Author: esgunter64

This week, we’re going to take a deep dive into omalizumab, otherwise known as Xolair, a monoclonal antibody drug used to treat asthma. So what’s a monoclonal antibody? This article from the American Cancer Society defines monoclonal antibodies as synthetic proteins that when incorporated into the human body, function as human antibodies. This is useful when a person’s own antibodies don’t target harmful cells and tumors like they’re supposed to, like in the case of cancer. In Xolair’s case, it’s used to treat asthma, which affects a vast population of the world and affects their quality of life.

Xolair works as an inhibitor of the IgE antibody in asthmatic patients. Asthma attacks are often brought about by interactions with allergens, which bind to receptors on the antibodies, causing them to bind to mast cells and basophils that cause the allergic reaction. Xolair works by binding to the receptors on mast cells and basophils, preventing IgE-allergen complexes from binding to them. Since the antibody-allergen complexes can’t cause the mast cells and basophils to elicit their allergic response, asthma attacks are prevented or their severity lessened as a result.

As with any drug, Xolair comes with side effects, which differ with the age of the patient, and whether or not they suffer from chronic idiopathic urticaria (chronic hives). Those side effects are:

• Adults, children over 12
  • pain, especially in arms and legs
  • dizziness
  • fatigue
  • skin rash
  • higher risk of bone fractures
  • discomfort in the ears
• Children 6-12
  • cold symptoms
  • headache
  • fever
  • sore throat
  • discomfort in the ears
  • abdominal pain
  • nausea/vomiting
  • nosebleeds
• Chronic Idiopathic Urticaria
  • nausea
  • headaches
  • swelling in nose, throat and sinuses
  • cough
  • joint pain
  • higher risk of upper respiratory tract infection

There are also some very serious side effects that could cause severe complications. Those are:

• risk of developing cancer
• blood vessel inflammation
• problems with the heart and blood circulation

The common side effects are pretty usual for a lot of drugs, and are usually indicative of an allergic response to the drug. However, the higher risk for things like cancer and circulatory problems are worth noting, and more research is necessary to determine how high of a risk it is, and whether or not there are ways to mitigate the risk.

Xolair also increases your risk of helminth infections. This seems peculiar considering that parasites and allergens aren’t exactly related, but they’re closer than you think. IgE, the antibody responsible for dealing with allergens, is also the antibody responsible for helminth infections. In fact, allergies are such a problem in the US because we don’t really have to deal with parasites, so the IgE antibodies started to get a little antsy and responded to harmless substances like pollen, resulting in hypersensitivities and allergic responses. Since Xolair prevents IgE from binding to mast cells and basophils, if IgE actually DOES bind to a helminth, it can’t interact with mast cells and basophils to destroy the invader, allowing it to grow and wreak havoc in your body.

Xolair prevents asthma attacks by weakening the immune system. Rather than beef up the defenses to allow them to destroy allergens or something, it just prevents the cells of the adaptive immune response that respond to allergens from doing their job, which prevent the allergic response, and thus the asthma attack. Overall, Xolair seems like a useful drug that, with more research into the severe negative side effects, could be a highly effective means of treating asthma.

It’s on everyone’s mind and I’m sure we’re all sick of hearing about it every time we partake in any sort of media, but COVID-19 is ravaging the world. But how exactly does this enigmatic disease work? Who is at risk of being infected, and can they be infected twice? Well the answer to those questions involve antibodies. Antibodies are like little troops that serve numerous functions in the immune system, from tagging a pathogen for phagocytosis to binding to the pathogen to preventing its movement. There are several different types of antibodies, all of which serve different functions and mean different things when it comes to COVID-19 testing.

One way that antibodies can prevent an infection is through neutralization. Neutralization is when the antibodies bind to sites on a virus or toxin to prevent their interaction with their target cells. This article from Scientific American discusses that neutralization antibodies would be the most effective way to devise a treatment for COVID-19, because if the human body naturally produces neutralizing antibodies against COVID-19, all we have to do is find what site on the virus they bind to in order to devise a treatment that mimics their action.

