Category Archives: Research

Combating Bacteria: A New Approach to Multi-Drug Resistance

BY YUSHA SHUN

Over the last decade, antibiotic-resistant bacteria have proliferated; according to the CDC, at least 90,000 deaths a year in the U.S. are due to bacterial infections, with a majority of these infections being resistant to some antibiotic. Alarmingly, hospitals and other health-care facilities have been the epicenter for the outbreak of drug-resistant bugs, simply because these places allow for bacteria to enter the bloodstream and open wounds most quickly. Bacterial infections caused by multidrug-resistant (MDR) bacteria are a serious threat to public health because of their virulence and resilience to many forms of treatment.

There are two major types of MDR bacteria — gram-positive and gram-negative, distinguished by how these bacteria stain on a Gram test. Although gram-positive MDR bacteria such as the well-known methicillin-resistant Staphylococcus aureus (MRSA) are still a major threat, there have been many developments of new antibiotics that should work effectively again them (at least for the time being). However, gram-negative MDR bacteria are much more concerning; these bacteria have an additional outer membrane that has effectively halted progress in drug development that can kill them. For this reason, there is currently a lack of drug candidates for this type of bacteria, posing a huge threat to global health.

Last month, though, in a study published in Nature Microbiology, researchers have described a new tool that has great potential in tackling these MDR gram-negative bacteria. They describe a new class of antimicrobial agents called structurally nanoengineered antimicrobial peptide polymers (SNAPPs); these so-called SNAPPs are engineered by a special type of peptide synthesis process. Two SNAPPs, S16 and S32, mimic naturally occurring anti-microbial peptides and have shown great results when tested against a range of MDR bacteria.

Specifically, researchers incubated SNAPPs with bacteria in a lab setting, and S16 and S32 were equally effective against strains of MDR gram-negative species, as drug resistance was not detected even after 600 generations of bacterial growth. They made sure that these peptides were not harmful to mammals by mixing the SNAPPs with human red blood cells and consequently observed no undesired interactions. The researchers also tested S16 and S32 in mouse models infected with MDR A. baumanii: treatment with S16 enabled survival of all mice for 24 hours, while 50% of the control mice died.

The scientists also ran experiments to determine what exactly in these SNAPPs can cause the death of MDR-resistant gram-negative bacteria. They found that the polymer peptide disrupts the outer membrane of these MDR bacteria because it can cross the membrane and the layers below that, leading to unregulated movement of ions across the membrane. SNAPPs can also cause the bacterial cell to spontaneously lyse (high concentrations) or cause the cell to follow programmed death (low concentrations).

This new research is crucial in facing this new global threat of multi-drug resistant gram-negative bacteria. For the first time, a suitable class of drug candidates that can not only destroy these bacteria but are also compatible with the mammalian body has been proposed. These SNAPPs may be the key to eliminating these unwanted pests that are resistant to any conventional method of antibiotic treatment. Hopefully, SNAPP-based drugs will be quickly developed and undergo clinical trials in the near future.

 

References:

http://www.nature.com/nrd/journal/v15/n11/full/nrd.2016.224.html

 

http://aac.asm.org/content/52/3/813.full

 

http://www.nature.com/articles/nmicrobiol2016162

 

http://science.sciencemag.org/content/sci/321/5887/356.full.pdf

Immunotherapy’s Rise Among Cancer Treatments

BY DEVORAH SAFFERN

Most cancer patients are treated with chemotherapy, radiation, and/or surgery, but recent promising research has given hope to another option: immunotherapy. This approach allows the immune system itself to fight the cancer. Tumorous cells often prevent the immune system from attacking, or even make themselves undetectable to the body’s white blood cells. Immunotherapy treatment types vary, solving all these sorts of issues. Treatments come in the form of drugs, vaccines, catheters, and even creams, sometimes combined with other cancer treatments. Researchers are currently studying various forms of immunotherapy, which have shown promising results. As studies are done and clinical trials run, the form of treatment is rapidly becoming more widely accepted. Just a few weeks ago, the FDA (U.S. Food and Drug Administration) approved Keytruda, a checkpoint inhibitor immunotherapy drug used to treat metastatic lung cancer, also known as the drug that cured former president Jimmy Carter from a deadly form of melanoma. Keytruda can now be used as a first step in treatment over chemotherapy, in certain cases. A number of other immunotherapy drugs have been approved in the past, including Provenge in 2010, a treatment for prostate cancer, and Imlygic in 2015, for metastatic melanoma. These recent advances indicate that immunotherapy will likely become more prevalent in treatments.

