person interactions for an uncertain stretch of time was excruciating. But it may be more palatable to hunker down if its only for a defined period.
To make the situation concrete, lets consider the upcoming Thanksgiving holiday. With cases growing rapidly around the country, especially in the northern Midwest, indoor social gatherings are more dangerous than at any point since the spring. Thanksgiving dinners are ideal settings for superspreader events: They crowd people from all over around a table to talk, laugh and drink, often in poorly ventilated rooms. Many families stuff themselves into houses for an entire long weekend.
Many of us havent seen our extended relatives for months. If we believe this pandemic will be raging for another year or more its tempting to think that the benefits of reconnecting over Thanksgiving might outweigh the risk of infection. We cant wait forever; maybe its worth rolling the dice.
The calculus is very different, however, if a vaccine is around the corner. While Pfizers still needs to be approved, manufactured and distributed, the company estimates that 50 million doses could be distributed before the end of the year. Another 1.3 billion would come in 2021. If other vaccines also show success, relief could come as soon as the spring.
Assuming this timeline holds, the case for skipping Thanksgiving becomes much stronger. People no longer have to pick between the risk of spreading Covid-19 and the risk of forgoing seeing family for the foreseeable future. They have only to sacrifice seeing them this fall in order to see them much more safely a number of months later. Why not wait?
The point generalizes. Without question, the sacrifices required to keep us safe from Covid-19 are costly. And the costs are not just financial; mental health is at risk as well as physical health as people forgo care, including self-care, to remain free from infection. All of that becomes easier to swallow if its for a shorter period of time.
The changed risk picture also has significant policy implications. As we speak, a nervous Europe has mostly locked itself down again, hoping to stave off the worst effects of a huge surge in infections. Germany, France and England have closed bars, restaurants, gyms and more.
For the most part, we havent done the same here in the United States, even in states that have been hit hard. Part of that is because our nations response to the pandemic has become politicized. But part of it, too, reflects the belief that indefinite business closings are just too costly. Countless small businesses would fail and unemployment would skyrocket. Many argue that we have to live with increased disease because we cant lock down for years.
But mask mandates, gathering restrictions and business closings are more tolerable and the impositions they require more justifiable if we have more confidence that theyll be temporary.
By the same token, Pfizers announcement strengthens the case for federal financial support. Covid-19 is still going to hurt some businesses disproportionately, either because theyll be forced to close again or because people have stopped going out as much. But Congress no longer needs to write a blank check to support them. It just needs to provide a lifeline for a number of months, a much more palatable prospect.
Providing these resources will have the added benefit of making it politically easier for states to adopt assertive measures to get a handle on case counts that are spiraling out of control. Its a bad idea for restaurants and bars to be open for indoor dining this winter. Temporarily closing them down would be easier to stomach if these establishments are given the wherewithal to reopen next year.
The same is true for aid to individuals who find themselves out of work as the virus-induced economic troubles deepen. Another round of topped-up unemployment insurance doesnt present the same financial risk to the United States as a never-ending financial obligation to the jobless.
The Pfizer announcement is unmitigated good news. But it would be a tragic mistake to relax our vigilance. Instead, continue to mask up, stay home and consider canceling or limiting your Thanksgiving plans. This is still a marathon, but the end is much closer than before.
Nicholas Bagley (@nicholas_bagley) is a law professor at the University of Michigan.
This article provides a basic overview of the immune system and how its successful engagement is necessary to produce a commercial vaccine, with a specific focus on the SARS-CoV-2 virus that causes the COVID-19 disease and the current pandemic. It also generally describes the different types of vaccines that could or are being used to make a commercial SARS-CoV-2 vaccine and identifies their current clinical status.
More than 200 years ago, the disfiguring and deadly smallpox virus was a major health issue until one scientist fully appreciated the significance of the phrase, as smooth as a milk maids skin. But how does that vain expression relate to vaccines? It connects the highly contagious causing smallpox virus with the much milder and related cowpox virus. In 1796, Englands Edward Jenner hypothesized why milkmaids, who routinely became infected with the cowpox virus, seemed to be immune to the smallpox virus and its disfiguring scars. He tested his hypothesis by inoculating a young boy with material harvested from a cowpox pustule, after which, the boy recovered from a mild cowpox illness. Two months later, Jenner inoculated the same boy with material from a smallpox pustule. Fortunately for the boy, he did not develop smallpox and he remained unscarred. (Reidel 2005.)
The scientific name for the cowpox virus is Variolae Vaccinae; its name partially derives from the Latin word for cow vacca. Thus, Jenner called this procedure vaccination and the material used in this process was called a vaccine. He devoted his life to promote vaccination and its use spread throughout England and Europe during his lifetime. In 1977, almost two centuries later, smallpox was eradicated as a result of vaccinations for that disease, which is a testament to Jenners lifes work. (Reidel 2005.)
The cowpox example demonstrates the basic principle of vaccination against a pathogen, typically a bacteria or virus that causes a disease. Any component in a vaccine that causes immunity against the pathogen is known as an antigen. An antigen is a molecule or a portion of a molecule recognized by the immune system as foreign that stimulates an immune response, which sometimes provides protective immunity from future infections. The cowpox virus vaccine induced protective immunity against the smallpox virus because the cowpox and smallpox viruses have structurally related antigens. In the case of the boy in Jenners experiment, his primed and prepared immune system was able to recognize and neutralize the incoming smallpox virus before it could cause disease. Thus, Jenner demonstrated that vaccination can protect an individual from disease.
The immune system is composed of an elaborate mixture of different cell types and cell signals that collaborate to provide a regulated and timely response to pathogens. The immune system can be sub-divided into two systems: (1) the innate immune system and (2) the adaptive immune system. The innate immune system is the bodys first line of defense that acts immediately or within hours of a pathogens appearance in the body. This system is a generic defense system in that it is not tailored to any specific pathogen. Conversely, the adaptive immune response develops over time to produce a tailored response that specifically targets the pathogen and includes antibody molecules and cells trained to recognize pathogens and pathogen-infected cells.
