Tuesday, July 31, 2018

Out of sight, out of mind: The massive hepatitis A outbreak no one is talking about

Since early 2017, over 4,500 cases of hepatitis A have been reported in outbreaks across 10 states in the United States, a massive increase from the 1,390 cases and 0 outbreaks seen in the entire country in 2015. And the cases keep rolling in. The states reporting outbreaks so far are Arkansas, California, Indiana, Kentucky, Michigan, Missouri, Ohio, Tennessee, Utah, and West Virginia, but additional cases have been reported in other states. Disease has been fairly severe in these outbreaks, leading to a ~60% hospitalization rate, compared to the typical ~30% for hepatitis A, and at least 62 deaths. These outbreaks have mainly plagued the homeless and illicit drug-using populations, which has kept outbreak coverage largely out of the national news. But there have also been reports of cases in people outside these groups, with a growing number of cases among food service workers.

The disease hepatitis A is caused by the hepatitis A virus (HAV). While "hepatitis" can be caused by several viruses that share similar names, the hepatitis viruses are quite different from each other. HAV is an unenveloped RNA virus from the picornavirus family, the same family as poliovirus and rhinoviruses.  Alternatively, hepatitis B virus is an enveloped double-stranded DNA virus from the hepadnavirus family, hepatitis C virus is an enveloped RNA virus from the flavivirus family, and hepatitis E virus is a quasi-enveloped RNA virus currently classified in the hepevirus family (hepatitis D virus is considered a subviral satellite since it cannot replicate without the presence of hepatitis B).

A cluster of HAV virions
CDC's Public Health Image Library.
Image # 2739; photo credit: CDC/Betty Partin.
HAV causes acute liver infections, which typically manifest with symptoms such as fatigue, nausea and vomiting, abdominal pain, low-grade fever, and jaundice (yellowing of the skin and whites of the eyes). Symptoms tend to appear 2-4 weeks after exposure to the virus and can last for a couple months. Previous hepatitis A outbreaks in the United States have been associated with eating contaminated food, such as an outbreak caused by imported pomegranate seeds in 2013. However, in the current outbreaks, the virus is being transmitted from person to person through contact with fecal material, leaving people with poor sanitation and hygiene at increased risk.

A vaccine for HAV exists and is extremely effective at preventing disease. Children are routinely vaccinated around age 1, providing protective immunity against the virus. Unfortunately, the vaccine was not approved for use until 1995, so many adults over the age of 25 have never been vaccinated and remain susceptible to HAV infection. Vaccination in adults is an option but is only routinely done for high-risk individuals, such as people traveling to countries where hepatitis A is common, caring for an individual with hepatitis A, or using recreational drugs. The vaccine can be given as a prophylactic before exposure or as a treatment post-exposure; as long as a person is vaccinated within 2 weeks of exposure, infection can still be prevented. However, mobilization of the vaccine to those at highest risk of infection in these outbreaks has been difficult due to the barriers in access to health care that exist for the homeless and drug-using populations. Additionally, other than the vaccine, there is no real treatment for HAV infection; giving patients rest, fluids, and adequate nutrition is the only course of action. 

While local health agencies and the Centers for Disease Control (CDC) have been working to contain these outbreaks and prevent further spread, vaccine availability and lack of funding have threatened efforts. When the outbreaks began, demand for the vaccine increased dramatically, leading to shortages in the vaccine supply. Fortunately, this issue has since been resolved thanks to vaccine suppliers GlaxoSmithKline and Merck ramping up production. However, the Section 317 Immunization Program from the CDC that has been essential in paying for these vaccines has already experienced funding cuts and may experience more in the coming year. Additionally, many public health officials feel they are not being provided with enough funding to support the other essential componenets of combating viral hepatitis.

Since the virus is spreading from person-to-person contact in these outbreaks, improved sanitation and hygiene are key to reducing spread. Achieving these goals in the populations at risk has not been an easy task. In California, officials resorted to cleaning their public buses, streets, and even sidewalks with bleach to complement their vaccine distribution campaigns. It is now believed that the outbreak in California is over, giving hope that employing similar strategies could improve outbreak containment in other states. Outside California, the number of cases per day has been trending downwards in some areas, but that trend has not been consistent, and officials warn that there is still a significant threat. Improving sanitation for the over 500,000 Americans experiencing homelessness is an essential measure to end the hepatitis A outbreaks and prevent future infectious disease outbreaks in the United States. In a tough funding climate, this will not be easy to achieve, but state health departments and private non-profits are working vigilantly towards this goal. Until then, wash your hands, wash your hands, and wash your hands to help fight the spread of HAV.