Following the new FDA approval and general successes in immunotherapy testing, the media has displayed this exciting ray of hope for cancer patients. Dr. Crystal Mackall of Stanford’s School of Medicine, who specializes in this type of treatment, told FOX news that the recent immunotherapy findings are “turning the practice of oncology on its head.” New York times writer Denis Grady wrote: “All this has brought new optimism to cancer doctors — a sense that they have begun tapping into a force of nature, the medical equivalent of splitting the atom.”

Keytruda, the new drug, is a checkpoint inhibitor. These inhibitors are the most common form of immunotherapy drugs, and are relevant in treating different types of melanoma, lymphoma, lung, kidney, and bladder cancers. Normally, T-cells (white blood cells that have the ability to kill cancer cells) can detect which harmful cell to attack through reception of the antigen on the cell’s surface. Some cancer cells, however, can activate an immune checkpoint “switch” on the T-cell during the process, and prevent the T-cell from carrying out its function. Checkpoint inhibitor drugs block the checkpoints of T-cells so that the cancer cell cannot “switch off” T-cells. A recent study published in the June 2016 edition of the Cancer Immunology, Immunotherapy journal discusses the increase in the number of T-cells and their functionality in eighteen glioblastoma patients who were treated with the inhibitor Axitinib. Many other significant studies on the treatment have been published in recent years. In an article from last May, an approach similar to the checkpoint inhibitor method is described. Scientists designed specific molecules to remove sugars from the coatings of tumor cells, preventing the tumor cells from deactivating T-cells via these sugars.

CAR (chimeric antigen receptor) T-cells are another of the more prevalent types of immunotherapy methods, frequently used in clinical trials. T-cells are removed from the patient’s bloodstream and mutated in the lab to produce the chimeric antigen receptors, which enables the cell to attach to the cancer cell antigens. The mutated cells are given back to the patient through an infusion. CAR T-cells are used to treat leukemia and lymphoma and have had positive effects. In a trial that took place in Children’s Hospital in Philadelphia, in which T-cells were used, twenty-seven out of the thirty patients achieved remission.  Other types of monoclonal antibody treatments are also being tested. Researchers are working to create more of these antibodies that attach to antigens of cancer cells, essentially “flagging” the cancer cells so that the immune system can sense and attack. The antibodies are also sometimes made to target and destroy the cancer cells on their own.

While there are still many unanswered questions regarding the efficacy and side affects of immunotherapy, studies demonstrate potential for further improved treatments. In future work, researchers will begin to examine surrounding tissue of the cancer cells to gain a better understanding of the paths of the T-cells. Another step to be taken is looking for undiscovered checkpoints to be blocked, as well as combining this inhibitor method with other treatments. Implementing inhibitors with other methods could be particularly useful, as remnants of destroyed cancer cells from the other treatments could trigger immune system responses that would be refined via these inhibitors. Like all cancer treatments, immunotherapy has side effects and risks associated. If those obstacles can be eliminated, though, immunotherapy could be highly effective, as the immune system is the body’s natural tool and would typically only target unhealthy cells, unlike chemotherapy and radiation therapies, posing less collateral damage to the patient. Future studies are expected to be done in this growing branch of cancer research, with the Fred Hutchinson Cancer Researcher Center, a new immunotherapy research clinic that will focus on treatment with T-CELLS, scheduled to open in Seattle this December. All of us hoping for new forms of effective cancer treatment can expect to see more of this exciting, growing field of immunotherapy.