The innate immune system has multiple layers, but begins with physical barriers, such as the skin and mucus. The skin creates an unfavorable environment for pathogens, for example, because it is relatively dry, contains beneficial microbes as well as naturally occurring antimicrobial compounds against pathogenic microbes. Moreover, the skins outer layer is continuously sloughed off. Beneficial microorganisms on the skin play a symbiotic role by outcompeting pathogenic microbes. These microbes are present all over the skin as well as throughout the digestive tract. Mucus is another physical barrier that contains antimicrobial components, but it is also able to physically trap infectious agents, and in the respiratory tract, pathogens entrapped by mucus can be expelled by a productive cough. (Murphy et al. 2012.)
White blood cells, which are important facilitators of inflammation, are another part of the innate immune system. Inflammation is a primary signal of, and is one of the first responses to, an infection. During inflammation, chemical signals called cytokines are released by damaged or infected cells. The cytokines are a diverse group of chemical compounds that convey instructions to cells surrounding the damaged/infected cells and are responsible for many of the physiological responses to an infection, such as dilation of blood vessels, heat and soreness. Cytokines signal the recruitment of other immune related white blood cells and stimulate defense mechanisms against intruders. For example, some white blood cells are equipped to detect the presence of unique viral RNA sequences and upon detection they release cytokines such as interferon, which activates a defense system that can capture the nascent virus. (Sparrer and Gack 2015; McNatt 2013 (discussing Tetherin protein capture of viruses).)
White blood cells are composed of a multitude of different cell types, are localized throughout the body, and are on constant surveillance for pathogens. Examples are:
One kind of phagocytic cell, known as a dendritic cell, present pieces of the digested pathogen as antigens on its cell surface, which is then available to activate other immune cells. As explained below, these presented antigens help activate the adaptive immune system by teaching the cells involved in the adaptive immune system how to recognize and react to the pathogen. (Murphy et al. 2012.) This interplay between the two immune systems is discussed more in Section II. B. below.
The complement system forms another part of the innate immune system. The complement system completes or complements the adaptive immune response because it comprises a set of specialized proteins in the blood that interact with antibodies (proteins produced by the adaptive immune system) and phagocytic cells to help clear foreign and damaged material. In a process called opsonization, antibodies and/or complement proteins coat a pathogen to facilitate its engulfment by phagocytic cells. In particular, complement proteins can bind with unique cell surface markers on the pathogen or with antibodies that have attached to the surface of a pathogen. These pathogen-bound complement proteins then interact with components on the cell surface of a phagocytic cell, which then engulfs and kills the pathogen. In addition, some complement components bind uniquely foreign pathogenic surface molecules, such as carbohydrates (made of sugars), and then destroy the pathogen by making holes in it. Finally, once the complement system has been activated, it causes interacting cells to release cytokines (i.e., chemical signals) that promote inflammation and recruit phagocytic cells. (Murphy et al. 2012.)
The adaptive immune system develops over-time, potentially taking many days or weeks to develop. That is time well spent because it provides a tailored and specific response to the pathogen that can last months, years, or even a life-time. Its capacity to remember past pathogens prepares the immune system to immediately pre-empt a new infection from the same or a related pathogen. This quick and effective response was demonstrated by the cowpox/smallpox example discussed in Section I and is fundamental to successful vaccination.
Cells that make up the adaptive immune system can be divided into two classes: B-cells and T-cells, each of which supply specialized soldiers to fight the pathogen. Each of these cell types originate from the bone marrow, but they mature in different places: B-cells remain in the bone marrow, whereas T-cells migrate to the thymus. Thus, their names signal the organ where they matured (B for bone marrow and T for thymus). During maturation, billions of B-cells and T-cells, each of which tailors its own unique cell-surface receptor, are selected or trained so that none of their receptors recognize self components in the body so as to eliminate any chance of autoimmunity (i.e., friendly fire.) The cell-surface receptor is like a lock that will recognize a specific key, which for present purposes is a pathogen-associated antigen. After maturation training, these newly formed nave B-cells and nave T-cells or nave trained soldiers march via the bloodstream and lymphatic system and take residence in their barracks, known as the peripheral lymphoid organs, such as the spleen and lymph nodes. The nave trained soldiers are considered nave because they have not yet received their orders to be activated and unleashed against the enemy pathogen. (Murphy et al. 2012.)
During an infection, information from the innate immune system gained from engaging with the pathogen is used to activate the adaptive immune system to mount a specialized and tailored attack on the enemy pathogen. Dendritic cells from the innate immune system perform reconnaissance and they follow the cytokine flare signals sent out by cells near the pathogen, which is where the battle is taking place. They are the immune systems super scouts. They are super because they directly engage the pathogenic enemy and also pass on enemy information to the specialized soldiers (nave B-cells and T-cells) of the adaptive immune system awaiting in their barracks. At the battle site, the dendritic super scout cells engage the enemy by digesting them and then displaying antigenic pieces of the enemy on their cell surface as keys. These cells are now super scouts that march to the barracks (e.g., the lymph nodes) with their antigenic keys proudly presented to the resident nave B-cells and T-cells. T-cells lose their navet if their locks fit the antigenic keys presented by the dendritic cells, transforming them into super trained soldiers, able to identify enemy invaders to fend off the pathogenic enemy. (Murphy et al. 2012.)
The dendritic cell super scouts, and super trained soldier T-cells collaborate to present the pathogenic key to those nave soldier B-cells that have the corresponding key hole in their lock, thereby converting those cells into super trained B-cells. Both classes of super trained soldier B-cells and T-cells, use the lock and key training method as a learned visual of the enemy in order to seek and destroy the pathogen. Thus, this training and selection by the adaptive immune system creates a tailored and specific immune response.