Latest case report statistics, July 2018
Not reported
≥ 1
≥ 2
West Virginia
≥ 2,787
≥ 62

Friday, June 29, 2018

I've got the power: How the potential bioterrorism agent Francisella tularensis manipulates host cells

In an age of advanced weaponry and warfare, the risk of bioterrorism is increasingly acute. One potential bioterrorism agent is the bacterium Francisella tularensis, which is responsible for the similarly named disease tularemia. F. tularensis is classified as a category A potential bioterrorism agent, the same classification as anthrax and the plague. A low number of bacteria are capable of causing disease, which can be fatal in up to 60% of cases if untreated. Outside the potential threat for bioterrorism, F. tularensis infection also happens naturally. While cases of tularemia in the United States have largely declined since the 1950s, this is not the case throughout the world, with multiple outbreaks occurring in Europe in the last 10 years.

F. tularemia.
CDC's Public Health Image Library.
Image # 1903; photo credit: Larry Stauffer, 
Oregon State Public Health Laboratory.
Disease management and bacterial elimination can be difficult because F. tularensis can survive in over 100 species of mammals, birds, cold-blooded animals, and arthropods, including rabbits, mice, rats, squirrels, cats, dogs, horses, pigs, and sheep. To further complicate matters, transmission of F. tularensis can occur in several ways, including the consumption of contaminated water or food; contact with urine, excrement, or blood from infected animals; bites from blood-sucking arthropods like ticks, flies, and mosquitoes; and inhalation of aerosolized bacteria. The symptoms of tularemia depend on the route of transmission and can include a skin ulcer at the site of bacterial entry; swollen glands; sore throat; and high fever. F. tularensis is naturally resistant to many antibiotics because it is an intracellular bacterium that spends most of its life hiding inside a host cell; an antibiotic must first get into the host cell before it can have any effect on the pathogen. Aminoglycosides, tetracyclines, and fluoroquinolones have been shown to be effective, but 5-15% of infections relapse following treatment, and the side effects from these antibiotics can be unmanageable, limiting their use.

Due to the low infectious dose, high mortality rate, ease of transmission, and difficulty in treatment, natural F. tularensis infection is a serious threat to public health, and a weaponized version of the bacteria could be catastrophic. To counteract these risks, researchers have been studying how F. tularensis causes infection to identify ways to inhibit or kill the bacteria. We know that once in the human body, F. tularensis is taken up by phagocytic cells, such as macrophages. The job of these phagocytic cells is to engulf the bacterium into a compartment called a phagosome for degradation. Typically, this is how the immune system would capture and kill a pathogen. However, in the case of F. tularensis, the bacterium escapes from the phagosome through a process that is not well understood to begin replicating in the cytosol of the host cell. A recent study shed a little light on this process and found that F. tularensis is manipulating the host macrophage in a unique way.

Macrophage (right) containing rickettsial microbes.
CDC's Public Health Image Library.
Image # 8731; photo credit: CDC, Dr. Ed Ewing.
Dr. Forrest Jessop and colleagues at the National Institute of Allergy and Infectious Disease found that F. tularensis alters the function of the mitochondria in the macrophage. The mitochondria are essential cellular organelles that are responsible for providing “power” to the cell, much like a battery provides power to a flashlight. When F. tularensis first enters the macrophage, it improves the function of the mitochondria, which keeps the macrophage alive and prevents an inflammatory response from the immune system. A few hours later, the bacterium reverses these effects and decreases mitochondrial function, decreasing the macrophage's power supply and leading to rapid bacterial replication and oncosis, a type of cell death that involves the swelling of the cell. This facilitates the pathogen’s ability to get out of the cell after replicating and move on to a new host cell.

The researchers were able to take this new-found knowledge of the bacteria’s effect on mitochondria a step further and test a therapeutic treatment in culture. They found that by treating F. tularensis-infected macrophages with drugs that protect typical mitochondrial function, they were able to reduce macrophage cell death and decrease levels of bacterial replication. It remains to be seen if this type of intervention will work in an animal system, but this is a promising step in the right direction towards increasing the number of treatments available for these infections. Since the environmental reservoir for F. tularensis is so vast, increased awareness of the risks of disease and research focus are important to stem the outbreaks and prevent future bioterrorism threats.