Sources:

 

http://link.springer.com/article/10.1007/s00262-016-1836-3

http://www.pnas.org/content/113/37/10304.abstract

http://myfox8.com/2016/10/30/can-your-own-immune-system-kill-cancer/

https://www.washingtonpost.com/news/to-your-health/wp/2016/11/01/seattle-cancer-center-bets-big-on-t-cell-immunotherapy

http://www.nytimes.com/2016/07/31/health/harnessing-the-immune-system-to-fight-cancer.html?rref=collection%2Fseriescollection%2Fimmunotherapy&_r=0

 

Antibody therapy offers promising lead for sustained HIV control

BY NOAH BEATTIE-MOSS

HIV/AIDS is a global pandemic, and has remained at the forefront of American consciousness since the 1980s, when hundreds of thousands of people, predominantly young gay men, passed away from the disease. Today, over 36 million people live with the disease worldwide, with over 1.2 million patients in the United States alone. It can be managed with continuous antiretroviral therapy, but there is still no known cure or vaccine. Recent research published in the journal Science, however, suggests the potential for a new combination therapy that may act as a functional cure.

Human immunodeficiency virus is categorized as a retrovirus, meaning it has an RNA genome enclosed by a protein capsid and a lipid envelope derived from the cell membrane of the host. Molecules on the HIV particle bind to receptors on the surface of T helper cells, especially CD4+ T cells, which play an essential role in the proper functioning of the immune system. Once inside a host cell, the viral RNA is converted into DNA, transported into the nucleus, and integrated into the cellular genome. This viral DNA is called a provirus, and is transcribed by the cell to produce new virus particles.

image-cycle-1-noah-beattie-moss
HIV-infected T cell, captured by a scanning electron microscope.

Antiretroviral therapy (ART) can target several different steps in this viral life cycle, such as blocking membrane fusion of HIV with the cell, or inhibiting reverse transcriptase, the enzyme which transcribes the viral RNA into DNA. But it has downsides: ART requires continuous daily medication, and viral loads regenerate if therapy is stopped, so it is not a cure. Long-term ART also has side effects such as toxicity, inflammation, and an elevated risk of aging-related diseases such as liver dysfunction and osteoporosis. In addition, access to medication poses a problem: in 2010, the average lifetime cost of treating HIV in the US was approximately $380,000, and distribution of ART medication in developing countries is extremely limited.

Research led by Dr. Aftab Ansari of the Emory University School of Medicine, published on October 14, 2016, investigated the effect of ART alongside an antibody targeting α4β7, a receptor on the surface of CD4+ cells which enables them to traffic into gastrointestinal tissues. During a typical infection, depletion of CD4+ cells in these tissues causes gut epithelial damage and allows the formation of persistent viral reservoirs, leading to general immune dysfunction. It was hypothesized that by blocking entry of CD4+ cells into this area, the immune system would remain strong enough to control the infection.

The investigation was conducted on macaques, using SIV, the simian analogue of HIV. Eighteen monkeys were infected with the virus and were started on a daily ART regimen after five weeks. Starting at week nine, eleven of the animals were treated with the α4β7 antibody, while the other seven received a nonspecific antibody as a control. ART was terminated for both groups at 18 weeks, and antibody treatment was terminated at 32 weeks.

The results were dramatic: macaques which received the α4β7 antibody had an absent or minimal viral load after ART was ceased, while the control group rebounded to high viral levels. Control over viral levels persisted through the end of the study, at week 90.

This indicates that α4β7-directed therapy not only stopped temporary entrance of HIV-infected T cells into gastrointestinal tissue, reducing tissue damage, but also allowed the immune system to subsequently control infection after therapy was discontinued.

