When browsing the web, I still follow rabbit holes. For example, I will click on a link, read an article, find another link in the body, follow that one as well, and keep on going until I get lost in the weeds and appear in wonderland. When I'm reading through my phone, I often have to go back to the browser history to see the trail of websites that lead me to my destination. But sometimes, I just can't find my way back. Why? Because somehow, I wasn't reading through the web browser. I was browsing through webview.
So when you are on instagram and click on a link shared by a friend. The page loads instantly, but something feels off. You are browsing the web, yet you don't see the familiar browser tabs or address bar. You are in a webview. Why webview and not your favorite browser? Well, this is what I call App attachment issues.
App developers don't want you to leave. And webview is the invisible fence they use to keep you tethered.
The Gilded Cage of Control
When an application loads content within an in-app browser (a webview) you are, technically, using the web. It's running the same rendering engine as a dedicated browser. But the app's sole purpose for doing this is to silo you. They want to maintain control over your experience, ensuring you are never truly free to roam the open internet.
The benefit for the developer is that no matter what page you browse, you are perpetually one button click away from being back in their app. It's a mechanism for user retention, a digital leash. Every company, from social media giants to news aggregators, is trying to fit you into their specific bucket, convinced that if they let you leave, you might not come back. They want to maintain that control over your experience, even when you are outside their reach.
On Android, this is super annoying. You might be able to click links and navigate from the initial website to a completely different, unrelated one, but you often cannot manually change the URL. You are trapped in the current browsing flow, unable to jump to a new destination without first leaving the app or performing a dedicated search. Why are you still under the app's thumb if you're surfing the public web? The answer is always control.
It's for your Protection
The web is a dangerous place. What if you click on the wrong link and your device gets compromised? We can't protect you in this case. At least that's what it feels like when clicking on external links on some websites. For example, on LinkedIn when you click an external link, you are often greeted with a warning message like this:
This link will take you to a page that's not on LinkedIn
Because this is an external link, we're unable to verify it for safety.
On the surface, it appears to be a helpful security measure. The platform is protecting you from the big, bad internet. But the only thing they are truly protecting you from is leaving their app.
If the link was already shared by a contact or surfaced on their platform, the implicit due diligence should have been done. Serving up a blanket safety warning for any external link, even those to major news organizations or well-known websites, is just a friction point to discourage you from leaving. It's a psychological barrier designed to make you hesitate, keep you inside the known confines of their platform, and reinforce their control. This security warning is nothing more than the final, passive-aggressive plea in the app's campaign against your freedom.
The Siloed Experience
If the in-app silo was just the web, but within the app, I wouldn't complain. But while developers are focused on retention, the user experience suffers in some infuriating ways. The webview is a fundamentally broken browsing experience for three core reasons:
The most frustrating drawback is the lack of permanence. Your browsing history is at the mercy of the developer. They can choose to record it, or not record it. And you will be none the wiser until you are trying to find that article you read just this morning. With my rabbit hole style of browsing the web, I often stumble upon great articles, helpful tools, or even products that I mean to return to. But if any of those pages were viewed under a webview, they vanish without a trace.
Related to the missing history is the risk of accidental loss. You might be deep into an article, hit the back button to navigate one step back on the site, and instead, the entire webview collapses, dumping you unceremoniously back into the main app feed. Because no history was recorded, there is no way to return to the page you were just on. The article is simply gone.
There is a common counterargument that says, "Most apps have a setting to disable webview and open links directly in your full browser." But two points to this. 1. Most people don't ever change the default settings. 2. Why is this even an option to select?
If the webview uses the browser engine anyway, why should the default setting be the one that compromises the user's web experience? Users do not dive into granular settings menus. The path of least resistance is the path most taken. By defaulting to webview, developers are prioritizing their retention goals over basic utility.
The entire architecture of the web is built on freedom, open access, and a unified browsing experience. By forcing a dedicated web environment, developers are fragmenting the internet and making our lives slightly harder.
I'm sure there are some metrics out there that say “using in-app webview increases engagement by x%.” But for n=1, aka me, it only increases my disengagement. All I can say to developers is: It's okay to let go.
The remedy for your attachment issues is user freedom. When I click a link, I expect to be in a full browser, with a permanent history, a functional address bar, and true control over my destination. It's time for applications to trust users, respect the open web, and stop trapping us in the confines of their digital cages.
For users, next time you click a link, look for that small icon, often a compass, an arrow, or an ellipsis, then choose to open in browser. It's your internet. It's okay to leave the app. Or even better, never download the apps.
Today, Rodrigo Ghedrin wrote the very well-intentioned, but incorrectly-titled, “I think nobody wants AI in Firefox, Mozilla”. As he correctly summarizes, sentiment on the Mozilla thread about a potential new AI pane in the Firefox browser is overwhelmingly negative. That’s not surprising; the Big AI companies have given people numerous legitimate reasons to hate and reject “AI” products, ranging from undermining labor to appropriating content without consent to having egregious environmental impacts to eroding trust in public discourse.
I spent much of the last week having the distinct honor of serving as MC at the Mozilla Festival in Barcelona, which gave me the extraordinary opportunity to talk to hundreds of the most engaged Mozilla community members in person, and to address thousands more from onstage or on the livestream during the event. No surprise, one of the biggest topics we talked about the entire time was AI, and the intense, complex, and passionate feelings so many have about these new tools. Virtually everyone shared some version of what I’d articulated as the majority view on AI, which is approximately that LLMs can be interesting as a technology, but that Big Tech, and especially Big AI, are decidedly awful and people are very motivated to stop them from committing their worst harms upon the vulnerable.
