Category Archives: covid 19
Akiko Iwasaki is a Professor of Immunology at Yale and a former student in my department (Dept. of Biochemistry, University of Toronto). She got her undergraduate degree in biochemistry in the mid-1990s1 and then did her Ph.D. in the Dept. of Imunology under my friend and colleague Brian Barber.
Alex Pallazzo is a keen podcast listener and he alerted me to an interview with Akiko Iwasaki on the EMBO podcast channel: The Right Place at the Right time. There are several reasons why listening to this podcast is worthwhile if you are interested in science and immunology. The most important reason is that it gives you a good idea of the depth of knowledge in the field because the level of the interview is pitched at those who have a considerable understanding of imunology. I'm not one of those people but I recognize good science when I hear it.
Another reason is that she discusses COVID-19 and how vaccines work. As you know from earlier posts, the serum antibody levels induced by the current vaccines wane after a few months so that vaccinated people can get infected by the SARS-CoV-2 virus. The secondary response then kicks in protecting you from serious illness. In order to stop the initial infections and prevent the spread of the virus we might have to get booster shots every six months or so and that's not a satisfactory solution.
Iwasaki works on something called mucosal immunity, which is new to me but very familiar to the experts. Here's a brief description from her website and a figure from Wikipedia.
The mucosal surfaces represent major sites of entry for numerous infectious agents. Consequently, the vast mucosal surfaces are intricately lined with cells and lymphoid organs specialized in providing protective antibody and cellular immunity. One of the most fundamental issues in this field concerns how antigens in the mucosa are taken up, processed, and presented by antigen presenting cells. Our laboratory's goal is to understand how immunity is initiated and maintained at the mucosal surfaces, particularly by the dendritic cells (DCs), through natural portals of entry for pathogens that are of significant health concerns in the world.
We focus on understanding how viruses are recognized (innate immunity) and how that information is used to generate protective adaptive immunity.
I hope I understand this well enough to explain it in simple terms. Mucosal immunity means that there are IgA antibodies in the mucosa that surrounds cells in certain parts of the body. For our purposes, the cells in the respiratory tract are important in COVID-19. The memory B-cells and T-cells that respond to the antigen are located right under the mucosa. Imagine that you could produce a vaccine that induced IgA against SARS-CoV-2 in the mucosa. The antibodies would be located right where the virus enters the body and they don't disappear over time like IgG in the blood stream. Furthermore, the secondary response is induced right near the site where the virus is attacking the body.
I think you need a nasal/throat spray vaccine to make this work and such vaccines are under development. They would probably have to be given in conjunction with the intra-muscular mRNA vaccines. I wish I could get Brian Barber to explain this but I can't seem to contact him. He gave a short lesson in immunology on his daughter, Jill Barber's Instagram account last year so I know he could do it.
I learned one other thing from listening to Akiko Iwasaki. We know that SARS-CoV-2 is more virulent in cold weather, especially during the winter months. She explains that the mucosal layer needs to be kept moist but during the winter months it can dry up due to the low humidity. The outside air is cold, therefore the humidity is low, and we import that air into our homes and workplaces. This dry air promotes spread of the virus.
Maybe we should be installing extra humidifiers to keep the humidity at higher levels?
It's a bit of a stretch from Akiko Iwasaki to Jill Barber but we've known Jill since she was little and my wife and I are big fans so here's a musical interlude to take your mind off COVID-19.
1. She must have taken my Molecular biology course and that's probably why she knows so much!
Danish scientists have looked at the first 785 cases of Omicron variant in Denmark. The most important lesson is that 83% of the cases were fully vaccinated. (Mostly two doses of an mRNA vaccine). This includes 7% of the total cases that had also received a booster shot. 76% of the Danish population are fully vaccinated.
Espenhain, L., Funk, T., Overvad, M., Edslev, S.M., Fonager, J., Ingham, A.C., Rasmussen, M., Madsen, S.L., Espersen, C.H. and Sieber, R.N. (2021) Epidemiological characterisation of the first 785 SARS-CoV-2 Omicron variant cases in Denmark, December 2021. Eurosurveillance 26:2101146. doi: [Eurosurveillance: Full Text]
This is similar to the results in other countries where a large percentage of the population are vaccinated. The spread of Omicron in those countries is largely driven by infection of the vaccinated group and the only way to blunt this spread is to limit contacts among vaccinated people. That means lockdowns or partial lockdowns for everybody and that seems to be working.