The precise mechanism by which this operates is yet unknown, but the combination of α4β7-directed antibodies with ART seems to have functionally cured SIV infection in the macaques, granted this is not a complete cure, because the viral genome is still present in the host. The human equivalent for the α4β7 antibody is already an FDA-approved drug called vedolizumab, currently used to treat Chron’s disease and ulcerative colitis. A clinical trial was begun in May 2016 to see if vedolizumab is safe for AIDS patients, and whether it allows the immune system to control HIV infection after ART is discontinued. The study is expected to be completed in 2020.

A great deal of work remains to be done to understand the molecular implications of this treatment, but the results of the clinical trial are eagerly awaited. Long-term immune control over infection promises to be a groundbreaking step forward in our ability to treat AIDS and could effectively eliminate the need for recurring medication. This would solve a major distribution challenge for developing countries, and could herald a new era in humanity’s relationship with this virus.

Image source: https://www.flickr.com/photos/54591706@N02/6813384933

The Community Pharmacy as a Delivery Agent for Crucial Public Health Interventions

BY ALISON HERMAN

The National Institute for Health Research’s Public Health Research programme in the UK recently conducted a meta-analysis to determine the role of community pharmacies as sites for crucial interventions related to the nation’s top public health priorities. Taking into account standards for quality, scientific replicability and accuracy, an independent research team selected 24 studies out of 14,000 citations related to this type of work in community pharmacies.

Among their major findings was showing that community pharmacies effectively and cost-efficiently encourage people to quit smoking through interventions like behavioral support and nicotine replacement therapy.

Unfortunately, as they point out in the limitations section of their review, little information was available to explain why the features of these interventions in particular were successful compared to others or no intervention at all. At the same time, they were unable to draw conclusions about the success of similar interventions in the realms of weight loss and healthy alcohol use due to a lack of primary research in those areas . The only relevant studies related to weight loss and healthy alcohol use were too different in their setups to be comparable or synthesizable with the other identified studies in order to make any general conclusions. Therefore, even though they find smoking cessation interventions to be successful, the meta-analysis does not provide any conclusive evidence about the mechanisms of successful community pharmacy interventions.

In addition to analyzing the effectiveness of community pharmacies in public health interventions, a primary objective of the study was to determine how demographic features, like race, gender, or socioeconomic status, affected the success of the interventions for different subsets of the population. Of the 24 studies analyzed, however, none included detailed information of the participants’ demographic features. As a result of this lack of evidence, they were unable to draw any conclusions in this section of the report. Given that demographic data was not a consideration in any of the studies analyzed, making demographic effects a central part of their analysis seems like an futile choice. Instead, these considerations should have been included in sections related to the limitations of the studies examined or discussed as future directions for research in this field.

An additional limitation of the study was that their claim that very few studies targeted disadvantaged populations is in tension with their claim that most community pharmacies exist in the “areas of highest deprivation.” This fact complicates the issue of the targeted population, since it would seem that, by default, community pharmacies treat and therefore target economically disadvantaged populations. The researchers do little to reconcile their claims that demographic features are unknown and yet, that they know that the studies do not target disadvantaged populations.

image-cycle-1-alison-herman
UK: A community pharmacist interacts with a customer as she picks up her prescription. Conversations like these could serve as crucial sites to institute public health interventions.

Nine of the 24 studies examined took place in the United Kingdom, so the conclusions of the meta-analysis are generalizable to the UK pharmacy context. Given the success of community pharmacies in smoking cessation, a recent news report announcing that the Department of Health plans to cut funding for community pharmacies in the UK could be worrisome for local communities. The meta-analysis carries implications for whether these cuts should move forward or not; as such, the public should be informed in a clear and accessible manner about the benefits of community pharmacies for important public health initiatives.

References

Brown, TJ, A. Todd, CL O’Malley, HJ Moore, AK Husband, C. Bambra, A. Kasim, FF Sniehotta, L. Steed, and CD Summerbell. “Community Pharmacy Interventions for Public Health Priorities: A Systematic Review of Community Pharmacy-delivered Smoking, Alcohol and Weight Management Interventions.” Accessed October 18, 2016.