Thursday, May 31, 2018

Broadly neutralizing antibodies take down bacteria, viruses, and yeast

Antibodies are an important player in the body's immune system. The job of an antibody is to recognize a very specific feature of a foreign protein, known as an epitope. Without high levels of epitope specificity, antibodies can often begin to bind to and attack self-proteins, leading to dangerous autoimmune reactions. By producing highly specific antibodies, the body can avoid these autoimmune disasters. However, this high level of specificity also means that antibodies typically only recognize one specific species or even sub-species of foreign invaders. Interestingly, a research group recently identified antibodies from healthy individuals that could recognize multiple subgroups of Klebsiella pneumoniae, as well as various other bacteria and even some yeasts and viruses. These “universal antibodies” have sparked a great deal of interest as a potential treatment option for patients suffering from infections.

K. pneumoniae is a species of bacteria that is found frequently in the environment and in people; it is estimated that over 1/3 of the world’s population is colonized by K. pneumoniae. In individuals with a healthy immune system, the level of bacteria is controlled, and illness does not occur. However, in immunocompromised and already-ill people, the bacteria can cause severe infections. Klebsiella are the third leading cause of hospital-acquired infections in the United States, with alarmingly high mortality rates: K. pneumoniae pneumonia can cause mortality in up to 50% of patients, and bloodstream infections can cause mortality in 20-30%. Equally concerning is the rising level of antibiotic resistance found in K. pneumoniae. This makes them increasingly difficult to treat.

K. pneumoniae (red).
CDC's Public Health Image Library.
Image # 18170; photo credit: NIAID.
The outer membrane of K. pneumoniae, and other bacteria, is covered in lipopolysaccharide (LPS) molecules. Because this molecule is exposed to the external environment, LPS serves as a good target for the immune system to produce antibodies against. LPS is made up of repeating sugar residues; in the case of the K. pneumoniae subgroups of interest in this research, that sugar is mannose connected by 1-2 or 1-3 linakages. Researchers identified a number of antibodies from the blood of healthy individuals that were highly efficient at neutralizing K. pneumoniae bacteria by binding to these mannose residues. Because mannose is a common surface sugar molecule and the mannose molecule arrangements used by K. pneumoniae are also used by other microbes, these antibodies had a very broad specificity. They bound not only K. pneumoniae, but also other intestinal microbes, HIV virions, and the yeast Saccharomyces cerevisiae

These antibodies open the possibility for their use as therapeutics. Giving pre-made antibodies to patients has already been established as an effective strategy to treat or prevent a number of infectious diseases, such as rabies, diptheria, tetanus, hepatitis B, and botulism. In the case of these infections, antibodies that are highly specific to the pathogen of interest have been made and used. However, the identification of these broadly neutralizing antibodies opens the door for a new opportunity. Giving a patient "universal" antibodies could help fight a variety of infections without even necessarily identifying the causative agent, which can be difficult and time-consuming in the face of a life-threatening infection. While it is a long process from antibody identification to the approved use of an antibody as a therapy in patients, this discovery provides researchers direction for the path ahead. Therapeutic advances that use alternative strategies to inhibit and kill pathogens are of the utmost importance in the current age of antibiotic resistance. Antibodies, instead of just antibiotics, that can fight disease will be one of the important tools in our arsenal against the ever-evolving microbes.

Monday, April 30, 2018

The Fast and the Furious...Antibiotic Discovery

Over 10 million deaths per year. That's the global death toll experts predict from drug-resistant infections by 2050 without new ways to combat these microbes. Unlike most disease areas, where new and improved drugs are being discovered and developed every year, bacterial infections are still largely treated with classes of antibiotics that were discovered over 50 years ago. Many of these drugs were found by screening microbes that live in the soil, which has proven to be a successful strategy for obtaining a vast variety of chemical compounds. However, most microbes in soil cannot be grown in the lab, leaving large gaps in our ability to study them and identify potential new antibiotics. Recent advances, however, have helped overcome this problem and lead to the identification of the first new classes of antibiotics in 30 years.

The iChip culture method.
Al Granberg. https://www.the-scientist.com/
In 2015, a team of scientists at Northeastern University isolated a new antibiotic using an ingenious method for growing soil microbes with the iChip, a device with wells for bacteria that are separated from a natural environment (like soil) by a diffusion membrane with tiny pores that allow the transfer of nutrients without allowing the bacteria to leave the well. Using this method, researchers were able to isolate new chemical compounds from these bacteria and identify teixobactin. Upon further testing, they found that teixobactin was highly effective at killing several types of bacteria in culture, including Mycobacterium tuberculosis and methicillin-resistant Staphylococcus aureus (MRSA), by interfering with the ability of the bacteria to build cell walls. Teixobactin was also shown to be effective at clearing infections in mice. Although teixobactin itself is difficult to produce, a group at the University of Lincoln, UK, recently synthesized a much easier-to-make version that maintains potency and could be used for commercial production.

