How I passed the ARE Exam 1, Practice Management, in 2 weeks

Summary

This is a post from Christian Lemon from the ARE 5.0 Community.

He reviewed Ballast’s ARE 5.0 Review Manual and did their practice problems. He also read Professional Practice: A Guide to Turning Designs into Buildings and watched the Schiff Hardin lectures.

He advises everyone to know their financials and basic accounting.

He spent an entire 2 weeks studying, including lunch breaks, hours after work, and any free time on the weekends.

To learn more information, check out my post on how to study for the ARE Exam 1, Practice Management, or check out the original post below.

Original post

Took Practice Management last Thursday & received notice of my official pass within 24 hours!

I have recently completed my AXP experience requirements & this was my first test, deciding to start from the top. I jumped in head first & scheduled my test about 2.5 weeks ahead of time, leaving a small window for studying. I’ve seen some other posts talking about studying for months prior but I always feel like a majority of studying gets pushed off until the last couple weeks anyways. Don’t let it weigh on you, just force yourself right into it!

In preparing for the exam, I began with a thorough review of the Ballast “ARE 5 Review Manual” , making detailed notes, highlights & flash cards along the way. I also skimmed approx. half of NCARB’s recommended “Professional Practice: A Guide to Turning Designs into Buildings” which I found intuitive, worth the $16. I read through & highlighted important aspects of both B101 & C401 contracts, also listening to the Schiff-Hardin lecture on B101 — definitely need to know these. The biggest help was the Ballast “ARE 5 Practice Problems” & “ARE 5 Practice Exam”, presenting relevant & challenging problems with full explanations. I did the Practice Probs over a few days prior & the Practice Exam the day before my test. 

I did purchase the “Architect’s Handbook of Professional Practice” but barely cracked it for this test. It’s an extremely detailed textbook that every architect should have on hand for reference but the amount of information required to review is overwhelming when faced with limited study time. I felt the Ballast “ARE 5 Review Manual” did an exceptional job covering the topics presented in Practice Management.

Without violating the NCARB’s Confidentiality Agreement, I will say know your financials & prepare for some basic accounting level math. Don’t get caught off guard by these types of question! I didn’t expect this content as it was not addressed in the Ballast Practice Probs / Exam. Luckily, I completed a finance minor in school so I had a bit of business background to lean on. Additionally, the actual exam case studies are significantly more developed than the Ballast guides. Lots more information to digest & analyze compared to the relatively brief case studies presented in the Practice Problems / Exam. Be sure to leave yourself plenty of time for these.

I won’t talk about a finite time commitment because everyone studies with different paces & methodologies. I did, however, commit a FULL two weeks to prep which entailed studying on lunch breaks, hours after work & any free time over the weekend. I felt I was adequately prepared and was confident going in.

Thanks for reading, hope this helps someone! No time to celebrate, onto Project Management…

Christian

How I passed the ARE Exam 1, Practice Management, in 1 month

This is a post from Patrick Edwards from the ARE 5.0 community.

He mentions that he first made the mistake of just reading the Architect’s Handbook of Professional Practice back-to-back, but didn’t find it helpful.

What he found helpful instead were these 6 steps over the course of a month:

  1. Start by familiarizing himself using the Ballast text
  2. Watch all the Schiff Hardin lectures
  3. Take the Designer Hacks PCM test
  4. Go to AHPP and focus on weak spots
  5. Retake Designer Hacks until you score above a 93%
  6. Watch the ARE live mock exam

To learn more, check out my post on how to study for the ARE Exam 1, Practice Management, or read below for the original post.

Original post

Howdy NCARB Community,

Glad to be posting from the other side of Pass #2. I passed PjM in early Jan, and posted my thoughts. I have general test-taking tips there, I’d recommend a look if you’re starting out and need some focusing.

Again, very impressed with NCARB’s test-writing. Nothing on the test was pure rote memorization, but because I had familiarized myself with all the testable areas, I was able to think critically and reason through to the right answers, just as if I were a practicing architect. And to those of you who are studying like a student – aka just to pass – you have the wrong mentality. You need to be studying like a professional – absorbing the material with the mindset of how you would apply it to your own practice and work experience.

I estimate I spent 3 months total studying. The first 2 months were reading the AHPP in sequence, according to PluralSight’s guide. I read 900 pages with little retention before realizing I needed to be much more efficient. Since I’m starting AXP at about the same time, most of the concepts were new and rarely used in my work (govt) and I couldn’t just intake mostly new concepts completely cold.

So – I switched tactics, and it worked out really well:

Strategy: In order to read the AHPP at the depth/nuance required, go general/overview first.

After watching NCARB’s PcM Intro Video,

Step 1: I used Ballast to familiarize myself with the basics. I read the PcM section a few times so that I made sure I had a good understanding of the concepts. They do a decent job of synthesizing the concepts down to the essence. On a related note, although their tests are the hardest out there, it doesn’t mean they’re the best.

Step 2: Schiff-Hardin lectures. I can’t speak highly enough about these. I know AIA contracts cold from just putting these on in my spare time. An outstanding post from Emily that is an “all 6 done” summary recommends listening to 6,7 – but I listened to them all and it was well worth my time.

(Review any other general/overview material you may have, to include Brightwood, or AEP if they ever get their act together and release it)

Step 3: Buy Designer Hack PcM test bank for $39. Although the questions are pretty elementary and lack nuance, the advantage it offers is a guarantee: 93% or better on their timed 85-question exam = pass PcM or money back. It was a fun way to go through questions and get opened to new concepts/terms. This allowed me to baseline where I was at overall, and identify my gap areas. Side note: DO NOT use this product in isolation. It is only useful if you’re studying and then use it as a barometer.

Step 4: Using your newly-identified gaps, go to AHPP and hone in on the sections you need to know. It will flow a lot smoother and you will have something to base on.

Step 5: Keep doing Step 3 until you CONSISTENTLY hit 93% (or higher)

Step 6: Watch ARE Live/Black Spectacles Mock exam

By Step 6, it should all be Blah Blah Blah Yeah I know this…

The test itself: it’s not surprising that it has the highest fail rate. That was a sturdy 2.75 hours, only 2-3 real gimmies. Again, like PjM, I went straight to the case studies. The advantages are: you’re fresh, and the resources usually help you out with a few answers in the first 60 multiple questions.