McKee, Selina. “Gov’t Announces Cuts to Community Pharmacy Budget.” Pharma Times, October 21, 2016. http://www.pharmatimes.com/news/govt_announces_cuts_to_community_pharmacy_budget_1173167.

The Role of Community Pharmacies in Public Health. January 16, 2014. Public Health England.

Image source: https://www.retail-week.com/sectors/health-and-beauty/alliance-boots-targets-uk-independent-pharmacies-with-alphega-pharmacy-brand/5055728.article

Gene Editing: What it means for the future of medicine

BY ALEXANDER V. SHAHIN

Earlier this month, an international group of scientists convened at Washington, D.C. and gave the green light for human gene editing research, even on germline cells. However, in their statement, they warned researchers to be careful, highlighting the need for “appropriate regulatory oversight.”

This news represents a landmark decision for the future of human gene editing. In recent years, scientists have developed increasingly sophisticated techniques for manipulating nucleic acid. In particular, the CRISPR/Cas system has emerged as a powerful new tool that has made it possible to insert, delete, or alter DNA cheaper and quicker than ever before.

This system uses the enzyme Cas9, which bacteria usually produce to fight off viral infections. Recently, an alternative enzyme called Cpf1 was identified that may potentially prove to be an even more powerful tool in gene editing.

The thought of being able to modify human DNA in order to cure genetic diseases seems like something out of a sci-fi movie. The truth, however, is that genetic editing of the human body is already underway in patients. Recently, researchers at a company called Sangamo biopharmaceuticals announced that they would begin clinical trials using the CRISPR/Cas system to replace a mutant copy of the Factor IX gene in hemophiliacs. Earlier this year, a gene-editing tool known as TALENs was successful in treating a baby girl with leukemia. Furthermore, gene editing has already been used to engineer different crops and livestock.

There are many in the scientific community who remain skeptical of these new gene-editing technologies. Some researchers believe that tampering with an organism’s genome could have unforeseen, negative side effects. This is especially worrisome in germline editing, where any genetic change could be passed along to future generations. There are also many who question whether tinkering with the human genome is ethical.

These are all important questions that should be kept in minds as we move into the future of gene editing research. These new technologies have the potential to revolutionize medicine in the coming years, but it’s our responsibility to make sure it is used correctly. Of course, there is still a lot to learn before these technologies such as CRISPR/Cas become mainstream in clinical research.

However, the promises they have shown in their early days reveal a bright future for the field. We might be a long way off from living in a world of designer babies, but gene editing is already having a significant impact on people’s lives and will, hopefully, continue to do so in the near future.

 

Interview: What Went Wrong with Ebola?

By Daniel Liu

The current Ebola crisis has claimed over ten thousand lives in West Africa, and continues to cause hundreds of new infections every week. Yet, media coverage of the crisis had been meager up until the summer of 2014, an entire half-year after the start of the outbreak in late 2013. The world’s delayed reaction has generated criticism for both public i
gnorance and for lackluster government response. But where did we go wrong? What could we have done differently that may have changed the course of this epidemic?

Adel Mahmoud
Princeton Professor Adel Mahmoud. Photo courtesy of Princeton University.

To get a better understanding of these difficult questions, we spoke with Princeton University’s Adel Mahmoud, a professor in both The Woodrow Wilson School of Public and International Affairs and The Department of Molecular Biology. Professor Mahmoud’s research focuses on the causes and emergence of infectious diseases, as well as the discovery, development, and global deployment and use of vaccines.

Question: What was the biggest shortcoming of the US and West African governments’ response to the Ebola crisis?

Answer: We were coming from behind in the response. This is a virus that we have known to exist since 1976. We know that it happens in outbreaks. We know that when it happens, the immediate need is for facilities to take care of patients and to deliver healthcare in a way whereby you don’t infect healthcare workers. The knowledge of how to deal with the issue is not rocket science, and it’s not new.