So what does the COVID-19 antibody response look like, and how can we use that to test for the disease? This article from the NCBI describes which antibodies are produced at which points in the infection, which can be useful in determining what stage of infection the person is in. The article describes the antibody IgM being most prevalent due to the primary response in the early stages of the disease, followed by production of the antibody IgG around week 2 in the secondary response. IgG then sticks around for about two years in other SARS-CoV virus infections, so it is likely that this could be the case with COVID-19 as well. So what does this mean for testing? If a person is tested and only IgM is present, it means this person is likely in the early stages of infection and should be quarantined immediately in order to prevent spread, as they may not be symptomatic yet. If both IgM AND IgG are present, it likely means they have been infected for a while, and should be quarantined for safety. If they only show IgG, it’s likely that they were infected at one point and overcame the infection, and are no longer infectious and hopefully unable to contract COVID-19 again.

Clearly, antibodies are extremely useful bits of the immune system that mean a lot. They can prevent infection from diseases like COVID-19, and it’s imperative that the antibody response start quickly in order to lessen the disease’s effects. In the NCBI article, it’s discussed how other SARS-CoV cases that have a delayed antibody response have a more severe outcome. Antibodies are also useful in determining who is safe to go out without fear of spreading COVID-19, which is super important in this moment as we try to flatten the curve to prevent from overwhelming our healthcare services. This is why universal testing needs to be made available, so we can see who has been exposed, who is infected, and who can’t contract the virus anymore. This would help get society opened back up as quickly as possible with the fewest restrictions, getting everything back to normal.

The T cells that is. In the huge and complex world of cancer treatment, one field of research is in CAR T cell therapy. But what exactly is CAR T cell therapy? Why is it useful, and what needs to be done to perfect this emerging field of medicine?

So what is CAR T cell therapy? An article from CancerConnect explains that it involves extracting a person’s own T cells, then genetically modified in a laboratory to give them what are known as chimeric antigen receptors (CARs) that are able to seek out and destroy cancer cells. The patient’s T cells are extracted via drawing blood, given the CAR proteins that allow them to seek out and destroy cancer cells, then transfused back into the patient en masse to attack the cancer cells. It’s like taking a bunch of your body’s soldiers and giving them the Captain America treatment where they’re cryogenically frozen for a while and brought back super buff and better able to take care of strong enemies inside your body!

As of right now, two CAR T cell therapy agents have been approved for use: Kymriah and Yescarta. Kymriah is used for people under 25 years of age with B cell precursor acute lymphoblastic leukemia, and Yescarta is approved for use on adults with diffuse large B cell lymphoma. These treatments genetically engineer CAR T cells that are able to bind to CD19, an antigenic protein found on the surface of cancerous B cells that are found in these cancers. Another CAR T cell therapy currently being investigated is Lisocabtagene Maraleucel, or liso-cel. Liso-cel is also designed to target CD19 on cancerous B cells found in lymphomas, but trials haven’t been entirely successful as of yet and has not been approved. Kymriah and Yescarta, while approved for use, are only approved for patients whose cancers haven’t responded to other treatments, or has returned after use of other treatments.

Despite CAR T cell therapy showing success in treating some lymphomas, it also has some unfortunate problems, side effects and cost. One side effect is cytokine release syndrome, or CRS. In CRS, the body responds negatively to the newly reinserted CAR T cells, resulting in high fever, blood pressure changes, and flu-like symptoms if left untreated. To address this side effect, clinics that administer CAR T cell therapy use the drug Actemra to treat CRS resulting from CAR T cell therapy. Other side effects of CAR T cell therapy include neurological effects and higher risk of infection. However, as discussed by the NCBI, these side effects and others that accompany CAR T cell therapy, like fatigue, dizziness, and pain, are side effects that also accompany other cancer treatments. Another big problem with CAR T cell therapy is the cost. The aforementioned NCBI article discusses the costs of Kymriah and Yescarta, which come out to around $511,000 and $403,000, respectively.

CAR T cell therapy is a unique and important field of research when it comes to cancer treatment. I think this could be a great new treatment for different types of cancers, especially the lymphomas already able to be treated by CAR T cell therapy. Further research should go into finding ways to prevent the harmful side effects that go along with CAR T cell therapy, as well as ways to drastically cut the cost of treatment, which being as high as it currently is, could mean the death of some terminally ill patients whose cancer is unresponsive to other methods of treatment like chemotherapy. Overall, I think this is a great step toward finding an effective treatment for different cancers as long as we can find ways to mitigate the damage caused by the treatments, both physical and financial.