Of the billions of potential soldiers, only a tiny fraction of them the few and the proud may have been activated with the learned visual antigens. Those few recruits, however, do not provide enough troop strength to defeat the enemy pathogen, which typically reproduce quickly, and so the number of recruits must be vastly increased. Consequently, both B-cell and T-cell super trained soldiers receive additional signals to clone themselves. By expanding the number of cells, the barracks begin to swell during an infection and that is why after infection the lymph nodes become swollen and tender to the touch. (Murphy et al. 2012.) (Note: do not touch them. Rather, let the soldiers expand and prepare for battle.)
The newly cloned troops are also strengthened by receiving special fire-power capabilities, such as antibodies for tagging and bagging the enemy for destruction. Some of the super trained T-cells are transformed into one of three different kinds of specialized T-cell. The first kind become like special forces that gain the ability to recognize and kill infected cells. The second kind become like drill sergeants that help train and activate the immune system, such as the B-cells, as described above, to facilitate antibody production. The third kind become like officers who manage/regulate the battles/immune responses.
The activated and clonally expanded B-cells also have their weapon capabilities upgraded. Instead of just expressing the receptor lock on their cell surface, they are equipped to produce and release large amounts of free-floating clonal copies of the locks called antibodies. These free-floating antibodies are specialized and tailored weapons, like missiles, that home-in on the antigen keys on the enemy pathogen and with help from the complement system, tag them for death by immune cells (as discussed above in Section II.A.3). The antibodies can also independently neutralize the enemy. For example, in the case of a virus, after antibodies have covered all of the viral keys, the virus will be unable to use its keys to access the cellular locks to gain entry into the hosts cells, thereby blocking any further viral infection.
After the battle has been won, these specialized super trained soldiers cells and associated antibodies slowly wane. Yet, while some battles are forgotten as time passes, others are always remembered. Thus, often a sub-population of the trained and converted B-cell and T-cell super trained soldiers become memory cells after they retire from battle. These cells retain the memory of their specific enemy, but they will be re-activated as soon as their former pathogenic enemy (or a close resemblance) appears. Upon re-activation, these already primed and prepared cells rapidly arrive for battle to fight in the first response of any reinfection. This time around, they quickly expand their clonal troops and produce their specialized weapons, antibodies and special forces, to quash the enemy. Sometimes there is extra support already roaming the body some antibodies from the last battle may still be present that can bind and neutralize the pathogen. This fast action alters the course of an infection to prevent disease. This is the principal purpose and role of vaccination victory without war. (Murphy et al. 2012.)
After it is administered, the ideal vaccine safely replicates the same immunological outcome from a natural infection (i.e., protective immunity), without causing disease or any substantial adverse effects. The adaptive immune response is the key to a successful vaccine. After vaccination, both memory B-cells and memory T-cells will be convinced that there had been a previous infection by the target pathogen that is now remembered, even though there was no prior battle. In essence, they will be on guard, surveying for what are considered to be past foes. T-cells derived from the memory T-cells will now be on hand so that they are ready to kill the pathogen and any newly infected cells harboring the pathogen. The memory B-cells will now be ready to replicate and produce massive amounts of neutralizing antibodies. Therefore, a successful vaccination will provide protective immunity and the affected individual may never realize there had been any contact with the pathogen. (Murphy et al. 2012.)
For safety reasons, many vaccines developed today are not living organisms or infectious viruses like the cowpox example that is they do not cause a disease. Jenners cowpox pustule vaccine caused a mild disease and contained a cross-reactive pox antigen to the smallpox virus, but there were probably other components in that pustule that helped to activate a robust and lasting immune response. (Riedel 2005.) However, infection with a related, mild virus, is rarely an option as a vaccine for a disease. Rather, modern vaccines typically have a selected subset of antigenic fragments from the pathogen, sometimes just a single fragment. Because of this, many modern vaccines need help because the reduced number of antigenic components from the pathogen on their own may fail to elicit a robust adaptive immune response. Such a vaccine design needs helping agents to activate a robust immune response. These helping agents are called adjuvants, because they help produce a fuller immune response. No adjuvant was required for the Jenner cowpox vaccine because it contained live cowpox virus that presented multiple antigens and persisted long enough to stimulate a robust immune response. (Murphy et al. 2012.)
Adjuvants are compounds that can stimulate phagocytic dendritic cells, which, as discussed above, are super scouts that digest the pathogens into small antigenic pieces and then present them as keys to other immune cells to achieve a full adaptive immune response. Adjuvants include a diverse group of chemicals, believed to act by different mechanisms, including aluminum salts, oil-in-water emulsions, and modified toxins from other pathogens, such as the pertussis toxin. (Murphy et al. 2012.)
Today, development of new adjuvants is a very active area of research because a limited number of adjuvants have been approved for use in humans and because modern vaccines, due to their reduced number of antigens, have failed when using the traditional adjuvants. (Shi 2019.) Often, each adjuvant must be tested with each potentially new vaccine. Some new adjuvants currently under investigation are based on molecules that are naturally found at a site of infection. These new adjuvants include structures that are unique to pathogens, for example: (1) flagellin, a protein that helps bacteria move, and (2) double stranded viral RNA, a hallmark of RNA viruses, such as SARS-CoV-2, discussed below. In addition, cytokines involved in host immunological signaling are being investigated as new adjuvants. (Murphy et al. 2012; Shi 2019.) For example, in the development of vaccines against the virus that causes COVID-19, the pharmaceutical company GlaxoSmithKline (GSK) has decided to share its proprietary vaccine adjuvant named AS03. GSK has been collaborating with four vaccine developers, including Sanofi. (Walker 2020.) The AS03 vaccine adjuvant is an oil-in-water emulsion made from squalene (a small molecule that animals use to make cholesterol), vitamin-E (e.g., DL--tocopherol) and polyoxyethylene sorbitan monooleate (e.g., the detergents, polysorbate 80 or tween 80 that are added to some foods). (Walker 2020; US Patent 9,700,605; Wu 2019.)