Case studies: USE YOUR RESOURCES. I kind of forgot that, and the first 6 case study questions I had a sinking feeling because I’d never even heard of some of these things. BUT keep in mind that if it’s a really minute specificity you’d only really know by looking it up – then it probably is, so try to find it in the case study resources. The Search box is your friend for unusual keywords. So I went and dug by efficiently searching the resources, and bingo found the information that led me to critically think my way to an answer. Keep in mind that almost nothing on these tests will be pure flashcard regurgitation. Always stop and think and make sure you’re answering what they’re asking, and providing the best response to the situation. Again – learn and test like a professional, not a student.

Then I went to the first 60 questions. All of them required thought and care based on things I should have known (financial reports, contract law, etc).

Probably the most important thing I can leave you with: if you memorize ‘what’ a term is, but only know the ‘words’ of what it is, but you don’t actually understand how it applies to the practice, what situations it would show up in, and what factors affect it, you probably won’t pass this exam.

Example (I made this up off the top of my head, and it’s not from the exam so don’t get your hopes up)

– Fast-Track delivery method uses multiple prime contracts and is used for compressed deadlines

vs

– Fast-Track is used by a client who is under a lot of pressure because they have big loans and want to pay off interest as soon as possible. They’re willing to compromise and have a more generic building so that the foundation and structure can get going quickly. The architect will take on risk and so they’ll need to worry about what supplemental conditions to the contract might be needed in case things go south, what “points of no return” need to be built in, etc…

Ask your co-workers and principals what the terms you’re studying mean to them. Ask your company accountant about cash vs accrual accounting. Your understanding of the application will help you answer these test questions.

Good luck!!!

How I passed the ARE Exam 1: Practice Management in 5 weeks while working full time. Story from ARE 5.0 Community.

Summary

This is a report from Scott Barber on the ARE 5.0 Community.

To study, he scheduled exams 1, 2, 3 in 5 weeks, after already taking 4, 5, and 6. He studied for an hour each day.

He used the Architect’s Handbook of Professional Practice and the Schiff Hardin lectures. He advises people to focus on business types, contracts, and finances and risk.

Check out my guide on how to study for the ARE Exam 1 if you want more information, or read on for the original post.

Original post

Just took PcM this morning and got the “provisional pass” at the end – definitely a relief!
I felt nervous about this one more than some of the previous exams, I had a tighter study schedule and even last night as I was reviewing I wish I had spent more time on some topics. I had a good grasp of the content overall, but some of the application of the knowledge wasn’t where I wanted it to be. Regardless, here’s my overview on study materials and two cents about what you need to know:

Study Schedule

For a number of reasons, I decided to schedule PcM, PjM, and CE all before Memorial Day. I scheduled them all on April 4 – so that left about 5 weeks before my first exam today. I had passed PDD, PPD, and PA and given the advice from others regarding overlap of these three exams and the smaller amount of content covered (compared to PPD/PDD), I decided to go for it.  

I kept the same approach as I did for similar exams: spent half of my lunch break studying, and stayed at the office after work for roughly an hour each day. The time spent studying for these exams can definitely cause a strain on family, so I tried to make the most of my time and be present when I got home. 

I think I could have used another week to review main topics, but if you’re just studying for PcM I think 5 weeks would be plenty. The first ~4 weeks were studying for all three exams (reading most of AHPP) so that divided up my time.

What to Study

  • AHPP – This book is essential for these three exams. I used Narmour Wright/Wiley’s list of suggested chapters and this helped me focus what I was reading. This is a big book but very helpful.
  • Schiff Hardin Lectures – I listened to these daily on my commute, focusing on the lectures for the A201 and B101, and then listened to a few others after I had gone through these a few times. These are a fantastic resource to understand contracts and other legal/professional concepts. The A201 isn’t heavily covered on PcM but it’s useful for my next two, so that’s why I spent time listening to it. 
  • Ballast – I started out studying this, but I don’t think it’s really necessary. Could be helpful but I focused my time on AHPP.
  • I also read the Owner’s Guide to Project Delivery Methods. This content is covered in the AHPP but I used it as a refresher and it’s helpful to read about concepts from different sources to get a well-rounded understanding. 
  • I also studied a few resources found throughout this forum, just based on what I felt weaker in.

What to Know

  • Business Types: Chart 5.1 on page 201-202 in the AHPP is a good summary, but make sure you know when each one is preferred (criteria could include ownership, control, personal asset risk, tax treatment, etc)
  • Contracts: This exam is heavier on the B101 but make sure you have a general understanding of contracts for different applications (project delivery types, etc).
  • Finances and risk (ARE Handbook, Section 2 stuff)

These areas are what stood out to me when taking the exam, but be sure to look at the ARE Handbook for the overall content. I think it aligned well with what I saw on the actual exam – the content listed above is what I felt weaker in and so that’s probably why it stood out.

Additional Thought: This exam has a lot of “pick 3” or “pick 4” out of a list of 6 choices. These can be tricky, but I typically wrote down numbers 1-6 on the scratch paper and crossed out or put a check next two options that I was more confident that would or wouldn’t be correct. Even so – there was generally one or two that I thought could go either way. Just be prepared for these types of questions.

Hope that is helpful! There are a lot of good posts on this forum from others who identified what they focused on, I definitely used their advice and would encourage others to do the same. Feel free to ask any questions and I’ll do my best to help! 

Going to spend the weekend preparing for PjM which I’m taking Monday morning. Hopefully I’ll have more good news then and can share advice after that exam too.

Good luck!

How to study for the ARE Exam 1: Practice Management

Intro to the ARE Exam 1

If I had to describe the ARE Exam 1, I’d describe it as an easy exam pretending to be a difficult one.

It’s easy because the topics on the ARE are not difficult and the questions aren’t particularly challenging. 

The ARE looks difficult, though, because it’s poorly organized. The handbook throws a bunch of huge, complicated books at you and tells you to memorize them.

You don’t have to do that! 

If you try to memorize everything in every ARE book your brain will explode. You literally cannot. Trying to is a big reason why a lot of people get overwhelmed by the ARE.

The trick with the ARE is to only study what you have to study, and only memorize the parts that you have to memorize. No more, no less. Everything else is your job to understand and not memorize.

What materials you’ll need for the ARE Exam 1

You should only need my Guide to the Overwhelmed for the ARE Exam 1. I don’t think you’ll need anything else.

Once you’ve mastered your flashcards, notes, and error log from this guide, test yourself by checking out the questions in the ARE handbook. There aren’t many of them, but they should be a useful indicator of what the test questions are actually like.

If you’re looking for alternative resources, you should check out my guide to all the recommended references from the Handbook.

How long it’ll take to study for the ARE Exam 1

The ARE Exam 1 is not a fundamentally difficult exam. It’s actually pretty short.