That’s precisely my reaction every time I see I’ve gotten a new email from good old Kevin telling me I have an extra week of Spring break, then that I can’t come back to campus for a bit, then that I have a week to pack up and move out. So much has happened in the past 3 weeks (!!) that it feels like I haven’t been back on campus for several months. It’s also my reaction watching my biochem lecture videos while trying to decipher what exactly IS going on in the electron transport chain. Nevertheless, COVID-19 has caused undue amounts of stress, irritation, and heartbreak over the past few weeks, for both me and millions of people around the world. While I have yet to be personally affected directly by COVID-19 (knock on wood), it has thrown a few wrenches in my plans for the rest of the semester and even the Summer.

The first thing that happened was the news that I would be continuing my semester via remote learning, which has had its ups and downs. On the positive, I no longer have a live 9:05am class on Mondays, Wednesdays, and Fridays, so I can sleep in to my heart’s desire (but not past 11:15, not really an issue usually). However, despite the relief of being able to get adequate sleep, I now have to traverse the odd and complex world of technology, at which I have the abilities of a man born in 1903. It’s also a LOT harder to motivate myself to do work. Since I don’t have a desk in my room/house to do work at in a quiet spot, I’m limited to working from my bed, which lacks the atmosphere of feeling like I should be doing actual work. Not only that, but it feels as though the workload should have decreased (illogical thought, I know, but I can’t help the feeling), but alas, that is not the case. I’ve just been trying to keep myself focused to knock out as much work as I can early in the day so I can have time to spend with family and friends later in the evening.

This next bit is what hit me the hardest: my Summer study abroad program in Sydney got cancelled.

I was extremely excited to travel to Sydney this Summer to study neuropharmacology, something I’m incredibly interested in that I would like to pursue further as a career. This program had excursions to discuss the unique flora and fauna in Australia and how they can be used as medications to treat neurological problems. But then came that fateful email that so rudely ripped Australia and the $50 non-refundable application fee right out of my hands. This cancellation, while a cause of despair, does have an upside, as it allows me to take Summer classes that I need at UNC. In order to graduate next May, I have to take biophysical chemistry (ew) this Fall since it’s (for some idiotic reason) only offered in the Fall. Its prerequisites are MATH 232 and PHYS 115, both of which I vehemently didn’t want to take and put off until it was stressfully late. So now I’m going to be taking these classes this Summer on their own instead of paired with the neuropharmacology course in Australia.

As with any stressful situation, I’ve had to handle quarantine and social distancing. This has involved 3 things: cooking (not as much as I’d like or what I’d like due to shortages and picky family members), video games (just bought Yoshi’s Crafted World and have been obsessed, holding off on getting the new Animal Crossing until my workload chills out and I can safely devote my entire life to Tom Nook and Isabelle), and blasting the soundtrack to A Gentleman’s Guide to Love and Murder on repeat, and lamenting at how bad I am at singing along. I’ve also started getting into anime, something I’ve wanted to try out for a while now. I started out with the show Vinland Saga, a historical drama set in the age of Vikings that seems to follow historical events. I highly recommend if it sounds like your thing, watchable on Amazon Prime Video.

So my quarantine has overall been uneventful. My family and I are taking all the precautions we can to prevent any of us getting COVID, and hopefully it continues to work out. For anyone who isn’t quite on board with all the social distancing orders going out, please remember this is about more than just you, this can seriously affect people in at-risk groups like the elderly and immunocompromised, and I’m sure you want this to go away as fast as possible. In order to get this thing under control, everyone just needs to limit their movement in public places as much as possible in order to flatten the curve and prevent the hospitals from being overwhelmed, leading to more unnecessary deaths.

Take this!

When engaging in sexual behavior, there’s a risk of contracting an STI from your partner, especially if either you or your partner have had sexual relations with other people before. Of course, the best way to prevent STIs is to not have sex, but condoms do work if you want to go for it, they just aren’t 100% effective. So what happens if you DO contract an STI? What can that look like, and how can we see that around us?