Viruses can be considered as tiny packets of genetic information. The amount of genetic information in a virus is minuscule compared to a human cell, consisting of as few as only thousands of nucleotides. In contrast, a human cell nucleus contains around 3 billion nucleotides. Viruses cannot replicate on their own, but rather they rely on a hosts cellular machinery in order to reproduce. In general, viruses encode just enough genetic information: (1) to produce the equipment necessary to hi-jack the host cells machinery for itself, (2) to avoid the hosts immune defenses, and (3) to produce unique viral components, such as viral coat proteins.
There are two classes of viruses: (1) enveloped viruses, which are encased in a lipid (i.e., fatty) membrane that contains viral proteins and (2) non-enveloped viruses, which have a more robust and durable outer layer (i.e., capsid shell) made of proteins. Both classes of virus contain spike proteins on their surface that act as keys to gain entry into a host cell. The spike protein key will only fit the right lock, which is a receptor on the hosts cell surface that the virus uses to locate a susceptible cell for infection. After the key-lock connection has been made, the virus gains control of the host cell and the infection begins. As described above, if antibodies block the viral keys, the virus cannot bind to the host cell and it is neutralized. A major role of vaccination is to have these protective neutralizing antibodies already present to stop an infection.
It is important to appreciate the distinction between a virus and the disease that it causes. The scientific name of the virus that has caused the present pandemic is Severe Acute Respiratory Syndrome Coronavirus 2 (SARS CoV-2) or the 2019 Novel Coronavirus (2019-nCoV). Only a sub-set of infected individuals develop the disease named Coronavirus Disease 2019 (COVID-19) when infected by SARS CoV-2. This is conceptually like HIV-1 and AIDS, where the Human Immunodeficiency Virus 1 (HIV-1) is the virus that causes the disease called Acquired Immune Deficiency Syndrome (AIDS). Not everyone who is infected with HIV-1 has or will develop AIDS, as is the case for SARS CoV-2 and COVID-19.
A vaccine should protect the site of primary infection. The SARS CoV-2 virus infects the epithelial (outer layer) cells in lungs and nasal passages and can spread to infect other less accessible blood vessel endothelial cells that line the interior surface of its lumen. (Hou 2020.) The SARS CoV-2 virus is an enveloped virus and its spike protein key recognizes the host human cell receptor lock protein, which is known as Angiotensin-converting Enzyme 2 (ACE-2). (Callaway 2020.) The human ACE-2 protein is found on various cell types, including: (1) those lining the nasal passage, (2) those lining the lung alveolar cells (these facilitate exchange of oxygen and carbon dioxide gases), (3) endothelial blood vessel cells found throughout the body, (4) arterial smooth muscle cells, and (5) enterocytes (cells of the intestinal lining). (Hamming 2004; Hou 2020.) Because they are exposed to air, alveolar and nasal cells are the most susceptible cells for infection from the SARS CoV-2 virus, which is spread through airborne microdroplets. (Hou 2020.) After entry into and replication in alveoli, the viruses can exit towards the blood vessels. Thus, after infection of the lung alveoli, it is possible the adjacent endothelial cells in the blood vessels become a secondary site of infection, which may be one way the infection spreads and becomes systemic. (Garca 2020; Nova 2019.) An ideal vaccine should provide protection to the alveolar and nasal epithelial cells of the respiratory tract to stop any potential secondary infections of the blood vessels.
The mutation rate of SARS CoV-2 is low, which bodes well for vaccine development. For more rapidly mutating viruses such as flu or HIV-1, successful vaccines have been either elusive, as for HIV-1 or have to be redeveloped each season, as for flu. (Callaway 2020.) The lack of success for HIV-1 and flu vaccines may be because the rapidly mutating viruses stay steps ahead of the immune system soldiers. So far, the mutations that have accumulated in the SARS-CoV-2 virus have not changed the capability of antibodies to neutralize the virus or provided an advantage for the virus. (Callaway 2020.) This may mean that additional development of vaccines will be unnecessary beyond the first round of successful vaccines currently being developed against SARS-CoV-2. See Table 1, below. However, how long an individuals immunity lasts against that virus (see discussion above re: memory cells at Section II. B. 5) has yet to be determined, meaning that re-vaccination may be necessary.
Various types of modern vaccines are generally described in this section, along with the pros and cons of each type. The various universities, institutes and pharmaceutical companies developing vaccines against SARS-CoV-2 are identified and classified according to the type of vaccine and its clinical stage in development in Table 1, below.
An obvious benefit of having multiple different vaccines in development is the increased chance of finding at least one successful vaccine. There are other benefits. Different vaccines may be useful because the virus could mutate to escape any one vaccine, making the escaped vaccine of little use. Additionally, different vaccines may provide protection against other related pathogenic viruses if those viruses are cross-reactive to one of the vaccines, as in the cowpox/smallpox example. In-fact, the spike protein from the related SARS-CoV from 2003 is 75% identical to the SARS CoV-2 spike protein and neutralizing antibodies from the SARS-CoV can also neutralize SARS-CoV-2. (Hou 2020.) Yet another reason for having different vaccines is that some may not work in certain human populations because not all individuals are able to present the same vaccine derived antigen for training the B-cells and T-cells. Finally, different vaccines can benefit vaccine production capacity if different manufacturing methods are used to make the different vaccines, as that can reduce competition for limited resources.
Live attenuated virus vaccination requires an infectious virus that has been mutated to become substantially weakened (i.e., attenuated) so that it causes no more than mild symptoms. Also essential is that the attenuated virus have the required antigen(s). The cowpox vaccine is a good example of an attenuated virus vaccine, which caused a much milder disease but resulted in protective immunity from the harsher smallpox virus. Modern genetic engineering enables precise and controlled mutagenesis of many viruses to reduce their pathogenicity. Historically, testing on attenuated virus vaccines for safety and efficacy has occurred over a relatively long period before they have been approved. This has been the case for the live-attenuated virus vaccines that are currently used to vaccinate against polio, measles, mumps, rubella, and varicella. (Murphy 2012). Because the SARS-CoV-2 virus has only recently been discovered and because the need for a vaccine is urgent, there presently is no effort to develop a live-attenuated vaccine for SARS-CoV-2.