It should take around 10 hours total to study for the ARE Exam 1.

If you’re looking to create a study plan for the ARE Exam 1, you should use 21st Night’s “My Study Plan” option to create a study plan that works around your schedule.

A complete list of topics on the ARE Exam 1

For a complete list of topics on the ARE Exam 1, you should sign up for my free email course on how to study for the ARE. You’ll not only receive a list of exactly what topics to focus on for each ARE exam, you also get advice on how to study for each exam and 10% off my Guide to the Overwhelmed.

How to learn all these topics on the ARE

Most students make the mistake of trying to learn all the topics the same way. I would not recommend that. Memorization is a separate process from understanding, and you need to treat it that way.

Memorization

The best way to memorize is to create and review flashcards. These flashcards should test one unit of information at a time (not a bunch), and include context or a mnemonic as an explanation. So, for example:

Question: “What does LLC stand for, and what does it mean?”
Answer: “LLCs are limited liability companies, which means their liability in a lawsuit is limited. The owner’s assets are protected. ”

Explanation: “LLCs offer more protection than sole proprietorships, which is why people use them.”

Understanding

The best way to understand is to create and review notes. These should not be copy-pasted from what I’ve written in my guide. Read what I wrote in my guide, then come up with your own note to summarize. Check back with my guide to make sure you’re happy with your summary.

To review notes, you can create flashcards from them, then review the flashcards. Or, you can just close your eyes, and make sure you can remember the content of the notes.

Using the practice problems

The best way to use the practice problems is to create an error log. 

What’s an error log?

Well, an error log is simply keeping track of all the questions that you have trouble with. Whenever you have trouble with a practice question, you put it in a card, along with an answer and a step-by-step explanation of the process to solve it.

When you go back to review the question, you make sure you can recall the step-by-step explanation, not just the answer.

This will help you master the processes you need for the ARE.

Studying app recommendation

Creating notes, flashcards, and an error log is easiest if you use 21st Night. 21st Night is a studying app that allows you to create flexible, powerful notes and flashcards and review them through your phone or laptop. 

It also allows you to link your flashcards and notes together, so you can easily create flashcards from your notes with a single click. Or, if you’re studying with a friend, 21st Night allows you to work together on a single collection of notes and flashcards.

Finally, 21st Night gives you analytics on what questions and topics you’re having trouble with, so you can make sure you’re studying the right way.

We shouldn’t be using R0 to measure the rate of COVID-19 transmission

There’s a pretty extraordinary clip that I saw on Twitter the other day of Angela Merkel discussing the R0 of COVID-19 in Germany. In it, she explains that R0 is how many people, on average, that an infected person transmits the virus to before they recover. If R0 is greater than 1, the number of infected people grows over time. Eventually, as Merkel explains, the hospital system is overwhelmed with infected. The date that this happens depends on R0.

This is extraordinary for two reasons. The first is the reason that Vox points out in the link above. Living in a country with Donald Trump as a leader, it’s weird to see a leader calmly and rationally explain somewhat complicated scientific concepts. The second is the way in which Angela Merkel discusses R0. She discusses it like yet another scientific parameter, the way she likely discussed temperature or pH in her work as a chemist.

Angela Merkel is not alone in this. This is the way that R0 tends to be discussed in the media and in scientific literature, as a parameter that can be measured and influenced. This is helpful for the purposes of, say, measuring the effectiveness of stay-in-place policies.

However, the supposed simple nature of R0 belies the fact that generating it is a complex process with a lot of assumptions. Those who use R0 should be aware of the process and of the assumptions that go into it. Any model you create using R0 has those assumptions built into it, and you ignore them at your own peril.

In this essay, I’ll explore the assumptions that go into generating R0 a bit, and then talk about the implications of them.

Let’s start with the definition of R0, as it’s actually a little more complex that Merkel lets on. R0 is the average number of people a given infected person will transmit the virus to, assuming an entirely susceptible population. R-effective is the same, but assuming a mixed population (some immune, some susceptible).

Right now, R0 is about the same as R-eff, as most people aren’t immune. As the virus progresses, this will change. Nobody knows exactly how immunity works for COVID-19 right now, which means R-eff is impossible to calculate. So, websites like Rt.live, which purport to calculate R-eff for each state daily, are total nonsense (very pretty, though).

So let’s just discuss R0. R0 has two obvious complications just from the definition.

1. R0 is heavily dependent on circumstance. It’s not an inherent property of the virus. Calculating a state or country-wide R0 means including circumstances with very high R0 (like a trade show or buffet) and circumstances with a low R0 (like isolated farms).

2. R0 assumes that the average is meaningful. This isn’t necessarily the case. If 10 people get COVID-19, and 9 of them are responsible and self-isolate, while the 10th opens a kissing booth at the county fair, you will get a high R0.

This high R0 will be way higher than the number of people who the 9 infected, and way lower than the number of people who the 10th infected. It will describe none of them well. You might think from this that you need to lockdown everyone in order to drive down your R0, while really you just needed to make sure the 10th guy didn’t open up a kissing booth.

Those are the two obvious complications from the definition. The less obvious complications come from how R0 is actually calculated.

R0 is usually calculated by taking a group of infected and non-infected people and observing them really carefully. You carefully track exactly when each non-infected person starts showing symptoms, testing them to make sure. You use your prior knowledge of the virus to guess when exactly that non-infected person became infected. You also use your prior knowledge of the virus to guess who infected them, based on how infectious people are each day after they’re infected.

From there, your model will show you how many non-infected people got infected by each new infectious person. You average them together, and that’s R0.

There are some complicated statistics that go into this (Bayesian inference! Markov chains! Matrices!), but that’s the gist. So let’s list out the inputs into the model:

1. Number of symptomatic people

2. Time from being infected to onset of symptoms

3. How infectious each person is on any given day after they’re infected

The first thing you might notice is that our model automatically ignores asymptomatic transmission. This is a big omission, as asymptomatic transmission is likely a big part of how COVID-19 spreads. Recently, some researchers decided to test every occupant of a Boston area homeless shelter for COVID-19. They found 146 out of 397 (36%) tested positive, but none had symptoms.

It’s impossible to say whether those people were presymptomatic or asymptomatic, but that’s still a big number. That fits in well with other viruses, which also tend to spread asymptomatically.

A lack of testing capacity generally forces us to calculate R0 only from symptoms, which leads into the problems with the second assumption. The relationship between when you’re infected and when you show symptoms is not a simple function of the virus. It depends a lot on your immune system and the viral dose, which is why different people react to the virus differently.