As usual, the United States is going to serve as a good control on these measures since the dominant message from American government, media, and health officials is that you are pretty much okay if you are vaccinated and you just have to be a bit more carefeul. No need to change your holiday travel plans.
The cases in Denmark cover all ages groups but the 20-29 age group had the highest number of infections. Quite a few of the cases could be traced to a "seasonal gathering" of 150 people and a large concert but most others seem to be due to community transmission once the variant became established. The original cases came from people who had travelled from South Africa and other countries.
Since the identification of the first Omicron case in Denmark, a steep increase in the number of cases has been observed. A major driver of this development was a large party with young adults – a population group with more social and close connections than adults and children.
We find several reasons for concern: (i) the rapid spread shortly after introduction despite extensive contact tracing efforts, (ii) the occurrence of several superspreading events with high attack rates and (iii) the high proportion of fully vaccinated Omicron cases.
So far, there haven't been many hospitalizations or deaths due to infection with the Omicron variant but that could come later.
Scientists are very interested in the omicron variant and why it is so dangerous. Since vaccinated people are getting infected, it must mean that the omicron variant isn't effectively neutralized by vaccine-induced antibodies. Several preprints on this topic have been posted and they all reach the same conclusion. I'll discuss one of them.
Garcia-Beltran, W.F., St Denis, K.J., Hoelzemer, A., Lam, E.C., Nitido, A.D., Sheehan, M.L., Berrios, C., Ofoman, O., Chang, C.C. and Hauser, B.M. (2021) mRNA-based COVID-19 vaccine boosters induce neutralizing immunity against SARS-CoV-2 Omicron variant. medRxiv. doi: 10.1101/2021.12.14.21267755
Recent surveillance has revealed the emergence of the SARS-CoV-2 Omicron variant (BA.1/B.1.1.529) harboring up to 36 mutations in spike protein, the target of vaccine-induced neutralizing antibodies. Given its potential to escape vaccine-induced humoral immunity, we measured neutralization potency of sera from 88 mRNA-1273, 111 BNT162b, and 40 Ad26.COV2.S vaccine recipients against wild type, Delta, and Omicron SARS-CoV-2 pseudoviruses. We included individuals that were vaccinated recently (<3 months), distantly (6-12 months), or recently boosted, and accounted for prior SARS-CoV-2 infection. Remarkably, neutralization of Omicron was undetectable in most vaccinated individuals. However, individuals boosted with mRNA vaccines exhibited potent neutralization of Omicron only 4-6-fold lower than wild type, suggesting that boosters enhance the cross-reactivity of neutralizing antibody responses. In addition, we find Omicron pseudovirus is more infectious than any other variant tested. Overall, this study highlights the importance of boosters to broaden neutralizing antibody responses against highly divergent SARS-CoV-2 variants.
This is an Amerian study so the authors looked at three different vaccines: Pfizer (BNT162b2), Moderna (mRNA-1273), and Johnson & Johnson (Ad26.COV2.S). For each vaccine they examined four different groups: (1) people who have received their full dose within the last three months, (2) people who had been vaccinated 6-12 months ago, (3) people who had been vaccinated at least six months ago but had subsequenty gotten infected with SARS-CoV-2, and (4) people who got a vacine booster shot within the past three months.
They isolated serum from every individual in the 12 groups and challenged them with a pseudovirus containing the spike protein from the WT variant (Beta?), the Delta variant, and the Omicron variant. What they're measuring is neutralization, or the ability of the antibodies in the serum to inactivate the virus so that it can no longer infect cells. The results are shown below.
Let's look at the top graphs (red) for the Moderna vaccine. You can see that if the vaccination was given recently (< 3 months), the antibodies do a good job of neutralizing the WT virus although there's considerable variation from individual to individual. It does less well with Delta and much less well with Omicron.
The results are more striking for people who were vaccinated more than six months ago. Neutralization of all three variants is much lower because antibody production wanes after a few months [On the effectiveness of vaccines]. Serum from this group cannot neutralize the Omicron variant—in other words omicron has evolved to escape neutralization from people who were vaccinated more than six months ago.
Omicron is neutralized fairly well in the group that had been infected after getting the vaccine. That's because their antibody levels were boosted by the infection. Similarly, people who got a vaccine boost also had high enough antibody levels to neutralize Omicron. The boost works better than getting COVID-19 but that may just be because the boosts were given more recently than the average infection.
Similar results were obtained for the Pfizer vaccine (red) and the Johnson & Johnson vaccine (green) except that the J & J vaccine gave poorer neutralization in all cases.