Advantages for live-attenuated virus vaccines include (Murphy 2012):
Disadvantages for live-attenuated virus vaccines are due to decreased safety. For example, these vaccines (Murphy 2012, Riedel 2005):
Inactivated and killed virus vaccines are typically made by growing and harvesting virus-like particles or viruses, respectively, in a controlled environment, after which they are treated by chemical, heat, or radiation treatment. To increase safety, an inactivated virus vaccine uses virus-like particles that are genetically inactivated. These virus-like particles are bioengineered to alter key genes and proteins of the virus to render it non-infectious. For example, it is common to remove most of the genetic material from the virus, which makes virus-like particles that are gutted shells of their former native versions. (Mohsen 2017.) Examples of inactivated vaccines include hepatitis B, human papillomavirus, and malaria. (Mohsen 2017.) Examples of killed virus vaccines include polio, rabies, hepatitis A, cholera, plague and most influenza vaccines. (Murphy 2012.)
Advantages for inactivated/killed virus vaccines include:
Disadvantages for inactivated/killed virus vaccines include:
DNA vaccines are composed of DNA fragments that encode viral proteins or protein fragments (i.e., peptides). The DNA encodes either surface or internal proteins of the virus. Internal viral proteins are chosen if they are predicted to be strongly antigenic and would be expected to be presented at the cell surface of infected cells, which would then be targeted by the immune system for killing. Surface viral proteins are often based on the spike protein that the virus uses to infect a host cell so that the vaccine induces antibodies that can neutralize the pathogen, as discussed in Section IV.
The DNA is then introduced to the host via an injection, usually in the deltoid muscle, and some small percentage of the DNA finds its way into host cells. (Liu 2019.) But to increase cellular entry of the DNA, there are generally two methods of delivering the DNA. The first method packages the DNA into nano-particles that facilitate entry into the cells. (Dalirfardouei 2020.) The second method does not package the DNA but rather relies on electroporation. Briefly, at the site of the injection, mild electric-pulses produce nano-holes in the cell surface. The nano-holes and electricity then facilitate the DNA to enter the cell. This electroporation method is used by Inovio Pharmaceuticals to deliver a potential DNA vaccine against COVID-19. See Table 1 below. (US Patent 7,328,064; US Published Patent Application No. 2019/0284263.)
The modified host cells use their machinery to make the mRNA corresponding to the vaccine DNA sequence, which directs the production of the viral protein/peptide. To the extent that the protein/peptide is made available to the immune system and is a good antigen, it will be recognized as foreign and elicit an immune response. As of 2018, there were no approved DNA vaccines for human use, although at that time there were more than 500 clinical trials on DNA vaccination. There is, however, one approved DNA vaccine for horses against the West Nile Virus. (Hobernik and Bros 2018.)
Advantages of a DNA vaccine are its safety and production benefits (Hobernik and Bros 2018):
Disadvantages of DNA vaccines relate to vaccine composition (Murphy 2012; Hobernik and Bros 2018.):
Conceptually, mRNA vaccines are very similar to DNA vaccines except: (1) the mRNA is directly encoded into protein/peptide and (2) the mRNA is typically packaged into lipid nano-particles, which protects the mRNA and facilitates delivery to the host cells, with or without electroporation.
Advantages to an mRNA vaccine are similar to DNA vaccines, but there are also added benefits:
Disadvantages to mRNA vaccines are similar to DNA vaccines except that:
Protein vaccines are composed of antigenic proteins or peptides derived from the pathogen. These vaccines are typically made using bioengineering techniques where DNA that encodes the pathogenic protein or peptide is introduced into a bacteria, yeast, or a mammalian cell line that allows for growth in large scale bioreactors. The purified antigenic protein or peptide is then formulated into a vaccine and injected into the individual. This method has been successfully used to vaccinate against the hepatitis B virus. (Murphy 2012.)
Advantages for protein/peptide vaccines are:
Disadvantages for protein/peptide vaccines are:
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The Board of SCDHEC met and spoke about preparations being made for the COVID-19 vaccine.
COLUMBIA, S.C. The South Carolina Department of Environmental Control (SCDHEC) Board met Thursday morning to discuss the COVID-19 response and vaccination plan, among other things.
Stephen White is the Immunization Branch Leader at SCDHEC and provided the board members a look at what that COVID-19 vaccine efforts look like at the department.
Theres a lot of things that we do know, and theres a lot of things that we dont know," White said.
According to White, DHEC created an interim plan on Oct. 16 that was submitted and approved by the CDC HHS.
The plan is still under revision as things continue to change, but the CDC has asked them to prioritize certain populations.
Were doing that in tandem with a vaccine advisory committee. Dr. Bell, Linda Bell, helps to coordinate that. Its a very large group of external stakeholders that meet on a weekly basis and they provide good feedback for DHEC to consider for our allocation purposes once the vaccine is made available to the state.
According to White, in order for a place to be a 'COVID provider' and administer the vaccine, they have to be enrolled per CDC requirements.
So currently DHEC has set up an enrollment team within DHEC. We are currently processing enrollments as we get those and currently to date we have 139 organizations which have registered, if you will or applied to be a COVID provider.
White said this vaccine will be one of the trickier ones they have handled.
Were used to in the past as far as refrigerated or frozen vaccines these are ultracold vaccines that are stored at -80 degrees Celsius which is really cold.
The vaccine is also a two-dose vaccine that requires the same brand for both doses.
Issues like these, along with how to properly store and distribute the vaccine are all logistical issues the team is hoping to solve before they are made available.