We don’t even know what the relationship of viral dose is to severity of symptoms of COVID-19, as we haven’t been able to do laboratory studies. For other viruses, like norovirus, researchers literally give small amounts of the virus to volunteers and see how little it takes to infect them. It’s hard to imagine doing that for COVID-19, given its deadliness.

Similar issues exist with calculating how infectious carriers are. Infectiousness also depends on the behavior of the subjects, like with my previous kissing booth example. So this input isn’t just a biological issue, but a sociological one.

Given the difficulties of calculating these inputs, we’d expect a variety of outputs. And that’s exactly what we’ve gotten. For COVID-19, for instance, we got an early estimate of 2.2 to 2.7 in Wuhan, then a revised estimate of 5.7 for the exact same region.

This tracks with other viruses. Take norovirus, for instance. Unlike COVID-19, norovirus is a really well-studied virus. It’s been studied since the 50’s, it quickly causes pretty unmistakeable symptoms (namely explosive vomiting and diarrhea), and we’re able to do laboratory studies on it. With all that being said, here are some estimates of the R0 of norovirus from a review paper (note: the names at the bottom are the authors of the papers reviewed).

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To some extent, this is what you’d expect, given that these are measuring R0 in different situations, from a scout jamboree to a hospital setting. However, imagine Angela Merkel looking at this graph, and then trying to make public policy decisions about managing the spread of norovirus. Would you assume that uncontrolled norovirus in Germany has an R0 of 14, like in Heijne’s paper, or a little less than 1, like in Sukhrie’s paper?

The difficulty in calculating R0 is compounded by the fact that it’s obvious every virus has to dip below an R0 of 1 in some situations. We’re not good at studying those situations, because they end up being papers about the dog that didn’t bark: “In this paper, we discuss a single guy infected with COVID-19, who went home and didn’t infect anyone and then recovered.”

However, we know that the R0 dipping below 1 has to happen, or else most of us (the symptomatic ones) would get an episode of explosive vomiting and diarrhea every year or so, or however long the immunity to norovirus lasts. That should happen especially whenever new strains of norovirus emerge to which our body is not immune. Why aren’t we constantly getting slammed?

I don’t think there’s an easy answer. Not only has there not been enough research done into the inputs of R0 (for COVID-19 or really for any virus), but there’s also so much we don’t know biologically about how this virus works.

So what are our other options? In a robust testing regime, it’d be about simply testing everyone possible, and then testing how we can change the rates of newly infected. Ideally, this would be combined with careful contact tracing, so we’d know who to test. Unfortunately, this is not the world we live in.

Our most realistic option, then, is probably to extrapolate from limited, well-done studies into more widespread policy changes. We measure the impact of the policies as best as we can, and we need to be open to changing them as the facts change.

Two COVID-19 studies done recently that I was particularly impressed by were an observation of a South Korean call center, and a Chinese restaurant.

In the South Korean call center, the virus spread widely among people sitting close to one another, and not widely among people sitting far from each other. This was true even though they shared the same elevators.

Floor plan of the 11th floor of building X, site of a coronavirus disease outbreak, Seoul, South Korea, 2020. Blue coloring indicates the seating places of persons with confirmed cases.
https://wwwnc.cdc.gov/eid/article/26/8/20-1274-f2. Blue is infected.

In the Chinese restaurant, again, infections were limited to close physical proximity.

From https://wwwnc.cdc.gov/eid/article/26/7/20-0764-f1. Note: A1 is the first one infected. The dates are when their infections were confirmed.

Instead of worrying about R0, it’d be more prudent to not pack people into close, confined spaces. We could also mandate the wearing of masks, so as to hinder the spread of virus through coughing or loud talking (like what would happen in a call center or crowded restaurant).

It’d be possible to implement these measures without having to resort to the extreme nature of the current lockdown. From there, we could see the effects of these policies on the hospitalization rate, and go from there.

Asymptomatic shedding of viruses is the norm

*edited to be more clear about relationship between shedding and contagiousness

Recently, there’s been scientific and media attention on how people can spread COVID-19 without showing symptoms. This is obviously a public health threat. However, this is also something that really should not be news.

Most infectious viruses can be spread without people showing symptoms. Symptoms are mostly what happens when the body’s immune system starts ramping up a fight against a virus. Symptoms do not indicate the virus itself.

Let’s take 4 examples for this, one from each of the major virus classifications: herpesvirus from enveloped DNA, adenovirus from nonenveloped DNA, influenza virus from enveloped RNA, and rhinovirus from nonenveloped RNA.

In herpes: “transmission of genital herpes in most study subjects (37 [56%]) appeared to have resulted from sexual contact in the absence of lesions…” (JID, 2008).

In adenovirus: “52% of asymptomatic children recruited from an Alaskan community tested positive for shedding respiratory virus in a one-time sampling scheme, with the majority having HRV and adenovirus.” (J Med Virol, 2010).

In influenza: “25 (11%) of asymptomatic cases displayed virus shedding” (Clin. Infect Dis., 2017).

In rhinovirus: “Rhinovirus can be detected in 15% of asymptomatic children” (Clin Micro and Infect, 2013).

It should be presumed that most viruses follow the same pattern. If someone is infected or shedding the virus, they can likely transmit the virus. It might not be easy, if it’s not a very infectious virus, but it can probably still happen.

More broadly speaking, this is an annoying pattern I’ve noticed with discussion and research into COVID-19 in general. It is a virus like any other. It broadly follows the same patterns we’ve seen with other viruses, especially other enveloped RNA viruses like the flu. The details of it are different, so it’s had a broad impact, but there’s no need to throw out prior research.

How to make bird flu (H5N1) cross over to humans

After writing my last post on why humans keep getting deadly viruses from bats, I got some interesting questions on why some viruses cross over from animals but most do not. What needs to happen for a virus to start infecting humans? Or, perhaps more pertinently, what new viruses do we need to worry about next?

The short answer is that a lot needs to happen for a virus to successfully infect humans. It needs to survive in human bodies, not get taken out by human immune systems, successfully infect human cells, then successfully pass from one human to the next.

This is a difficult enough task that the only viruses that we probably need to worry about are the ones that have successfully crossed over to humans in the past. Bird flu caused pandemics in 1918 (probably), 1957, and 1968. It’s likely that it’ll do so again. On the other hand, it is unlikely that a virus with no history of crossing over to humans can mutate enough to successfully infect humans.

That’s the short answer. The long answer is a lot more complicated.

Before I start, it’s important to note that virology is still in its infancy. No scientist could design a virus from scratch to successfully infect humans, or even predict in advance whether a virus can infect humans. Virologists are still at the point where they’re only collecting data on which viruses have successfully infected humans and how they’ve done so.