Late in 2013, when the outbreak first started, we should have immediately been pursuing identification, isolation, barrier nursing—and we could have influenced the course of events. In some ways that’s not very helpful because it’s historical. Now, when we are in the middle of the dilemma, the US says we’re going to send a few hundred of our troops, and we’re going to build facilities to take care of patients. That’s very well and good. The problem is, these things take time. And in the meantime, the infection is progressing, and the transmission is happening.

It would be unfair to ask “why didn’t [West African governments] respond better?” We today are facing a very serious challenge because most of the resources, most of the attention is going towards Ebola now, but what about all the other diseases that are there? What are you going to do with the polio campaign? What are you going to do with the immunization campaign? The resources are very limited, and there is no question today—there is a shift to put it for Ebola. The depth of resources and the depth of capabilities is very thin. You suck it in one direction, you lose it in other direction.

Question: In retrospect, what could the world have done differently to diminish the extent of the Ebola crisis?

Answer: There are a few things that would have changed the nature of what we have seen in West Africa. For example, we have been working on candidate vaccines for Ebola for the last fifteen to twenty years. Rather than working on a candidate, testing it in a couple of experimental animals, and throwing it in the freezer, what we should have done is to take these vaccine candidates, examine which is the best, take them through phase I, and take them through phase II, so you know you have an effective vaccine in the freezer. You face an outbreak like this, then you only have two steps: scale up, and deploy. What we’re doing today is, taking candidates from the lab, going through phase I, and then phase II, and only then would we be able to scale up and deploy. You really have to invest some effort in getting ready. And getting ready does not mean you spend billions and billions making things that nobody would use. No—getting ready means that you have explorations, and you have the first couple of steps to put you in a much more capable position to respond. Have a candidate drug available. That’s the difference.

Question: The CDC has set recommendations that individuals who have been potentially exposed to Ebola be monitored for twenty-one days, but not quarantined. A few states in the US, such as New Jersey and Connecticut, have ignored these guidelines by instating mandatory quarantines anyways. In fact, this issue has been contested in Maine’s district courts, which ruled against the mandatory quarantines. Do quarantines here in the US serve a real public health benefit, or are these states just acting out of fear?

Answer: The difficulty in answering this question is related to assessing the risk of someone coming from an Ebola-infected area. What is the risk that that individual would have the infection? That’s the first serious question you have the answer. And if the risk is high, then I would say quarantine is a reasonable approach; for example, a healthcare worker who was delivering care to Ebola patients in a West African country. In quarantine we’re not asking people to be put in jail, we’re just saying: stay home for twenty-one days. For the sake of public health safety, that is not an undue burden. But if the exposure is marginal, or if the contact is marginal, then monitoring temperature for the twenty-one days is a reasonable approach. When you are in the heat of the battle and people are just yelling and screaming at each other, logic gets lost. The issue here is very simple: assess the risk, and if the risk is reasonable, then put the person in isolation.

Question: In many West African countries, there is a very negative image of Public Health workers. Many families are reluctant to hand their loved ones over to be transported to hospitals because it is seen as a death sentence. How can Public Health Policy be used to address these social issues to change public perception of the disease?

Answer: When you have a village in West Africa, and several people drop dead, and then you have a team descend upon them in moon suits—what do you expect? You are injecting fear, immediately. Ebola happened in countries where they have known Ebola, and it has been around, in and out, for some time. But as long as it is not the disease of the day, no one wants to talk about it. So we lost ground, the ground of public education, of information, of dissemination, of trust. Those are the issues that make people part of the solution. People are not the enemy here!

What we have to consider is a campaign of education, of context, of information dissemination, by local people who are trusted in the community. Explaining, what are these moon suits? How is this disease transmitted? What is Ebola? Unfortunately, when you are in the heat of the battle and you have thousands of people in West Africa dying—that element gets forgotten. But it needs to be brought back on the forefront. These are countries with suspicion about the health profession, with suspicion about Western medicine, with suspicion about vaccines. We can’t just say “we’re going to build a hospital, and we’re going to put you in quarantine, and we’re going to do this and that.” You need real human interaction at a very personal level.