In 2017, another new class of antibiotics was discovered at Rockefeller University using just bioinformatic analysis of DNA extracted from the environment; this group didn’t even have to grow the bacteria in the lab. They based their strategy on the knowledge that there is a family of calcium-dependent antibiotics. By isolating DNA directly from environmental samples and searching for sequences that featured the known calcium-binding signature, they could identify genes that potentially encoded new calcium-dependent antibiotics. They then transferred these DNA sequences into bacteria that can be cultured for further study. The new antibiotic class they found, the malacidins, also interferes with the ability of bacteria to properly form cell walls. Malacidins were shown to clear MRSA infections in the cut wounds of rats. Importantly, even after 3 weeks of exposure to the drug, there was no sign of resistant bacteria. This finding suggests that the mechanism of action for the malacidins is one that cannot be circumvented easily by the bacteria, which bodes well for their use against multidrug-resistant pathogens.

A third novel class of antibiotics was just described earlier this month in the journal Molecular Cell by researchers from the University of Illinois at Chicago and the biotech company Nosopharm. This class, called the odilorhabdins, was isolated from a bacterium that lives in a symbiotic relationship with a nematode worm in soil. This bacterium secretes a number of compounds that help the nematode colonize and kill insects and keep the insect carcass from being invaded by other bacteria or fungi. The odilorhabdins exert their antimicrobial activity by interfering with bacterial protein production. While several other antibiotics also target this process, the odilorhabdins bind to a unique site on the bacterial ribosome (the part of the cell responsible for making proteins); this means that bacteria that are resistant to other antibiotics that interfere with protein production will not be resistant to the odilorhabdins. When tested for their ability to kill several pathogenic bacteria in culture, the odilorhabdins were highly effective. One of the odilorhabdins, NOSO-95179, was also tested in mice and could significantly reduce Klebsiella pneumoniae septicemia and lung infection.

MRSA (green) being enveloped
by a white blood cell.
CDC's Public Health Image Library.
Image # 18126; photo credit: NIAID.
While these new antibiotics are still in the early stages of development and are at least 6-10 years from being available for use in people, the rapid identification of multiple new antibiotic classes after a decades-long “discovery void” provides hope. The new techniques for culturing soil bacteria, along with bioinformatic approaches that avoid this step all together, offer new avenues for drug discovery. Additionally, there is ongoing work to re-investigate previously sidelined drug candidates and modify existing antibiotics to improve their efficacy and overcome resistance. No matter the approach, the road to develop a new antibiotic is long and expensive, making it impossible for academic research labs to go it alone. Luckily, pharmaceutical companies are beginning to get more involved. In 2016, the Antimicrobial Resistance Industry Alliance presented the “Davos Declaration” at the World Economic Forum. Nearly 100 companies signed the declaration, pledging to support the research and development of new antimicrobials and improve access to current and future treatments. With this renewed commitment from the pharmaceutical industry, which had largely been turning away from antimicrobial development in recent years, the financing and man-power to produce these new antibiotics might just be available. While nothing short of a strong, concerted effort to deal with drug resistance will allow us to avoid the looming projection of 10 million deaths per year, the current pace of advancement bodes well for our ability to rise to the challenge.

Thursday, March 29, 2018

New funding (and new hope) for a Lassa virus vaccine

Nearly 2 years ago in 2016, I wrote a post about a deadly virus that was causing a worrying outbreak in Nigeria: the Lassa virus. For the rest of 2016 and 2017, the outbreak lessened in severity, but it was not completely eliminated. Unfortunately, this year has featured a new surge in infections with the virus. In just the first 2 months of 2018, at least 317 people have been infected with Lassa virus, far surpassing the 143 cases confirmed in all of 2017. Additionally, around 20% of those infected in 2018 have died from the infection.