As such, our answers as to how viruses are spread to humans are still frustratingly specific. We’re going to have to look at a case study, H5N1 (the most recent bird flu), and ask the question: how could H5N1 spread to humans?

H5N1 was a flu that seemed prime to spread to humans. It successfully crossed over a few times in poultry markets and environmentally, although not as often as one would expect considering how widespread it was among ducks, geese, chicken, and other farm birds. It was also related to the bird flus that did successfully spread to humans in 1957 and 1968. Finally, the relatively few times it did cross over, it killed people very effectively, reaching a mortality rate of about 60%.

So what were those extra steps that H5N1 needed to take? How did it need to change to successfully spread from person to person?

Well, let’s start by looking at it in the wild, or what’s called its wildtype. Then we can look at how it had to change.

H5N1 is 8 strands of RNA (which humans use for messaging DNA info), wrapped in a lipid coat, studded with the proteins NA, HA, and M2 (note: the entire coat is studded with these proteins, they just drew only 3 of them).

Diagram and description of wildtype H5N1 from here: https://www.annualreviews.org/doi/10.1146/annurev.med.57.121304.131333

This is an incredibly simple and tiny setup. It’s way smaller and simpler than a cell. There’s a good reason for that: a cell has to have all the machinery to run. A virus just needs to hijack the cell’s machinery: it’s a strike team, as opposed to a factory.

H5N1’s ultimate goal is to get its instructions running in the cell. In order to do so, it first needs to actually survive in a bird’s body.

Then, the virus needs to evade the body’s innate immunity, like the mucus that lines the respiratory tract, the macrophages that eat up anything unfamiliar, and the tough skin cells that don’t let anything through.

Next, it needs to evade the body’s adaptive immunity, made up of antibodies looking to spot viruses that it’s encountered before. The most recognizable parts of the H5N1 virus are the relatively large HA and NA proteins, followed by the relatively small M2 ion channel. Influenza A viruses all have these features, so, generally speaking, antibodies are on the lookout for them. They might not have seen H5N1 before, but they’ve seen its cousins.

To respond to this, influenza A viruses like H5N1 constantly change around the shape and structure of their HA and NA proteins to make it harder for the antibodies that are trying to spot them. This is, of course, a random process, driven by viruses’ constant replication and poor error-checking of their RNA build-out instructions. Any mutations that are beneficial will make that virus type way more common (more of them will survive). This is a balancing act, though: HA and NA need to change enough to be unrecognizable, but they do still need to be functional.

If H5N1 does evade the immune system, it then needs to find an appropriate cell. When it does, the virus uses HA to attach itself to sialic acid residues on the outside of the cell. Like all protein-protein interaction, this is really specific and works on a lock and key method.

In fact, it’s so specific that the best theory on why H5N1 could not infect humans at first was that HA needed to be modified to attach to a different side of the same acid of the same protein that humans and birds both share. It’s like a lock that not only just accepts one key, but only accepts a key that’s bent in exactly the right way, and viruses have to accidentally bend their key in the right way to fit.

This was the shift. In birds, sialic acid attaches to glucose with the 2-3 linkage, and HA could attach to that. In humans, it generally attaches with the 2-6 linkage, and HA had to undergo mutation (probably in pigs, which have both 2-3 and 2-6 linkages) to be able to attach to that. There are some 2-3 linkages in humans, but not enough to be a viable attachment strategy for H5N1. From https://www.annualreviews.org/doi/10.1146/annurev.med.57.121304.131333

On a side note, this is where NA comes in handy, too. HA not only only attaches to very specific protein residues, but it also doesn’t care where those protein residues are. This is a problem for the virus if those protein residues are in mucus, which has a lot of sialic acid but no viable cells to infect. NA serves to bushwack the virus’s way through decoys until it can get to the real prize.

After the virus attaches to a cell, it works its way to an endosomal compartment, which is a gateway into the cell. Normally, it’s difficult for viruses to pass through this gateway, for obvious reasons.

However, H5N1 has a trick. It found a way to use proteases (the body’s tools to break down and manipulate proteins) to transform the HA protein into two proteins that can fuse with the endosomal gateway, allowing the virus to enter. Proteases, like proteins, are really specific, and this trick only works on proteases that are found in the respiratory and gastrointestinal tract (which is why avian flu causes pneumonia and diarrhea).

Then, it uses M2 as a channel to inject its RNA into the cell. From there, the virus uses its own polymerases to make more copies of its RNA, so it can start taking over the cell.

Finally, it needs to spread from human to human, like through a cough or a sneeze. This is a complex process that’s not super well understood, but likely requires high levels of virus in the upper respiratory tract. This results in inflammation, which then results in coughing or sneezing.

The main barriers to wildtype H5N1’s success came with attaching to cells (as previously mentioned), making more copies of its RNA in the different temperature and pH of the human body, and making humans cough or sneeze. So, in order for H5N1 to successfully transmit from human to human, it’d probably need to figure that out.

Fortunately for us, we have experimental confirmation on exactly how that would happen, with the really interesting and kind of frightening paper “Airborne Transmission of Influenza A/H5N1 Virus Between Ferrets“. In this paper, they turned H5N1 into a virus that could probably be transmitted from human-to-human using ferrets as a vector.

Why ferrets? Well, because ferrets can be infected by both human and avian flus. When ferrets get human flus, they react to them much like humans would, and can spread them to each other. They’re an ideal mixing bowl, like pigs are, but a lot easier to keep.

In order for H5N1 to be spread between ferrets, there were a few changes that needed to be made. Two of them they knew about, and did so in the experiment by directly editing the viral genome to change the protein HA and the viral polymerase PB2:

  1. Making sure that HA in H5N1 bonded to 2,6 sialic acid instead of 2,3
  2. Changing PB2 to replicate more efficiently at the lower temperature of the mammalian respiratory tract (33 degrees C) rather than the higher temperature of the avian respiratory tract

However, once they made those changes (which, for the record, can be done with off the shelf parts), they found that the virus still did not transmit between ferrets. So, they decided to introduce artificial selection into the process, and let guided evolution find the missing piece.

They started inoculating the ferrets intranasally with the mutated H5N1 (literally squirting it in the ferrets’ noses). They would inoculate one ferret, let the virus work for a bit, then euthanize the ferret, extract the mutated virus from the now deceased ferret’s lungs and nose, blended all the extract together, and then inoculated a new ferret.