A 25-year-old Nevada man was the first American confirmed to have caught COVID-19 twice, and his second infection was worse than the first. USA TODAY
By medical standards,Nicole Worthley is considered extraordinarily rare. She was diagnosed with COVID-19 on March 31 and again in September.
She was walloped both times, with a fever for six weeks and side effects all summer before round two kicked in.
But she can't prove she had COVID-19 twice. That requires genetic testing of both infections, which has only happened a few dozen times in the world, and never in South Dakota where she lives.
Many states are keeping track of claims of reinfection South Dakota, for example, is studying at least 28, while Washington state is investigating 120 but they are still considered extremely unusual, according to health experts, including the World Health Organization.
In Colorado, 241 people have had a second positive PCR test more than 90 days after the first one. "All are investigated as cases, including isolation instruction for the case and quarantine instruction for their close contacts," according to a Colorado Department of Health and Environment spokesperson.
There may be a COVID-19 vaccine by the end of the year. But 'normality' may not come until the end of 2021
The U.S. Centers for Disease Control and Prevention said in a statement that it is investigating some possible reinfections but has not yet confirmed any. It only considers infections more than 90 days apart to be possible reinfections; otherwise, someone's illness is likely a lingering infection.
Worthley said she's not sure which is worse: Being able to be reinfected, or having a lingering virus that could flare up anytime.
Nicole Worthley believes s he's been infected twice with COVID-19, forcing herself and three kids, ages 6, 8 and 10, to isolate at home for months.(Photo: Courtesy Nicole Worthley)
"Whether or not I personally have a proven reinfection isn't to me as important as it's possible that you can get it again," she said. "Or, if you don't believe that, then it's possible that for six straight months you can have COVID-19, still test positive for COVID-19 and still be actively ill from it because I don't think there's a lot of understanding of that right now."
No one knows how long the immune system can keep someone safe from COVID-19 after infection.
Some diseases like measles are one and done. Once infected or vaccinated and the immune system typically provides protection forever. With other viruses, like the common coldsome of which are closely related to the coronavirus that causes COVID-19protection might not last a year, or even a season.
COVID-19 was discovered less than a year ago, so scientists don't yet know how long the body can fight it off.
The answer has implications for the longevity and effectiveness of vaccines, the possibility of communities developing so-called herd immunitywhere the virus no longer spreads because so many people have already been infected, and how those infected once should feel and behave.
Worthley, 37, could be considered a "long-hauler"someone whose COVID-19 lasted for months after infection.
She was diagnosed the last day of March after suffering sharp chest pains. A few days later, she was so short of breath thatshe could barely walk across her apartment.
A single parent to three kids, ages 6, 8 and 10, Worthley struggled to function. "The room would be spinning and I'd be wheezing and stuff. Sometimes I could feel my teeth tingling," she said.
She ran a fever for four straight weeks, then had a break for a day or sonot enough to meet the 72-hour window to be declared healthy and then spiked again for two more weeks.
She and her kids were stuck in their Sioux Falls apartment from late March until early June.
Cold weather, holiday visitors and pandemic fatigue: Experts warn COVID-19 will get much worse this winter
The children never got more than a few tired days and a yucky cough. But she knows her illness affected them. During his bedtime prayers, her oldest son often said he was thankful she was still alive.
In early June, the family was finally allowed to go out. Worthley was told she didn't need another test; she was no longer considered infectious.
She went back to work at the daycare center where she's an assistant teacher but only part-time because the pandemic had driven away some families.
Still, all summer, Worthley, previously healthy though admittedly overweight, had weird symptoms. Her doctor prescribed a beta blocker for heart palpitations and an anticonvulsant for nerve pain in her legs.
She donated convalescent plasma in September, hoping the antibodies her immune system had developed could help someone else fight off COVID-19.
Nicole Worthley had a fever for six weeks during her first bout with COVID-19, but "only" 17 days with her second.(Photo: Nicole Worthley)
Then, at the end of September, about a month after her kids started in-person school, her 10-year-old came down with strep.
Worthley was feeling lousy, too, so she got tested for strep. Negative.
A few days later, still feeling weak, she called her doctor. Can you smell anything, the doctor asked.
"I got the Vicks out," Worthley said. Nothing.
Four days later, she got a positive COVID-19 test result.
"It was easier this time," she said. "I was only feverish for 17 days."
She had diarrhea, upset stomach, loss of taste and some respiratory issues, but not as bad as the first infection. More than a month later, though, she still can't smell and a half-hour phone call was punctuated with her coughs.
Worthley believes she is among the 28 people that the South Dakota Department of Health has said it's investigating for reinfection, although she's yet to hear from anyone at the state.
So far, only a few dozen people worldwide have been confirmed to have been infected twice with SARS-CoV-2, the virus that causes COVID-19.
One man in Hong Kong didn't know he'd been infected a second time. He only found out when he was routinely tested on his return home from a trip to Italy. Another man, just 25, in Nevada, was sicker the second time.
In both cases, genetic analysis of the infections proved that they were infected twice, with slightly different versions of the virus not just long-suffering. The World Health Organization has received reports of reinfections, but they are relatively rare so far.
"Our current understanding of the immune response is that the majority of people who are infected mount an immune response within a few weeks of infection," a WHO spokesman said via email. "We are still learning about how long the antibodies last. So far, we have data that shows that the immune response lasts for several months."
In a statement, a CDC spokesperson said the agency is actively investigating a number of suspected cases of reinfection, though none has been confirmed.
"CDCs investigation of the reinfection phenomenon is in its early stages," he said.
'Pleasantly surprised': Pfizer's COVID-19 vaccine candidate shown to be 90% effective in early findings
Jeffrey Shaman, a professor at the Columbia University Mailman School of Public Health, who has been investigating reinfections, said scientists still have a lot of open questions.
Among other things, he said, they want to know: How often reinfection can happen, are people contagious with the second infection and for how long, and do people who are reinfected have less severe cases the second time or are they worse off?