While the reports from March suggest that the current outbreak is slowing, major hurdles for the containment and management of Lassa fever cases still exist. The disease is carried by multimammate rats, which are difficult to keep out of homes and away from human food, especially as populations in Africa grow and the once-empty fields where the rodents live are developed. The long asymptomatic period at the beginning of infection makes it difficult to diagnose and treat effectively. Even once symptoms do manifest, they tend to be mild and non-specific, with 80% of those infected suffering from mild fever, general malaise, and/or headache. Additionally, the sub-optimal treatments have not improved in recent years, and there is still no vaccine.

lassa, virus, virions, adjacent, cell, debris, virus, member, virus, family, arenaviridae
Lassa virus particles. CDC's Public Health Image Library.
Image # 8700; photo credit: C.S. Goldsmith.
In an attempt to deal with these issues, the Coalition for Epidemic Preparedness Innovations (CEPI) awarded $37.5 million to Themis Bioscience earlier this month for the development of their Lassa virus vaccine. CEPI was created in the wake of the Ebola epidemic and receives funding from the Wellcome Trust, the Bill & Melinda Gates Foundation, the European Commission, and the governments of Germany, Japan, Norway, Belgium, Canada, and Australia to support the development of vaccines for potential or existing pandemics. While there are many diseases that could fall into this category, the main focus in the next 5 years for the group will be Lassa virus, the Middle East Respiratory Syndrome (MERS) virus, and Nipah virus.

With the funding from CEPI, Themis plans to move into human trials with their Lassa virus vaccine as early as this year. Following the Ebola crisis, the World Health Organization developed a procedure to fast-track the approval of products for use in public health emergencies. The hope is that these procedures could be used in the context of the Lassa virus outbreak to accelerate the development of the Themis vaccine. To further speed development, the Themis Lassa virus vaccine will be based on the measles vaccine vector previously created by the Institut Pasteur, which has already been used effectively in humans. By inserting Lassa virus proteins into this vector, a new vaccine that will prime the body to respond to a Lassa infection will be created. This strategy opens the door to allow for the rapid creation of additional vaccines, as well.

The funding from CEPI will support the preclinical and initial clinical development through a phase 2 trial of the Themis Lassa virus vaccine in order to test its safety and efficacy. The ultimate goal is that the funds will allow the production of a vaccine stockpile that will be ready to test in an outbreak, which may be needed sooner rather than later. While the current outbreak appears to be slowing, and the dry season, when the majority of Lassa fever cases in Nigeria have historically occurred, is coming to an end, a report from Sierra Leone has suggested that the incidence of Lassa fever may actually be higher during the rainy season. This leaves uncertainty about the outlook for the current Lassa fever outbreak. But whether the outbreak continues now or goes dormant for the next 10 years, a vaccine will be a vital weapon in the fight against Lassa virus for the future.

Monday, March 5, 2018

Good reason for my writing gap

I must apologize for my extended absence from writing these posts. But I promise I had good reason! Since my last post at the end of August, I've completed my dissertation and graduated with my PhD, hunted for a job, gotten a job, moved, and started that new job. But now I'm back and ready to provide you all with more exciting biology posts. Enjoy!

Flu vaccination: Arm yourself against the anti-vax arguement

The flu vaccine. Always a hot topic, especially in years when the vaccine has poor efficacy as it does this year. At times like this, the anti-vax community can gain leverage. So let's take a look at some of the top arguments used in the anti-vax movement and see if we can shed some light on the controversy.

The flu vaccine makes you sick.
People will often say that they got the flu because of the flu shot. This is actually not possible. The flu shot is made with an inactivated, DEAD form of the virus that cannot replicate and transmit. While there can be side effects from the shot that make you feel "sick," this is not the flu. Additionally, the flu vaccine stimulates your immune system, which actually strengthens your ability to fight infections and avoid getting "sick." It is important to note, though, that getting the flu vaccine does not mean you are immediately protected. It typically takes about two weeks to gain the full advantage from the vaccine. People who were already exposed to the virus before receiving the vaccine or who are exposed shortly after vaccination will not be protected.
Image result for flu vaccine
Brian Snyder/Reuters/Landov

The flu vaccine contains mercury that will poison you.
Flu shots that come from a multi-dose vial do typically contain thimerosal, an ethylmercury-based preservative to prevent any bacteria or fungus from contaminating the vaccine. Flu shots that come in prefilled syringes and the nasal flu vaccine do NOT contain this preservative (with the exception of the Fluvirin prefilled syringes from Seqiris, which contain trace amounts of thimerosal). It is important to note the distinction between ethylmercury (found in thimerosal) and methylmercury. Methylmercury is the form of mercury found in foods, like seafood, that is associated with neurological complications. While in vitro studies (in cell culture systems and not in the body) have found little difference between the effects of methyl- and ethylmercury, the story is quite different in vivo (in actual living creatures). Ethylmercury is cleared from the bloodstream significantly more quickly than methylmercury, minimizing the exposure of the body to mercury. Ethylmercury is also compartmentalized by the body more successfully than methylmercury, further limiting exposure. Some may argue that based on the in vitro evidence, ethylmercury is unsafe, but the in vivo data and years of studies have shown that this is not the case. But, if you still want to avoid mercury all together, you can get a prefilled syringe version of the flu shot that contains no thimerosal.