In this process, they were essentially forcefully recombining the viruses again and again. Each time they blended the extract together, the viruses had a chance to swap parts, so whatever mutations one virus had could be shared with the other viruses. Any mutation that caused a virus to be particularly successful (i.e. be more prevalent in the lungs or nose) would be shared with its counterparts.

They did this 6 times, leaving 12 dead ferrets in their wake (their control group was doing the same thing with wildtype virus). Then, they changed tactics, and, after inoculating, didn’t extract the virus directly from the ferrets’ nose and lungs. Instead, they squirted the ferrets’ noses with water and forced them to sneeze, then collected their sneeze. Then, same process: blend the sneeze, inoculate the next ferret with the sneeze, euthanize the old one.

While before they were selecting for any mutation that would cause a virus to be more prevalent in the lungs or nose, in this case they were selecting for mutations that would cause a virus to be more prevalent in sneezes. Any mutation that allowed a virus to be common in sneezes would be shared with its counterparts.

They did that an additional 3 times, leaving 20 dead ferrets in their wake. By this point, they had their virus, and sequenced it. As one might expect, there were a lot of different mutations in the flu virus, which varied from virus to virus, even within the last ferret. But, there was one mutation that almost all the viruses shared: a mutation that removed a piece of HA. As it turned out in a subsequent experiment, this mutation allows HA to fuse with cell membranes at lower pHs (i.e. the pH of human respiratory tracts, rather than avian).

In the process of doing so, they produced a hilariously uninformative diagram. Pity the poor grad student who had to make an image of a ferret in Photoshop.

All that was left to do now was test their new, artificially selected virus. And it worked! It successfully spread from ferret to ferret through the air when they were kept in cages next to each other.

The mutated virus had a weird effect when it came to virulence, though: the mutated virus was as deadly as the wildtype intratracheally, less deadly intranasally, and supposedly not deadly at all when transmitted through the air. I say supposedly because they stopped keeping track of the ferrets’ health 3 days after they got infected, which seems way too short to me.

The scientists were also eager to point out that the mutated virus was sensitive to the flu drug oseltamivir, and that it wouldn’t affect people who had antibodies against other H5 flus. My only guess as to why they pointed that out, and why they stopped tracking ferret health after day 3, was that they wanted to forestall criticism about having created a pandemic in a laboratory. They also spent a large amount of their paper talking about their security protocols, which seemed to be for the same purpose.

Regardless, this experiment showed, in a limited way, how viruses can go from animals to humans. It’s not easy: the wildtype virus never became transmissible from ferret to ferret, even after going through the artificial selection process. And it is limited: H5N1 was already mediocre at going from birds to humans, it just wasn’t particularly good at it or at transmitting from human to human.

There’s still a lot of work to be done on viruses. For one thing, scientists still have no ability to predict which mutations a virus needs to undergo in order to transmit to humans. We can observe what happens naturally and copy it, but we can’t predict it.

For another, there’s still not great information on what makes a particular virus so deadly, and how that connects with how well it spreads. There’s some obvious connection, namely that a virus that kills ferrets or humans in 3 days (like H5N1) will result in pretty quick social isolation. But whether making H5N1 airborne actually made it less deadly is a much more interesting and complicated question.

Additional research on predicting how deadly viruses will be humans is complicated, for obvious reasons. Even this paper was really controversial. I think the best avenue of exploration would be predicting how deadly a created virus would be in birds, fish, or insects. There’s still so much to discover on how viruses work on literally any level, so there’s no reason to limit the discovery to humans.

Why do human beings keep getting diseases from bats?

Humans get a surprising number of very infectious diseases from bats. We get SARS (including the recent COVID-19/SARS-CoV2), Ebola, rabies, and possibly mumps. These are all incredibly infectious, deadly diseases.

This seems weird because human beings aren’t in particularly close contact with bats. They’re nocturnal, don’t have large city populations (for the most part), and humans don’t eat them that often. It should be harder for diseases to pass from them to us. They’re also not very similar to us genetically, so their diseases shouldn’t be able to leap to us so easily.

Part of the answer is that bats are very social creatures. When one bat gets a virus, they pretty quickly pass it onto the other bats in their colony. However, that’s also true of goats and cows, who don’t seem to pass on infectious diseases to us as often.

The more important part of the answer is that bats are “reservoirs” of some particularly virulent viruses. Bats live with long-term infections of SARS or Ebola and are seemingly ok with it. While humans and other mammals either have to clear these viruses from their body or die, bats do not. They will just keep on keeping on, sometimes shedding the virus, sometimes not. It’s more likely that the bat will shed the virus during stressful times (i.e. when it’s in a cage and about to get eaten).

That’s what seems to have happened with COVID-19. A bat shed the SARS-CoV2 virus at some point, probably in a wildlife market. The virus at this point was not in state where it could infect humans. However, viruses can both mutate (change shape) and recombine (swap parts) rapidly. Coronaviruses are especially good at recombining.

The SARS-COV2 virus was shed from a bat (possibly from its saliva or droppings), seems to have recombined with a coronavirus in a pangolin (who was probably in a cage right next to it), and then was in a form where it could be transmitted to a human. Once it by chance was in the right form, that virus could successfully spread itself to humans everywhere.

That’s the short version. There’s an interesting question, though: why don’t these viruses kill bats? Ebola, SARS, and rabies all kill their hosts pretty quickly. How can bats live with these viruses year after year?

Well, that’s complicated. This is going to require a dive into the immune system. Before I start, two brief caveats:

  1. When I discuss bats, I’m discussing 1300+ species across almost every continent. Not all bats are the same, and we haven’t really studied most bats. Generalizations are necessary, but just be aware that they’re happening and might not apply to specific bat species. I’m also generalizing across all bat cells, and what’s true for a cell in the abdomen is not going to necessarily be true for a cell in the testes or brain.
  2. When I discuss immunology, I’m discussing an incredibly complicated subject that we still don’t know a ton about. The immune system is the defense force for the entire body, which is a hard enough job in the first place. However, it’s also been in an arms race with bacteria, viruses, and parasites for billions of years, developing defenses, countermeasures, and counter-countermeasures. Discussing the immune system is like discussing season 4,500,000,000 of a TV show that started complicated to begin with.

With those caveats out of the way, let’s start exploring why the bat immune system is so different from humans. Both bats and humans are mammals, which means we have roughly similar immune systems and roughly similar responses to viruses.

When a virus comes into the body, its goal is to invade cells, take over their production capabilities, and use the production capabilities to produce more viruses. Then those viruses produced do the same. It also wants to spread itself outside the body (i.e. by a cough). Viruses want to do this ideally without being noticed by the immune system, and certainly without being disrupted by the immune system.