During a press release in October 2019, the CDC informed the public that cases of certain STIs were on the rise, especially syphilis. They confirmed 115,000 syphilis cases, a 14% increase in primary and secondary (the most infectious stages of syphilis) syphilis cases from the previous year, and a 40% increase in syphilis cases among newborns. Of the cases of congenital syphilis, 70% of those cases came from only 5 states. The CDC proposes that the increases seen in cases of STIs is a result of several factors. Drug use, poverty, and stigma surrounding STIs can limit access to treatment, allowing for the spread of these STIs to other people. The CDC also reports decreased condom use among vulnerable groups, which include young people and gay and bisexual men. We have also seen cuts to local and state level STI programs, which has resulted in reduced screening and patient follow-up, and even in some cases clinic closures.

Something clearly needs to be done to try to prevent the spread of STIs. The CDC is providing resources and surveillance at the local and state level health departments to try to prevent the spread of STIs and eliminate issues like congenital syphilis. They also advocate for STI screening to be made a part of standard medical care in order to catch and treat STIs as early as possible, and assist in preventing their spread. Outbreak Observatory links the rise in cases of STIs like syphilis to the growth of online dating and the defunding of Planned Parenthood as well. With online dating being such a big thing that allows people to meet all sorts of people, it opens the door for more sexual relations, which increases the risk of spreading STIs. Planned Parenthood provides resources for reproductive health, which includes STI screening and treatment. With these programs being defunded, it limits access to useful resources that people suffering from STIs need to prevent the spread of STIs.

In order to prevent the spread of syphilis, it is important to understand why it is spreading. Limited access to resources due to funding cuts makes getting screened and treated much more difficult. It’s also important to know that syphilis can be spread despite not showing symptoms. Syphilis can cause a latent infection during which it is still infectious between sexual partners. This is why it is crucial to use STI prevention methods, like abstinence, monogamy, or condoms. Assuring precautions are taken to prevent the spread of STIs like syphilis, it is likely that we’ll see a drop in cases and with proper screening, congenital syphilis can be eliminated.

As cool as invincible ninjas may sound, in this case they’re rather subpar. The invincible ninjas in this case aren’t on your side, but are instead working to take you down. The ninjas are superbugs, or infections that are resistant to almost all known antibiotics. So how does this happen? What gives these bacteria their protection against all of our lines of defense?

Antibiotic resistance is naturally a slow process. As bacteria are exposed to antibiotic agents, the ones that aren’t killed are able to reproduce, spreading whatever gene they have that makes them resistant throughout the rest of the population. Due to the increasing use of antibiotics, both to treat infections and in other areas like the meat industry, bacteria have an increased exposure to these antibiotics, allowing for resistance to occur much quicker. A huge root of the antibiotic resistance problem is that people don’t seem to know how to use antibiotics. Lots of people will go to a doctor and demand antibiotics for any sort of problem they have without even knowing the cause. If that infection is the cause of a virus, antibiotics will have no use at all, and the only thing being accomplished would be the killing of some beneficial bacteria. Another problem is that if people DO have a bacterial infection and are prescribed antibiotics, they don’t take them properly. You have to take antibiotics at the same time every day, and for the full amount of time prescribed. Lots of people end up taking them at variable times and stop taking them before they’re finished because they feel better. Well, news flash, you didn’t kill all the bacteria, you left a couple that are now going to reproduce, a little bit stronger than before.

Another reason that antibiotic resistance is becoming more widespread is the use of antibiotics in the meat industry. Antibiotics have the effect of making animals gain weight, which is good for maximizing how much meat you get from an animal. The problem arises that these animals are also in contact with bacteria that can cause infections, allowing them to be exposed to antibiotics without even having to infect a human. You may think you can circumvent this by buying labelled “antibiotic free” meats, but this is a bit of a misnomer. “Antibiotic free” in regards to meat just means that there are no antibiotics detectable in the animal at the time it was killed for meat, not that there were no antibiotics used.

More and more bacteria are developing drug resistance every year due to this misuse of antibiotics. An article from LiveScience discusses two new infectious agents that were placed on the CDC’s urgent threat list, Candida auris, an emerging fungal infection that poses a major global health threat, and the family Acinetobacter, which causes infection in various parts of the body. The article cites the CDC saying that drug resistant Acinetobacter caused around 8,500 infections and 700 deaths in 2017, and is common in healthcare settings. The fact that antibiotic resistance is spreading throughout many different species is worrying. As more and more bacteria are unable to be treated by antibiotics, there’s a higher chance of contracting a life-threatening infection.