What this shows is that the initial vaccinations aren't very effective at blocking infection so vaccinated people will get infected. The amount of antibodies in the serum will rise after the initial infection because the memory B cells and memory T cells will be activated so these people will eventually fight off the infection and most of them will not suffer severe effects. This is because the Omicron variant cannot evade higher levels of antibodies and also because cellular and innate immunity are a bit different than antibodies alone.
The strange result is that after a booster shot the neutralization of Omicron relative to Delta is higher than before the booster shot. This suggests that the third dose of antigen in the vaccine is capable of eliciting additional antibodies that weren't stimulated in the first two doses. (These are polyclonal antibodies. There are many different antibodies to different parts of the spike protein. Everyone has a slightly different antibody profile and nobody has a complete repertoire of all the possible antibodies.)
As I mentioned above, this is just one of several studies that show the same result. Omicron can evade neutralization in people who have been vaccinated so they will develop mild symptoms and spread the virus until their secondary defenses are sufficient to stop the infection. Getting a booster will help keep Omicron under control.
The fact that vaccinated people can help spread the virus is one of the reasons why the Omicron wave will be significant and deadly. However, in addition, the Omicron variant is more infectious than Delta and much more infectious than previous variants. The authors observed this in their experiments when they tested for neutralization by seeing if the viruses could infect cells in culture. Omicron is 2× more infectious than Delta and this is another reason why the Omicron wave will be dangerous.
The reasons for the increased infectivity are not known at present. About a dozen papers/preprints have been published but some of the results are contradictory. For example, modeling of the interaction of spike protein and the ACE2 receptor has shown increased binding in some papers but other papers refute this claim by showing that they didn't take into account the mutations that reduce binding. There's a suggestion that the efficiency of cleavage at the furin cleavage site is enhanced in the Omicron variant but this has not been confirmed. Some scientists have speculated that changes in the glycosylation pattern of spike protein will enhance uptake of the virus and others point to changes in a helical bundle that will probably cause the virus to enter cells more readily.
We'll have to wait and see why infectivity is higher in the Omicron variant and also why transmissibility seems to be higher (higher viral load?). Meanwhile, one thing is clear. Booster shots are important to keep this variant under control. The bad news is that the effect of the booster in producing antibodies is likely to diminish over time so that after six months or so the levels of antibodies might not be sufficient to neutralize Omicron and additional boosters will be necessary (or an Omicron-specific mRNA vaccine.) People (mostly American) who got their booster shot several months ago may not be as protected as they think.
Some of the problems with this study are similar to the problems with the studies out of Israel. Many countries have spaced out their first and second vaccination doses to several months instead of 4-6 weeks as in Israel and the USA. The strategy followed in other countries may lead to higher antibody levels than those shown in this study. Also, in most other countries the AstraZenica vaccine has been widely employed and the Johnson & Johnson vaccine is not approved. Furthermore, a significant number of people in those other countries have received mixed vaccine doses (e.g. AstraZenica + an mRNA vaccine) and this is known to be beneficial. It would be nice to see a similar study from Canada or the UK.
I've learned a bit of immunology from hanging out with immunologists so I'm going to try and explain how vaccines protect you from the worst consequences of an infection and why booster shots aren't as necessary as you think. This will be an illustration of how difficult it is for the media to keep you correctly informed about real science and why we should have more scientists explaining these things instead of doctors
Dozens of papers on this topic have been published over the past year or so and they all say the same thing. SARS-CoV-2 vaccinations induce an immediate production of antibodies in response to the spike protein antigen whether it's presented on the surface of a viral vector such as adenovirus or synthesized in your cells by mRNA. The antibodies are produced by a small number of B cells that just by chance happen to recognize the viral protein. These cells multiply rapidly so that within a few days you have enough antibodies being produced to fight off any infection.
Over time, the antibody production declines if there's no infection but some of the B cells become memory B cells that lie in wait for the next infection when they can be rapidly stimulated if you get infected months, or years, later. There's another type of cell called a T cell that also forms memory T cells that are very long-lasting and help fight off future infections.
Imagine that you encounter the virus several months after you've been vaccinated. As soon as the virus enters your body the memory cells are activated and the virus is attacked. You may have a mild case of COVID-19 for a few days but you are protected against the most severe forms of the disease. The point is that a reduction in antibody levels is perfectly normal. What's important is whether you have a robust level of memory B cells and memory T cells that can be activated. The hype in the media has convinced people that the vaccines are no longer effective after six months and you have to get a booster shot to protect you from COVID-19.