Question: Senegal and Nigeria have successfully contained and ended their outbreaks of Ebola. Is this success a reflection of proper public health response, and if so, which ones?

Answer: In some ways, you have to say yes. Obviously, they did not face a major outbreak—but they managed to control it by, basically, quarantining all the patients and their contacts. It’s all about the proper isolation, and the proper care. And the proper care today is not specific therapies; the proper care is fluids, electrolytes, and maintaining body function, which we physicians learned how to do years back. It’s an issue of getting these well-known techniques of medical treatment deployed.

Question: How much responsibility should the US take in fighting Ebola in affected West African Nations? What would be the best way to help?

Answer: The best thing that the US can offer is scientific know-how. The current front candidates for Ebola vaccines all came from the US. I would have liked to have seen them partially developed earlier, but the first thing that the US can offer, is scientific input. The second is exactly what President Obama did, which is to deploy humanitarian support in situations where it is urgently needed. There aren’t many other countries that can match what the US can do in this regard. The third element is financial support. I think we are doing all three.

Question: How significant of a role have NGOs such as Doctors without Borders (MSF) played in containing Ebola?

Answer: They are an essential element of the response. Developing countries have a very complicated agenda to face the future and—don’t take this as an insult or as a criticism—their ability to spend on the infrastructure for health is limited. So when something like [Ebola] comes up, it taxes the total capability of these countries. They can’t do it their own! They need support from abroad.
Private, non-profit organizations have the ability to move quickly. The edge of advantage of MSF is that they can deploy doctors tomorrow. That’s phenomenally important.

Question: What can we learn from the Ebola epidemic when addressing future public health crises?

Answer: There are quite a few lessons. One of them is that the threat of microbes to the human population is a constant feature of life on earth. If it is not Ebola, it will be something else. We have no other alternative but to learn how to predict, and how to get ready, and how to respond. It’s one thing to have noticed that Ebola has started—that was the end of 2013. It’s another to try to face it in the middle of 2014. Where have we been?

Second, what elements of response do you have? You should have had some ideas of vaccines, some ideas of drugs beforehand. Most of these infections are going to emerge in areas that are not 100% prepared to deal with it. The world has to be prepared to respond, and Ebola showed that the world was not. The virus was running around amok in Guinea in 2013, and no one talked about it. We started waking up in the middle of 2014. Come on guys, where have you been? The world was caught unprepared.

Ebola: What went wrong?

The current Ebola crisis has claimed over ten thousand lives in West Africa, and continues to cause hundreds of new infections every week. Yet, media coverage of the crisis had been meager up until the summer of 2014, an entire half-year after the start of the outbreak in late 2013. The world’s delayed reaction has generated criticism for both public ignorance and for lackluster government response. But where did we go wrong? What could we have done differently that may have changed the course of this epidemic?

To get a better understanding of these difficult questions, we spoke with Princeton University’s Adel Mahmoud, a professor in both The Woodrow Wilson School of Public and International Affairs and The Department of Molecular Biology. Professor Mahmoud’s research focuses on the causes and emergence of infectious diseases, as well as the discovery, development, and global deployment and use of vaccines.

Question: What was the biggest shortcoming of the US and West African governments’ response to the Ebola crisis?

Answer: We were coming from behind in the response. This is a virus that we have known to exist since 1976. Continue reading Ebola: What went wrong?

Measuring up a Vaccine: The Meningitis B Immune Response Study

This past November, students from Princeton University’s incoming freshman class lined up atop Icahn Laboratory’s Oval Lounge to participate in an immune response study to the meningitis B vaccine. That clinic was the second round of a large-scale public health study being conducted by Professor Nicole Basta, an infectious disease epidemiologist in the Department of Ecology and Evolutionary Biology.

After nine cases of meningitis B broke out at Princeton in 2013, University Health Services (UHS) worked with the Centers for Disease Control and Prevention (CDC) to approve an emergency vaccination campaign. Continue reading Measuring up a Vaccine: The Meningitis B Immune Response Study