Another group of drug resistant bacteria are the Enterobacteriaceae family, which includes E. coli, Shigella, and Salmonella, lots of which have developed resistance to carbapenems, typically a last resort antibiotic for drug resistant bacteria. These bacteria are discussed by the NCBI. These infections can take place in many parts of the body, like the urinary tract, lungs, bloodstream, and digestive tract. They are usually hospital-acquired infections, and most patients who are infected by antibiotic resistant Enterobacteriaceae spend a lot of time in healthcare settings due to unrelated issues, like surgeries. These are dangerous infections because they can cause awful symptoms, and the fact that they’re common as hospital-acquired infections means they’re most likely to infect immunocompromised individuals, making the infection even worse.

In my opinion, superbugs are some of the scariest things out there. They’re tiny unstoppable juggernauts ready to just barrel through all of our antibiotic defenses without even taking a hit. If we don’t start figuring out how to use antibiotics, and stop using them so frivolously for minor infections, viral infections, and in meat farming, superbugs could very easily wipe out millions and millions of people all over the world. We’re at a point where it’s extremely difficult to discover new antibiotics, so once we hit the end of our options, there’s nowhere else to turn to. We’re letting so many diseases that were once easily treatable with antibiotics take over and wreak havoc, and it’s only going to get worse without taking action against improper antibiotic use.

Polio is a pretty awful disease that used to affect a large proportion of people in the US. Now, thanks to one rad dude by the name of Jonas Salk, polio is a lot less of a threat than it used to be, where it could paralyze and incapacitate people for the rest of their lives.

So what happened that made polio much less of a problem today? One word — VACCINES! Those handy-dandy little needles full of lifesaving goodness has kept the poliovirus in check since my man Jonas Salk developed it back in the 1950’s. So what’s the deal with the polio vaccine? How does it work, and since it obviously hasn’t eradicated polio completely, what’s happening in the not-so-wonderful world of polio now?

There are two types of polio vaccine: the inactivated polio vaccine (IPV) and the oral polio vaccine (OPV). The IPV is made up of inactivated polio viruses that are no longer pathogenic. These are injected into the patient, usually in a series of four injections over the course of the first 6 years of life. The OPV is drastically different in that it is administered via drops to the mouth. Both vaccines work very well, but the OPV offers better mucosal immunity, preventing the virus from entering the cells of the throat and intestinal tract to replicate. However, the OPV is an attenuated vaccine rather than inactivated, which carries its own set of problems. One problem is that, very rarely (approximately 1 patient per 2.4 MILLION doses of vaccine given), the virus used in the vaccine can mutate to become pathogenic. However, just switching over to the IPV instead of the OPV doesn’t solve the problem. Due to the fact that the polio virus replicates in the victim’s throat and intestinal lining, wild type polio can still enter the body, replicate, and spread. This isn’t a problem with the OPV, which prevents the spread of the virus, so if the goal is polio eradication (and it should be) the OPV is the way to go.

So since polio ISN’T eradicated, what the heck is going on with polio? In short, it’s not looking too good. The WHO Emergency Committee convened in December 2019 to address polio outbreaks, and in a January 2020 press release, confirmed 113 cases of polio globally, about 4x higher than the 28 confirmed in the same period the previous year. They also reported outbreaks of vaccine-derived polio infections in 7 countries since the last convention. One of those outbreaks occurred in the Philippines. In response to this outbreak, agencies in the Philippines heightened surveillance and launched field investigations in order to detect the virus and understand the scope of the outbreak. The Department of Health is reinforcing their statement that vaccination schedules should be maintained to protect from the outbreaks.

So should you be worried about polio? Odds are, no, you shouldn’t. The polio vaccine works wonders to protect from this awful and debilitating disease, so as long as you’re vaccinated, you have nothing to worry about. If you intend to help out the rest of us who would LOVE to see polio disappear in our lifetime, vaccinate you and your kids. This includes advocation for the OPV, which has been discontinued in the US. If we want to get rid of polio once and for all, the OPV needs to be instated as the standard, considering it works to prevent the spread of polio altogether.

When you’re feeling lonely, just remember that you’ve got trillions of little bacteria having a grand old time living somewhere on or in your body to keep you company!

Ok, so maybe they can’t carry on a conversation or engage in a discussion about the Good Place finale, but they can do something else that’s much more useful than that. Basically every function our bodies perform is impacted in some way by our microbiome. Some of our gut bacteria help break down compounds to help our bodies digest food. Our microbiome can even impact how we experience diseases and illness.