To answer those questions, researchers like him have to figure out what's behind these reinfections, Shaman said.
People might fail to generate immune memory with the first infection, and need repeated exposure to build up immunity. If so, a vaccine might have the same problem, and it won't bevery effective.
Or people might get antibodies to the virus and then lose them, Shaman said. In that case, a vaccine's benefit might not last long.
The worst-case scenario would be what happens with dengue.In the case of that mosquito-borne tropical disease,someone can get sicker if infected a second time, or infected after getting a vaccine.Then, a vaccine could actually be harmful though theres no evidence thats the case with COVID-19.
Sometimes diseases that start as outbreaks can become endemic, returning year after year.
The 1918 flu, for instance, was so devastating because it was new and no one had built up resistance, Shaman said. It came back repeatedly but "didn't have the huge pulses of people dying," he said, possibly because their bodies had built up some immunity to it.
If that's the case with COVID-19, then a vaccine, even a partially effective one, could have a big benefit by exposing people to the virus and helping them build up tolerance, he said.
It's not yet clear how long someone is contagious with COVID-19 if their symptoms linger or recur.
A study published Thursday in JAMA Internal Medicinefound that 18% of COVID-19 patients in an Italian hospital tested positive again after recovering from symptoms and having a negative test.
Only 1 of the 32 patients tested showed signs of replicating virus in their bloodstream, suggesting that they were either still infectious or reinfected but that couldn't be confirmed because no genetic testing was done. That patient was still suffering symptoms 39 days after initial diagnosis, though the others who tested positive again were unlikely to be contagious, the study concluded.
Until scientists learn the answers to these questions, people who have been infected once shouldn't assume they're protected indefinitely, and should continue to wear masks, wash hands, maintain distance and avoid crowds, Shaman said.
"The only way we're going to get a sense of it is over time," he said.
Worthley admits she could have been more careful about wearing a mask. When she first caught COVID-19 in March, few people were wearing them, and Worthley didn't know of anyone at church, work, her kids' schools who had COVID.
In the summer and early fall, she wore a mask at work, but not at church. She assumed she'd be protected because she'd been sick for so long.
Now, Worthleysaid she's not confident of being protected against the virus, so she always wears a mask.
"I have a whole bunch of them in my van," she said.
Contact Karen Weintraub at kweintraub@usatoday.com.
Health and patient safety coverage at USA TODAY is made possible in part by a grant from the Masimo Foundation for Ethics, Innovation and Competition in Healthcare. The Masimo Foundation does not provide editorial input.
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New Current Procedural Terminology (CPT) codes have been created that streamline the reporting of immunizations for the novel coronavirus (SARS-CoV-2, also known as COVID-19).
Unique CPT codes approved for COVID-19 immunizations
The CPT Editorial Panel has approved addition of six Category I codes (0001A, 0002A, 0011A, 0012A, 91300, 91301), new and revised guidelines and parenthetical notes, and a new Appendix Q.
These CPT codes, developed based on extensive collaboration with Centers for Medicare & Medicaid Services (CMS) and the Centers for Disease Control and Prevention (CDC), are unique for each of two coronavirus vaccines as well as administration codes unique to each such vaccine and dose. The new CPT codes clinically distinguish each COVID-19 vaccine for better tracking, reporting and analysis that supports data-driven planning and allocation.
With this newest release of SARS-CoV-2-related CPT codes, along with releasing the standard code descriptor PDF, we are also releasing an easy to use Excel file of just the SARS-CoV-2-related CPT codes. The file contains the SARS-CoV-2-related CPT codes released since the 2021 data file release on Aug. 31, 2020 and includes:
As new SARS-CoV-2-related CPT codes are approved by the CPT Editorial Panel, the AMA will publish updates to these files.
Category I vaccine descriptors
Vaccine resources
CPT Assistant provides guidance for new codes
CPT Assistant provides fact sheets for coding guidance for new SARS-CoV-2 (COVID-19)-related vaccine codes.
The fact sheets include:
Download the November special edition of the CPT Assistant guide (PDF, includes information on SARS-CoV-2 Vaccines)
The coronavirus made its mark first in densely populated parts of the United States. And after seven months, rural communities are seeing a rise in cases.
The 13,000 residents of Grundy County, Tennessee, are fairly isolated. Its scenic mountains are home to parks with names like Savage Gulf and Fiery Gizzard. Until recently, residents felt that distance protected them from COVID-19.
Folks got relaxed, Mayor Michael Brady said. They felt like lifes coming back to normality. And, of course, thats really not the case right now.
Grundy County has gone from basically no COVID-19 to seven or eight new cases a day a per capita rate higher than Tennessees largest cities.
At first, residents had to drive to another county to get tested. Now the local health department can do it, but the hours are limited.
At times Ive had to deploy the sheriffs department up there to navigate traffic, Brady said. Theyll be lined up in the road.
Across the country, rural counties from South Dakota to South Carolina are now seeing spikes.
And yet the mindset that distance is enough defense persists, said Jacy Warrell of the Rural Health Association of Tennessee.
Business as usual is kind of the mantra in a lot of our rural communities, she said. Theres still this perception that the spread of COVID is more of an urban issue.
Rural residents are also facing the pandemic with more risk factors like diabetes, high blood pressure, high rates of obesity, chronic obstructive pulmonary disease, emphysema and heart disease, according to Dr. Lisa Piercey, Tennessees health commissioner.
So they are not only more likely to contract the disease, but to have worse outcomes, she said.
And when people get severely ill, help may not be as close as it used to be. In the last decade, more than 120 rural hospitals have closed nationwide, according to the American Hospital Association.
Brady, the mayor in Grundy County, Tennessee, said his area doesnt even have an urgent care.
We just have the health department, he said. Rural Grundy County desperately needs a medical facility.
For now, residents are traveling to other counties if they become seriously ill. And some of those hospitals are starting to reach capacity.