Here's a very recent paper that presents the data. It was published in Science on December 3, 2021.
Goel, R.R., Painter, M.M., Apostolidis, S.A., Mathew, D., Meng, W., Rosenfeld, A.M., Lundgreen, K.A., Reynaldi, A., Khoury, D.S. and Pattekar, A. et al. (2021) mRNA vaccines induce durable immune memory to SARS-CoV-2 and variants of concern. Science 374:eabm0829. doi: 10.1126/science.abm0829
Vaccination against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has proven highly effective at preventing severe COVID-19. However, the evolution of viral variants, and waning antibody levels over time, raise questions regarding the longevity of vaccine-induced immune protection. Goel et al. examined B and T lymphocyte responses in individuals who received SARS-CoV-2 messenger RNA vaccines. They performed a 6-month longitudinal study of individuals who never had SARS-CoV-2 infection compared with people who had recovered from SARS-CoV-2. Humoral and cellular immune memory was observed in vaccinated individuals, as were functional immune responses against the Alpha (B.1.1.7), Beta (B.1.351), and Delta (B.1.617.2) viral variants. Analysis of T cell activity suggested that robust cellular immune memory may prevent hospitalization by limiting the development of severe disease.
The authors looked at the immune reaction in three different groups. The first was the naive group of people who have never had COVID-19 but got the vaccine (blue). The second group was people who had already survived COVID-19 and then got vaccinated (red). The third group was composed of people who had mild cases of COVID-19 and never got vaccinated (purple).
This is a long paper with lots of experiments but the data can be summarized in the figure below. The authors looked at antibodies to the spike protein and to its specific ACE2 binding site. They also looked at neutralizing antibodies or the abiity of circulating antibodies to neutralize whole virus particles. The results are summarized in the first graph and they show that the antibody levels rise to maximum levels about one week after receiving the second dose of vaccine (administered four weeks after the first dose).
The antibody levels fall to about 10% of the maximum value over the next six months. (The x-axis is a log scale.) This is exactly what you expect for a typical vaccine. Note that the levels for people who had already been infected were higher to begin with but the rate of decline was similar to the naive group. This suggests that booster shots will have a similar effect on antibody levels.
The levels of memory B cells and memory T cells rise to a maximum at four months, right at the time of the second dose. They remain high at the end of six months.
Taken together, these data demonstrate that mRNA vaccines induced a population of memory B cells that was durable for at least six months after vaccinaton, and these cells were capable of rapidly producing functional antibodies against SARS-CoV-2, including neutralizing antibodies against VOCs [variants of concern], upon stimulation....
Taken together, these data indicate that mRNA vaccination generates durable SARS-CoV-2-specific CD4+ T cell memory in individuals who were not previously infected with SARS-CoV-2 and only transiently boosts these responses in SARS-CoV-2-recovered individuals.
What this means is described by the authors in the concluding remarks,
These data may also provide context for understanding potential discrepancies in vaccine efficacy at preventing infection versus severe disease, hospitalization, and death. Declining antibody titers over time likely reduce the potential that vaccination will completely prevent infection or provide near-sterilizing immunity. However, the durability of cellular immunity, here demonstrated for at least 6 months, may contribute to rapid recall responses that can limit initial viral replication and dissemination in the host, thereby preventing severe disease.
In other words, if you are fully vaccinated (two doses of mRNA vaccine) then you are well-protected against severe disease although you may suffer mild symptoms for a few days. You may be able to avoid the mild symptoms if you have gotten a recent booster shot but that effect is likely to decline in a few months.
The hype about booster shots is extremely misleading. The media is making it sound like all of your vaccine protection declines after six months and you need the boosters to have any chance at all against the omicron variant. How many times have you heard that your vaccine protection drops to 33% after six months?
You could argue that boosters aren't even necessary but that ignores the possibility that even a mild infection may be harmful to some people. It also ignores the possibility that by preventing even a mild infection you could be blocking the spread of the virus. I don't know of any data on viral loads after vaccination but I suspect that a booster offers some protection against spread.
AHA “regrets any confusion” and is reviewing meeting policies after outcry over Covid-19 vaccine abstract
Michael Hiltzik is first off the mark writing for the Los Angeles Times: These authors wanted to push the COVID-19 lab-leak theory. Instead they exposed its weaknesses.
Hiltzik is one of the few science writers who know what they'r talking about.1 You should read his entire review—here are some excerpts to tempt you.