One such way that our microbiome can impact illness is through dysbiosis. Dysbiosis is when some factor like antibiotic use causes a disruption in the normal microbiota. This scenario gives way for infections by pathogens like Clostridium difficile, which causes diarrhea and a sometimes fatal inflammation of the colon. In order to treat infections by C. difficile, an article in Nature tells of a study where fecal microbiota from healthy patients was transplanted into infected patients. Despite how utterly gross it is to imagine having the bacteria from someone else’s feces put into your body, it worked phenomenally, to the point where the trial had to end because it was no longer ethical to give the control group normal antibiotic treatment!

Yes, more! An article from Gut Microbiota for Health highlights a species of gut bacteria that helps protect against the harmful byproducts of food processing. The article tells of researchers from Washington University School of Medicine that discovered Collinsella intestinalis that is able to break down a certain Maillard reaction product (MRP), e-fructoselysine (FL), into less harmful substances. For those who aren’t familiar with MRPs (like me before I read the article), MRPs form when amino acids react with reducing sugars in the presence of heat. These compounds are present in lots of processed foods, and are associated with problems like diabetes and heart disease. These researchers found that C. intestinalis uses FL as a carbon source, breaking it down into lysine, formate, and acetate, which are naturally produced by the body.

Based on that you probably want to make sure you’re taking proper care of your little buddies you’ve got living inside you. So how can you make sure your lil microscopic dudes get what they need? The most important thing you can do is know when to use antibiotics. Antibiotics can kill off a large portion of your microbiome, which makes it a lot easier for agents like C. difficile to cause an infection.

You can also help your microbiome through your diet. This article from The Conversation gives diet tips that can help improve the health of your microbiome. Their tips include eating a diet that involves a diverse range of fruits and veggies, resistant starches like potatoes and legumes, and different fibers. The article also claims that exercise is good for your microbiome due to the fact that the lactate produced helps feed certain microbes. Another good tip is consumption of probiotic foods, like kimchi, yogurt, and pickles (not combined, of course). These foods contain microorganisms to help them ferment, which when ingested are incorporated into your microbiome.

So yeah, your microbiome is pretty important. It’s important to realize just how much all those bacteria actually do for us. It’s easy to just figure our body can do everything it needs to on its own, but honestly, that’s a little egotistical. We need those bacteria to make sure we can adequately function to digest everything we eat, to protect us from harmful pathogens, and keep us in good health overall. So when you’re lonely, don’t forget about all those bacteria working to make sure you can function properly.

It’s that time of year again: flu season is in full swing. As occurs every year, the flu is spreading through the US and wreaking havoc. So what’s going on this year specifically? How is this year’s flu comparing to those of the past?

The CDC has reported that an estimated 19-26 million people have been affected by the flu this year. As reported from ILINet, as of week 4 of this flu season (ending January 25), ILI (influenza-like illness) activity is high in most states, including here in NC. In a study of how widespread cases of the flu are, every state except Hawai’i has reported widespread flu activity. Of these reported flue cases, some 8.6-12 million have resulted in medical visits. Around 180,000-310,000 have resulted in hospitalization, and an estimated 10,000-25,000 have died from the flu this season.

So how does all this compare to previous flu seasons? In reference to the past 6 flu seasons (starting with 2014-2015), this year’s flu is about a midpoint. As of week 4 of the season, the rate of incidence is about 29.7 per 100,000 people. As a comparison, last year at week 4, the rate of incidence was around 18.6 per 100,000, while 2 years ago saw a rate of 57.7 per 100,000. So based on this, the flu could definitely be worse, but at the same time, it could, and has been, much better, considering that at this point in the 2015-2016 season, the rate was only 3.1 per 100,000. At this point in other seasons, the slope of the curve was still on the climb, so we can only expect it to get worse from this point before it gets better. If the trend continues, based on data from previous years, the seasonal high will be around 60-70 per 100,000.