The body’s goal is, basically, to stop all that. The body wants to stop viruses from coming in. If a virus does come in, the body wants to kill it before it invades any cells. If it does invade a cell, the body wants to know about it immediately. Then it wants to kill that cell and anything inside it. The cell’s role is to let the body know if it’s been invaded, let other cells around it know that it’s been invaded, and to contain the invasion as best as possible.

That is a really, really high level overview. There’s a lot of complexity hidden in there. But, it’s enough that we can dive into the specific difference between bats and humans: the cell’s role in the immune system.

In humans, the individual cell’s role in the immune system is a lot like those “if you see something, say something” posters. Human cells recognize viruses as a sort of lock and key by their pattern recognition receptors. Once they recognize a virus, they start producing interferon.

Interferons interfere with viruses, hence their name. They work as both suppressant and alarm, making it harder to make proteins and RNA (building materials of viruses and human cells), promoting gene p53 (which starts the cells’ self-destruct sequence), alerting the body’s T and NK cells (which kill infected cells), and promoting high temperatures (which make it harder for viruses to replicate).

There are 3 types of interferon: alpha, beta, and gamma. They have a lot of overlap in functionality, but the most important difference is that it seems like alpha acts as the gas in the immune system and beta as the brakes.

That distinction is really important, because that ends up being the key difference between the bat immune system and humans’, as well as the key to why bats can carry these deadly infections.

Bat cells do not work on a “see something, say something” model. Instead, bat cells just continually “say something”. Instead of recognizing viruses and then producing interferon, they continually produce interferon alpha and seem to produce almost no interferon beta: all gas, no brakes.

In other words, bat cells just continually assume they’re under attack and never stop fighting viruses, regardless of whether they’ve detected any. This is surprising. Interferon is a really powerful molecule, and continually producing it should have the same effect on a cell as continually putting a factory on red alert. It should make the cell run much worse, and cause a lot of collateral damage.

After all, when this sort of immune system overreaction happens in humans, humans get serious disorders, like Multiple Sclerosis and Lupus. Bats do not tend to get these. In fact, many bat species live around 20 years on average, which is not only way longer than it should have with its overactive immune system, but is exceptionally long for such a small animal. To give a comparison, rats live a year or two, as do rabbits.

So, how do bats live so long with a hyperactive immune system? Well, the answer seems to be that although their interferon is continually produced, their immune system is never allowed to go to the same extremes as human immune systems.

There’s a couple ways in which they don’t go to extremes. For one, bats seem to lack Natural Killer (NK) cell receptors, which may mean they lack NK cells. NK cells are as heavy duty as their name implies; while their cousins, T cells, kill any cell that displays signs of being infected, NK cells kill any cells that don’t display signs of being not infected. Viruses will frequently prevent cells from indicating that they’re infected, so NK cells just kill any cell that looks like it’s hiding something. Needless to say, this results in a lot of collateral damage.

For another, bat cells also lack a lot of the pathways to go into apoptosis (self-destruct mode). In a human cell, the production of interferon starts readying the cell to self-destruct and stop the virus from using the cell’s machinery. Bat cells lack an associated protein, and seem to have some significant changes at the related p53 gene.

So, bat cells are always ready to fight viruses, but never ready to go the extremes of “kill or be killed” that human and other mammal cells are. This actually works out well for bats. A lot of the damage done in a viral infection is by the overreaction of the immune system in “cytokine storms”, like in the 1918 flu epidemic. Bats avoid all of that.

So, bats just live with the infections instead. They fight them enough that the viruses can’t take over their body, but they don’t clear the infections. This balance can get upset, though, when the bat gets stressed. For instance, when bats get white nose fungus, a really deadly and stressful disease, they also end up with 60-fold higher levels of coronavirus in their intestines.

An added bonus to this is that the lower levels of inflammation in bats might cause their relatively long lifespan by making their biological aging slower. This is an interesting avenue of research for people as well.

Last question, and here’s the most interesting one. Why are bats like this? What made their immune system so weird?

Well, it actually has to do with their flying. Bats are the only mammals that fly. Flying is a really energetic process and can raise bats’ internal body temperature up to 41 degrees Celsius (106 degrees Fahrenheit) for an extended period of time.

That’s really hot. In humans, that would cause serious brain damage. In bats, it’s enough to damage DNA through the production of reactive oxygen species, as well as to release the DNA into the cytoplasm or bloodstream.

This meant obviously that bats had to be really good at regularly repairing their DNA, a tricky process that can lead to cancer. But it also meant that bats couldn’t rely on the classic immune system trick of recognizing foreign pieces of DNA. In other animals, those were likely strands of DNA from a virus or bacteria. In bats, those were likely just pieces of bat DNA that had been damaged and let loose in the wrong place.

Recognition couldn’t work in the same way. So bats’ immune systems decided to be always on, instead. Then, to avoid the problems with that, bats’ immune system also evolved to never reach the same levels of inflammation as other mammals. The end result was that bats were much more able to live with deadly viruses, neither ignoring nor overreacting to them.

Neat, huh?

How to study for the MCAT

This post shared by Trevor Klee, Tutor.

1. Your overall MCAT studying process

a) Start with a diagnostic test. What are your specific strengths and weaknesses? Use the error log app to discern the patterns.

-The error log is like flashcards, but more flexible and better for analytics.

b) If you’re missing content, review the Khan Academy videos for the required information. Employ active review: pause the video, write notes, and form mental connections between what was just covered, what’s been covered, and the overall topic. Do not just watch the videos all the way through like a TV show.

c) Do Khan Academy and AAMC questions to focus on what you’ve reviewed, as well as the content surrounding it. Really try to understand the process of how to solve questions: you’ll find a lot of examples online. Ask yourself why the right answers are right, and the wrong answers are wrong.

Don’t worry about speed, that comes with being confident and fluent in the techniques. As the old Army saying goes, “Slow is smooth and smooth is fast.” Focus on being smooth in your answering process.

d) Once you feel like you’ve covered your initial weaknesses, or you feel confused about about what to do next, take a practice test. Then start with a) again.

e) There are two parts to studying for the MCAT.

One part is like being a marathon runner. You need to put the miles in on the pavement to run a marathon. Anyone can do it, but it takes effort. Doing questions, getting them wrong, and then learning how to do them correctly is the equivalent of putting those miles in. It’s going to suck, but that’s how you learn.

The second part is like being your own coach. You need to reflect on your own progress and what you get wrong and right. What are the patterns in what you get wrong? What techniques do you have difficulty applying?