... “Viral” is a laboratory-perfect example of how not to write about a scientific issue. The authors rely less on the scientists doing the painstaking work to unearth the virus’ origin than on self-described sleuths who broadcast their dubious claims, sometimes anonymously, on social media. In the end, Chan and Ridley spotlight all the shortcomings of the hypothesis they set out to defend....
“Viral” is built on vague innuendo, dressed up with assertions that may strike laypeople as plausible but have long since been debunked by experienced virologists. An entire chapter, for example, is devoted to the “furin cleavage site,” a feature of the virus’ structure through which the enzyme furin makes the spikes on its surface — which it uses to penetrate and infect healthy cells — more effective.
The furin site was originally described by lab-leak advocates as so unusual that it could have been placed there only by humans. Virologists have since determined that the feature is not all that rare in viruses similar to SARS2, and in any case, it could have emerged through natural evolutionary processes well known to experts. Chan and Ridley place a heads-I-win-tails-you-lose gloss on these findings, writing that if the site “proves to have been inserted artificially, it confirms that the virus was in a laboratory and was altered. ... If, on the other hand, the furin cleavage site proves to be natural, it still says nothing about where the virus came from.” Why write about it at all, then?
Alina Chan's reputation is already about as low as it can get and now it looks like she's dragging Matt Ridely down with her. He was already part way there so he didn't have far to go.
The book is published by HarperCollins. Should American lawmakers look seriously at regulating the publishing industry for spreading misinformation since they're already investigating Facebook for the same crime?
Harper is set to publish Viral: The Search for the Origin of COVID-19 in just a few days. The authors are Alina Chan, a postdoc at the Broad Institute of MIT and Harvard, and Matt Ridley, a science journalist who has written several respectable books.
The book promises to reignite discussion of the lab leak conspriracy theory with a focus on Alina Chan's role in promoting it. In preparation, you should read this article about her: They called it a conspiracy theory. But Alina Chan tweeted life into the idea that the virus came from a lab.
I'm curious about someting else. The book deal was signed less than six months ago so it's clear that Harper has rushed it into print. That's a lot faster than my book is taking and a lot faster than the books by several other scientists. My publisher insists on a rigorous review of my book to make sure the science is accurate and other scientists have had similar experiences. In my case, the reviews will take three months.
I wonder who reviewed the Chan/Ridley book and told Harper that the science was accurate and the book should be published? I think we all know the answer. I'm guessing that this book will contribute to the mistrust and undermining of science that's common in today's society and that Harper will not be criticized for contributing to that mistrust. Instead, they will be praised for making tons of money from gullible book buyers.
Here's the Amazon blurb that Harper has written to promote the book. Judge for yourself whether this is real science or hype masquerading as science.
A new virus descended on the human species in 2019 wreaking unprecedented havoc. Finding out where it came from and how it first jumped into people is an urgent priority, but early expectations that this would prove an easy question to answer have been dashed. Nearly two years into the pandemic, the crucial mystery of the origin of SARS-CoV-2 is not only unresolved but has deepened.
In this uniquely insightful book, a scientist and a writer join forces to try to get to the bottom of how a virus whose closest relations live in bats in subtropical southern China somehow managed to begin spreading among people more than 1,500 kilometres away in the city of Wuhan. They grapple with the baffling fact that the virus left none of the expected traces that such outbreaks usually create: no infected market animals or wildlife, no chains of early cases in travellers to the city, no smouldering epidemic in a rural area, no rapid adaptation of the virus to its new host—human beings.
To try to solve this pressing mystery, Viral delves deep into the events of 2019 leading up to 2021, the details of what went on in animal markets and virology laboratories, the records and data hidden from sight within archived Chinese theses and websites, and the clues that can be coaxed from the very text of the virus’s own genetic code.
The result is a gripping detective story that takes the reader deeper and deeper into a metaphorical cave of mystery. One by one the authors explore promising tunnels only to show that they are blind alleys, until, miles beneath the surface, they find themselves tantalisingly close to a shaft that leads to the light.
I'm currently discussing the meaning of "function" with a small group of scientists and philosophers and it's not easy to come up with an acceptable definition. Imagine how much more difficult it is to identify research that results in a gain of function!
Gain-of-function research has been in the news recently because there are a group of conspiracy theorists who accuse the scientists at the Wuhan Institute of Virology of conducting gain-of-function research on bat caronaviruses leading to the creation of SARS-CoV-2 which then escaped from the lab to cause the pandemic. Some of these conspiracy theorists even accuse the American NIH of funding this gain-of-function research.