So what’s the deal with the flu this year? The first thing to look at is this year’s vaccine. This year’s vaccine covers 4 strains of the flu. But how effective is it? Due to how early it is in the season, it’s impossible for the CDC to say definitively how effective this year’s vaccine is. However, since the Southern Hemisphere’s flu season runs from about April to September, we can look there for clues as to how effective it will be in the Northern Hemisphere. According to Contemporary Clinic, there was some error in the vaccine in relation to the H3N2 strain that circulated. This led to lower vaccine effectiveness against that strain due to a mutation causing a loss in a glycosylation site. Based on this, we can expect infection rates to be a little higher than normal due to this mismatch.

I’ve never been one to worry excessively about flu season. I rarely get debilitatingly sick to begin with (knock on wood), and I try to always get vaccinated pretty early, keeping myself from contracting the flu, and if by some chance I do catch it, I know it won’t be as bad as it would be if I hadn’t gotten the vaccine. For anyone else, I highly recommend getting the flu vaccine if you’re physically capable. Not only can it prevent you from getting the flu, but you can prevent it from spreading to other people (and do you want to be responsible for getting someone sick? Do you want that on your conscience?), and even if worse comes to worst and you DO get the flu, would you rather have the flu for a few days, or a few weeks? Not really a hard question in my opinion: GET A FLU SHOT!

The short answer is vaccines. PLEASE vaccinate your kids and yourself if medically possible. Vaccines aren’t whack.

Now for the long answer: what makes people think vaccines ARE whack, and how has that impacted the world as a result.

The main outcry started back in 1998, when a man named Andrew Wakefield published a paper that suggested links between the MMR vaccine, gastrointestinal disorders, and autism. However, that article has since been retracted by Wakefield amid response from the scientific community that failed to corroborate his findings. In a paper from the journal Psychological Medicine, the researchers involved found no association between the MMR vaccine and autism, and cited 11 studies, ranging from epidemiological investigations to vaccine safety reviews to passive surveillance data with the same findings. A paper cited by Wakefield himself even shows no link between the MMR vaccine and autism.

So how did Wakefield’s study go wrong? One potential problem lies within his research sample. Wakefield sampled only 12 children, all of whom had histories of developmental disorder. Additionally, all of his sample patients were consecutively admitted to the same hospital. From a statistics standpoint, this methodology is a nightmare. When conducting research of any kind, you need a large random sample in order to determine the significance of your research. 12 subjects is by no means considered large, and selecting all your patients from the same facility that were consecutively admitted is far from random selection. This sort of statistical malpractice likely contributed to his false data. The study cited by Wakefield that appears to refute his own claims used a sample size of 770 children with neurodegenerative disorders, only 16 of which had received the measles vaccine within 7-14 days of the onset of illness. This study, much more statistically sound, found no link between the vaccine and the onset of autism.

Oh, but that’s not where the problems with Wakefield’s paper end. Wakefield had partnered with a lawyer who had been trying to sue a vaccine manufacturer. This lawyer had been sending Wakefield patients with symptoms of Crohn’s disease (targeted toward families with children with neurological disorders) and his firm had been paying Wakefield £150 an hour, plus expenses, for the two years leading up to Wakefield’s publication. It’s evident that Wakefield was in this lawyer’s pocket, valuing the potential profit of the situation rather than doing what is scientifically ethical. In order to help this lawyer pursue his lawsuit, Wakefield distorted and falsified data. He reportedly claimed that the symptoms of one of the children used in the study appeared later than actually reported by the child’s parent due to the fact that the symptoms actually first appeared a month before the child received the MMR vaccine, and upon investigation, the cases described in the paper supposedly don’t match up with the child, as was the case with child 2 in Wakefield’s study.

So how has this dubious paper changed the attitudes of the general public in regards to the MMR vaccine? It doesn’t look too good. A 2003 paper found that, since Wakefield’s study was published in 1998, there has been a sharp decline in % coverage by the MMR vaccine. According to said paper, the vaccination rate was climbing toward a maximum, and vaccination rates discrepancies between affluent and deprived areas were equalizing.

However, once Wakefield published that awful paper, everything started to go downhill. The rates are now below what the WHO recommends to be within the threshold for herd immunity to be effective in preventing spread to those who can’t be vaccinated. This poses a serious problem for immunocompromised individuals who can’t be vaccinated, as the ones who were supposed to protect them have abandoned the responsibility. Wakefield’s paper and the subsequent response shows us that we have to be extremely careful in what information we take in as fact. It’s important to look deeper at the potential ulterior motives one might have for publishing something, and do extensive research to corroborate those findings.