Pfizer said early data show its coronavirus vaccine is effective. So whats next?
In the last few months, Pfizer and its partner BioNTech have shared other details of the process including trial blueprints, the breakdown of the subjects and ethnicities and whether theyre taking money from the government. Theyre being especially transparent in order to try to temper public skepticism about this vaccine process. The next big test, said Jennifer Miller at the Yale School of Medicine, comes when drug companies release their data, so that other scientists who the public trust can go in, replicate findings, and communicate them to the public. And hopefully build appropriate trust in a vaccine.
How is President-elect Joe Biden planning to address the COVID-19 pandemic and the economic turmoil its created?
On Nov. 9, President-Elect Joe Bidenannounced three co-chairs of his new COVID-19 task force.But what kind of effect might this task force have during this transition time, before Biden takes office? The transition team can do a lot to amplify and reinforce the messages of scientists and public health experts, said Dr. Kelly Moore, associate director for the Immunization Action Coalition. Moore said Bidens COVID task force can also start talking to state leaders and other experts about exactly what they need to equip them to roll out the vaccines effectively.
What is it like to search for a job right now?
Unemployment fell in October to 6.9%, and people have been coming back into the workforce after losing jobs or giving up on looking for one earlier in the pandemic. But looking for jobs isnt getting any easier. The key stat right now when it comes to finding a new job? There are nearly twice as many job seekers as there are job openings.
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This Fishers man is participating in a COVID-19 vaccine trial. Here's what he has to do. The Indianapolis Star
Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases and the leading government expert in infectious diseases for the past four decades, gave his estimate of when a vaccine will be available to all Americans: Were talking probably by April. The veteran immunologist said frontline workers, those with pre-existing conditions, and vulnerable members of the population will be first in line.
But for those who wish to avail themselves of Pfizer and BioNTechs vaccine, assuming it progresses smoothly, Fauci has a timeline. I believe within the first quarter, he told CNNs Jake Tapper Wednesday. We have a lot of people in this country who may not want to get vaccinated right away. Thats why were talking about this leading to the second or third quarter to get people convinced to get vaccinated.
The news of this vaccine is really extraordinary.
Help is coming, and its coming soon, he added. We likely will be able to start dispensing vaccines in December. When we get both of those things together vaccine and public health measures that would really be a game changer.
On Monday, Pfizer, BioNTech said their COVID-19 vaccine candidate BNT162b2 is 90% effective in first interim analysis of Phase 3 study in trial participants without previous evidence of SARS-CoV-2 infection. Pfizer Chief Executive Dr. Albert Bourla sounded an optimistic tone in a statement: Today is a great day for science and humanity.
Health professionals say the news has come not a moment too soon: The U.S. has recorded more than 1 million COVID-19 cases in 10 days.
The vaccine will need to be kept in freezing temperatures for distribution and will require two doses, and its not yet clear how long it will last. But Fauci told CNN that was not unexpected. Its a challenge that was anticipated, he said. That was part of the Warp Speed agenda.
The companies said they are planning to submit for Emergency Use Authorization (EUA) to the Food and Drug Administration soon after the safety milestones are met, which is currently expected in the third week of November. Assuming the vaccine is effective and reaches the market, there will be many logistical and distribution issues to solve in the months ahead.
The news of this vaccine is really extraordinary, Fauci said. He said the extremely high level of expected efficacy should help persuade more people to get vaccinated early, but he cautioned people not to abandon public-health measures like wearing a mask, washing hands, avoiding crowds and meeting others in public places outdoors.
Related: Joe Bidens pandemic plan
Some 60% of people said they are willing to take a vaccine if and when its released if they can reduce their chance of infection by half, according to a new survey by STAT News and the Harris Poll. Whats more, almost two-thirds said they would take a vaccine if it reduced their risk of contracting the coronavirus by 75%.The online survey was taken by 1,954 online between Oct. 29 and Oct. 31.
If were actually at 90%, its going to reinforce for two-thirds of Americans who are then much more likely to take the vaccine, although I think its fair to say that it doesnt need to be 90% effective to get that pull through, Rob Jekielek, managing director of the Harris Poll, told STAT. However, younger people are less likely to say theyll get the vaccine than older Americans.
While the U.S. makes up approximately 4% of the worlds population, it has had approximately 20% of all COVID-19 cases. As of Friday, the U.S. had reported 10.5 million COVID-19 infections and 242,436 deaths, just ahead of India (8.7 million cases to date). To put that in context: The U.S. has a population of 328 million people versus 1.35 billion in India.
The U.S. daily tally of coronavirus infections topped 160,000 on Thursday, a new daily record and 10th consecutive day of 100,000-plus new cases. Hospitals in the Midwest and southern states including Texas and Florida continued to feel the strain. Hospitalizations are at their highest level since the pandemic began, up 30% since Nov. 1, according to the Covid Tracking Project.
Before the BNT162b2 announcement, Fauci said that he was hopeful that a coronavirus vaccine could be developed by early 2021, but said he believed it was unlikely that a vaccine would deliver 100% immunity. Two months ago, he said the best realistic outcome, based on other vaccines, would be 70% to 75% effective. The measles vaccine is among the most effective, with 97% immunity.
In addition to BioNTech SE BNTX, +4.10% and partner Pfizer PFE, +1.85%, AstraZeneca AZN, +0.29%, in combination with Oxford University; Johnson & Johnson JNJ, +0.93% ; Merck & Co. MERK, -0.31% ; Moderna MRNA, +0.53% ; Sanofi SAN, +3.72% ; and GlaxoSmithKline GSK, +1.20% are among those also working toward COVID-19 vaccines.
The Pfizer-BioNTech vaccine collaboration did not receive public funding under the Trump administrations so-called Operation Warp Speed program, though an advance order was placed through that program in the event that the vaccine wins regulatory approval. Moderna and AstraZeneca did, the New York Times notes, accept Operation Warp Speed funds.