How do you define gain-of-function research in a meaningful manner? That's the question posed by Amber Dance in a recent Nature article. (Amber Dance is a freelance science journalist.) The first reference below is the title and subtitle of the article that was published in the magazine and the second reference is the online version.
Dance, A. (2021) The Truth About Gain-of-Function Research: Granting new abilities to pathogenic microbes sounds dangerous, but what has the research told us? Nature 598: 554-555. [doi: 10.1038/d41586-021-02903-x]
Dance, A. (2021) The shifting sands of ‘gain-of-function’ research: The mystery of COVID’s origins has reignited a contentious debate about potentially risky studies and the fuzzy terminology that describes them. Nature 598: 554-555. [Nature website]
The only relevant gain-of-function research is the type specified by NIH as "gain-of-function research of concern" (GOFROC). This is research that makes a potential pathogen more likely to cause disease in humans. This is the kind of research that would be carried out in a lab devoted to biological warfare but it could also apply to some research that was carried out in the past, as described in the article. There is no evidence to support the accusation that scientists in China, or anywhere else, were doing such research on coronaviruses.
There are other kinds of research that involve constructing chimeric viruses in order to test whether they have the potential to cause a pandemic. This is perfectly normal, even necessary, research but conspiracy theorists have claimed that this is forbidden gain-of-function research. The article does a good job of explaining this research and why it's not a problem.
Image Credits: The coronavirus figure is from Alexy Solodovnikov and Wikmedia Commons.
The COVID-19 pandemic has highlighted long-standing gaps in infection control knowledge and understanding among the frontline healthcare workforce. Since the onset of the pandemic, healthcare-associated infections and antibiotic-resistant infections have increased, reversing national progress made before 2020.
Infectious disease threats like Ebola, COVID-19, and antibiotic resistance will continue to emerge. It’s more important than ever that we equip our nation’s healthcare workforce with the infection control knowledge they need to protect themselves, their patients, and their communities.
One year ago, this month, CDC launched Project Firstline. Project Firstline provides engaging, innovative, and effective infection control education and training for U.S. frontline healthcare workers.
Meeting the Needs of the Diverse Healthcare Workforce
Project Firstline’s innovative content is designed for all healthcare workers, regardless of their previous training or educational background. The program’s training and educational materials provide critical infection control information in a format that best meets healthcare workers’ needs.
During its first year, Project Firstline and its partners hosted more than 300 educational events on infection control and developed more than 130 educational products. The products are accessible on a variety of digital platforms, including Facebook, Twitter, and CDC and partner websites. Products currently available on the CDC Project Firstline site include:
- A video series featuring CDC’s infectious disease expert, Dr. Abby Carlson
- Explainer videos on infection control basics
- A facilitator toolkit with guided session plans on infection control for COVID-19
- Job aids for on-the-go access
Maximizing Impact through Partnerships
Project Firstline brings together academic, public health, and healthcare partners plus 64 state, local, and territorial health departments to provide infection control educational resources to healthcare workers nationwide.
Our partners have used a diverse range of products and activities to reach healthcare workers with tailored infection control information during the COVID-19 pandemic. Some of these activities include Twitter chats, podcasts, videos, and virtual training events simulcast and translated into multiple languages.
Additionally, Project Firstline launched the Community College Collaborative in partnership with the American Hospital Association and the League of Innovation in the Community College. The program is integrating enhanced infection control content into the health programs of community college classrooms. The program was piloted this summer with faculty cohorts from 16 participating colleges across a range of community college settings. Faculty came together to tailor the infection control curriculum for each professional area, with a plan to phase it into their coursework. Professional areas included:
- emergency medical services
- respiratory care
- practical nursing and nursing assistants
- medical assisting
This effort will help ensure that the future healthcare workforce starts their careers with key infection control knowledge to protect themselves and their patients.
The Future of Project Firstline
Project Firstline aims to become the go-to resource for infection control among healthcare workers. It will focus on building a strong culture of infection control within all healthcare facilities.
Using insights learned during its first year, the program will create a new suite of readily available and easy-to-consume education materials. The new materials will be designed to help strengthen infection prevention and control capacities beyond the COVID-19 pandemic.
Thanks in advance for your questions and comments on this Public Health Matters post. Please note that CDC does not give personal medical advice. If you are concerned you have a disease or condition, talk to your doctor.
Have a question for CDC? CDC-INFO (http://www.cdc.gov/cdc-info/index.html) offers live agents by phone and email to help you find the latest, reliable, and science-based health information on more than 750 health topics.
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