2. Your MCAT materials

Mandatory

-AAMC Full Length tests

-AAMC Section bank questions

-Khan Academy videos

Flashcards/an error log. The reason I call it an “error log” is that it shouldn’t just be for facts. Anything that you want to remember for test day (like practice problems, diagrams, or techniques) should also go in there.

Optional

-Other AAMC question packs (if you need additional review)

-UWorld question packs (Ditto)

3. Your MCAT study plan

Short MCAT study plan

-Plan for roughly 300 hours of serious studying to get a good score (90th percentile or above)

-So, plan to spend 4 months spending 20 hours a week studying (to give yourself some wiggle room)

-That’s 2 hours a day on weekdays, 5-8 hours a day on weekends (the longer stretches of time are for full length practice tests)

-It’s a lot! But packing it all into a few months is the best way to do it. People get discouraged when they spend a year or two  working on the MCAT, especially when it’s hard to see yourself making improvements week by week. Packing it into a short time prevents that.

Long MCAT study plan

-Here’s a link to a free, detailed 16 week MCAT study plan by Nick Morriss, 99th percentile MCAT tutor.

4. How to study the content tested on the MCAT

This is how you should approach the content for the first and subsequent times

a) Be engaged with the videos. Make sure you are taking notes that aren’t just transcripts of what the video said. Think about the material presented and write it down in your own words.

b) Between 2-6 days after learning/reviewing content for the first time, go back through your notes you’ve taken for a given topic/set of topics. I strongly recommend rewriting them or typing them up- this forces you to take longer to think about what the notes say, while also letting you feel like you’ve accomplished something at the end.

Added bonus: you know have a nicer, neater study guide to draw from if you need to quickly find something later.

c) Take note of content you are struggling with and revisit this 1 week later. You may need to rewatch some videos or look for other explanations if you are can’t figure out why you aren’t understanding. Don’t stress if you feel like it should be easy- it’s a lot of complex information!

d)  Every 4 weeks or so, go back through this content and rewrite key points.

5. When to seek out MCAT tutoring

You might expect a tutor to say, “Seek out tutoring, all the time, for as many hours as possible, no matter what” (as my Dad says, “Don’t ask the barber when you should get a haircut”).

But, this isn’t the case. Or, at least, it’s not what I recommend.

You should seek out tutoring in two cases:

  1. You took a practice MCAT or a real MCAT, and it didn’t go the way you expected or wanted
  1. You’ve been studying for a while, and you’re overwhelmed

In either case, you shouldn’t seek out tutoring until you’ve put in some serious effort on your own. It’ll save your wallet, and give you a better idea of what you can get out of tutoring

You can start your MCAT tutoring journey by emailing me at trevor@trevorkleetutor.com .

How to study for the GRE

This post shared by Trevor Klee, Tutor.

Your overall process when preparing for the GRE

a) Start with a diagnostic test. What are your specific strengths and weaknesses? Use 21st Night to discern the patterns.

If you put the questions you get wrong into the error log app, then head to the analytics section, you’ll get an idea of what exactly you need to focus on next.

b) Do questions to focus on your weaknesses as revealed through the error log app. Really try to understand the process of how to solve questions: you’ll find a lot of examples online. Ask yourself why certain techniques are used, and why your initial instinct may be wrong.

Don’t worry about speed, that comes with being confident and fluent in the techniques. As the old Army saying goes, “Slow is smooth and smooth is fast.” Focus on being smooth in your application of techniques.

c) Once you feel like you’ve covered your initial weaknesses, or you feel confused about about what to do next, take another practice test. Then start with a) again.

d) There are two parts to studying for the GRE.

One part is like being a marathon runner. You need to put the miles in on the pavement to run a marathon. Anyone can do it, but it takes effort. Doing questions, getting them wrong, and then learning how to do them correctly is the equivalent of putting those miles in. It’s going to suck, but that’s how you learn.

The second part is like being your own coach. You need to reflect on your own progress and what you get wrong and right. What are the patterns in what you get wrong? What techniques do you have difficulty applying?

Your materials

Mandatory

-Official GREPrep tests

-21st Night as an error log

-Error log helps you organize yourself, and show you what questions you still need to do, which questions you need to understand, and the patterns in what you’re getting wrong. It will also help you repeat questions so you can remember the strategies necessary on test day.

-The official GRE books (official guide, quant supplement, verbal supplement)

Optional materials

Manhattan Prep 5 Lb GRE book, for extra quant questions (the official books don’t have enough)

-Strategy guides, for the necessary techniques

-My recommendations: my strategy guides

Your study plan

If you want a detailed 3 month study plan, you can receive ours.

Otherwise, plan for roughly 100 hours of hardcore studying to go up 10-15 points on quant or verbal.

So, if you’re starting at 150V/150Q and want to get to 165V/165Q, plan to spend 4 months spending 20 hours a week studying (to give yourself some wiggle room, if you have some unproductive days).

That’s 2 hours a day on weekdays, 5 hours a day on weekends.

It’s a lot! But packing it all into a few months is the best way to do it. People get discouraged when they spend months working on the GRE, especially when it’s hard to see yourself making improvements week by week. Packing it into a short time prevents that.

How to review the sections

This is both how you should approach the questions, and, more importantly, how to analyze a question you got incorrect.

Review through the error log is key to understanding. If you don’t review your incorrect questions, you’ll never understand them.

Vocabulary: how can we break down the sentence to tell us what goes in the blank, especially key sign posts (like butlikewise, etc.)? Is what we missed simply not knowing the word, or was our comprehension off?

Reading Comprehension: what precise part of the passage did I need to read to get the correct answer?

Critical Reasoning:  how does the argument work (premise, reasoning, conclusion)? how does the correct answer fit into the argument?

Quant: what equations do I need to start with? how do I get from there to the answers?

Data interpretation: where’s the trick in the graph?

When to look for a tutor

You might expect a tutor to say, “Seek out tutoring, all the time, for as many hours as possible, no matter what”. As my Dad says, “Don’t ask the barber when you should get a haircut”.

But, this isn’t the case. Or, at least, it’s not what I recommend.

You should seek out tutoring in two cases:

  1. You took a practice GRE or a real GRE, and it didn’t go the way you expected or wanted
  2. You’ve been studying for a while, and you’re overwhelmed

In either case, you shouldn’t seek out tutoring until you’ve put in some serious effort on your own. It’ll save your wallet, and give you a better idea of what you can get out of tutoring.

In that case, you can start your GRE tutoring journey by emailing me at trevor@trevorkleetutor.com .