The flu vaccine causes the virus to mutate, becoming more virulent.
This is a popular argument used in the anti-vax community. While that is always a theoretical possibility, there is currently no scientific evidence that this is happening. The influenza virus has an extremely rapid mutation rate, whether you put selective pressure on it or not, so it’s going to be mutating all the time regardless of what we as humans do. This is just the nature of the virus’s replication; the enzyme it uses to replicate its genome makes a lot of mistakes, and the virus is perfectly happy to continue on with those mistakes (aka mutations).

The idea that vaccines create more virulent viruses is typically based on the fact that the use of antibiotics can lead to more pathogenic bacteria, which has been observed. But the vaccine works very differently from an antibiotic. In the case of bacteria, they directly come in contact with and are affected by the antibiotic, which gives bacteria that can survive while in contact a direct advantage. In the case of the vaccine, since it is priming an individual’s immune system and not directly contacting the virus, there is no such direct advantage to the virus. Even if the influenza virus you encounter is different from the vaccine strain, your immune system will be primed and you will have a better chance of successfully clearing the virus. While it is theoretically possible that by vaccinating, you remove the predominant influenza strains, leaving an opening in the environment for a “resistant” strain to fill, most of the highly virulent and dangerous strains have emerged in parts of the world where vaccination rates are very low, so this doesn’t seem to be happening.

Vaccination causes super strains of the flu virus to emerge that are immune to our vaccines. 
Image result for flu vaccine
Influenza virus. Carrington College
People often further argue that our lack of vaccine effectiveness in recent years comes from the emergence of “super” strains of the virus that are “immune” to our vaccines. But the research suggests otherwise. Vaccinemakers use a less-than-ideal system for choosing the vaccine strains that relies on a test using ferrets exposed to the virus. This can lead to incorrect selection and a poor vaccine. Also, improved diagnostic techniques make it more likely for us to capture influenza infection than ever before, so people who would have been diagnosed with some unknown viral disease (and therefore considered “protected”) in the past are now being properly diagnosed as influenza patients. And we are learning that our vaccine production system making the vaccine in eggs leads to its own set of mutations in the vaccine strain that often dampen protection in people. A lot of groups are working to improve the vaccine production pipeline and find alternative ways that don’t involve growing the vaccine in eggs, so that will likely be the way of the future in 5-10 years.

Vaccines cause autism.
This claim is not unique to the flu vaccine and has been spouted at the forefront of the anti-vax community ever since 1998, when Andrew Wakefield and colleagues published a study looking at 12 children that claimed there was a link between the measles-mumps-rubella vaccine and autism. What people in the anti-vax community typically fail to realize is that since that article was published, it has been retracted (the authors themselves admitted their conclusions were inaccurate), Wakefield and colleagues have been found guilty of ethical violations and fraud, and Wakefield has been removed from the UK medical registry. They hand-picked the patients for their study and falsified data to ensure that they would conclude there was a link between vaccines and autism. Additionally, they had received funding from lawyers who had been hired by parents to bring lawsuits against vaccine companies. Since the Wakefield study, many large-scale studies have been performed to see if their initial findings could be confirmed in spite of the ethical issues with the study, but no corroborating evidence has been found. The link between vaccination and autism is based on fabricated data and has no true scientific merit.

In spite of the potentially poor efficacy, healthcare providers will still push for vaccination. Any protection is better than none, especially if you are in contact with the populations at high-risk of dying from infection, i.e. the elderly, babies, and immuno-compromised individuals. The more people who are protected (even if the protection is sub-optimal), the less likely it is for the virus to come in contact with these highly susceptible individuals, and healthcare providers rely on this to keep patients safe. The bottom line is we may have a sub-optimal vaccine, but a lot of people are actively working on that, any protection is still better than none, and there is no evidence that getting the vaccine has any negative impacts on the pool of viruses we are exposed to. So please do not be discouraged, and use your new flu vaccine knowledge to help educate others!