But.
Another reality that people were a little more quiet in acknowledging, and sometimes reluctant to engage with out loud, is the reality that hundreds of millions of people are using the major AI tools every day. When I would point this out, there was often an initial defensive reaction talking about how people are forced to use these tools at work, or how AI is being shoehorned into every tool and foisted upon users. This is all true! And also? Hundreds of millions of users are choosing to go to these websites, of their own volition, and engage with these tools.
Regular, non-expert internet users find it interesting, or even amusing, to generate images or videos using AI and to send that media to their friends. While sophisticated media aesthetics find those creations gauche or even offensive, a lot of other cultures find them perfectly acceptable. And it’s an inarguable reality that millions of people find AI-generated media images emotionally moving. Most people that see AI-generated content as tolerable folk art belong to demographics that are dismissed by those who shape the technology platforms that billions of people use every day.
Which brings us back to “nobody wants AI in Firefox”. (And its obligatory matching Hacker News thread, which proceeds exactly as you might expect.) In the communities that frequent places like Hacker News and Mozilla forums, where everyone is hyper-fluent in concerns like intellectual property rights and the abuses of Big Tech, it’s received wisdom that “everyone” resists the encroachment of AI into tools, and therefore the only possible reason that Mozilla (or any organization) might add support for any kind of AI features would be to chase a trend that’s in fashion amongst tech tycoons. I don’t doubt that this is a factor; anytime a significant percentage of decision makers are alumni of Silicon Valley, its culture is going to seep into an organization.
The War On Pop-Ups
What people are ignoring, though, is that using AI tools is an incredibly mainstream experience now. Regular people do it all the time. And doing so in normal browsers, in a normal context, is less safe. We can look at an analogy from the early days of the browser wars, a generation ago.
Twenty years ago, millions and millions of people used Internet Explorer to get around the web, because it was the default browser that came with their computer. It was buggy and wildly insecure, and users would often find their screen littered with intrusive pop-up advertisements that had been spawned by various sites that they had visited across the web. We could have said, “well, those are simply fools with no taste using bad technology who get what they deserve”
Instead, countless enthusiasts and advocates across the web decided that everyone deserved to have an experience that was better and safer. And as it turned out, while getting those improvements, people could even get access to a cool new feature that nobody had seen before: tabs! Firefox wasn’t the first browser to invent all these little details, but it was the first to put them all together into one convenient little package. Even if the expert users weren’t personally visiting the sites riddled with pop-up ads themselves, they were glad to have spared their non-expert friends from the miseries they were enduring on the broken internet.
I don’t know why today’s Firefox users, even if they’re the most rabid anti-AI zealots in the world, don’t say, “well, even if I hate AI, I want to make sure Firefox is good at protecting the privacy of AI users so I can recommend it to my friends and family who use AI”. I have to assume it’s because they’re in denial about the fact that their friends and family are using these platforms. (Judging by the tenor of their comments on the topic, I’d have to guess their friends don’t want to engage with them on the topic at all.)
We see with tools like ChatGPT’s Atlas that there are now aggressively anti-web browsers coming to market, and even a sophisticated user might not be able to realize how nefarious some of the tactics of these new apps can be. I think those who are critical can certainly see that those enabling those harms are bad actors. And those critics are also aware that hundreds of millions of people are using ChatGPT. So, then… what browser do they think those users should use?
What does good look like?
Judging by what I see in the comments on the posts about Firefox’s potential AI feature integrations, the apparent path that critics are recommending as an alternative browser is “I’ll yell at you until you stop using ChatGPT”. Consider this post my official notice: that strategy hasn’t worked. And it is not going to work. The only thing that will work is to offer a better alternative to these users. That will involve defining what an acceptably “good” alternative AI looks like, and then building and shipping it to these users, and convincing them to use it. I’m hoping such an effort succeeds. But I can guarantee that scolding people and trying to convince them that they’re not finding utility in the current platforms, or trying to make them feel guilty about the fact that they are finding utility in the current platforms, will not work.
And none of this is exculpatory for my friends at Mozilla. As I’ve said to the good people there, and will share again here, I don’t think the framing of the way this feature has been presented has done either the Firefox team or the community any favors. These big, emotional blow-ups are demoralizing, and take away time and energy and attention that could be better spent getting people excited and motivated to grow for the future.
My personal wishlist would be pretty simple:
* Just give people the “shut off all AI features” button. It’s a tiny percentage of people who want it, but they’re never going to shut up about it, and they’re convinced they’re the whole world and they can’t distinguish between being mad at big companies and being mad at a technology so give them a toggle switch and write up a blog post explaining how extraordinarily expensive it is to maintain a configuration option over the lifespan of a global product.
* Market Firefox as “The best AI browser for people who hate Big AI”. Regular users have no idea how creepy the Big AI companies are — they’ve just heard their local news talk about how AI is the inevitable future. If Mozilla can warn me how to protect my privacy from ChatGPT, then it can also mention that ChatGPT tells children how to self-harm, and should be aggressive in engaging with the community on how to build tools that help mitigate those kinds of harms — how do we catalyze that innovation?
* Remind people that there isn’t “a Firefox” — everyone is Firefox. Whether it’s Zen, or your custom build of Firefox with your favorite extensions and skins, it’s all part of the same story. Got a local LLM that runs entirely as a Firefox extension? Great! That should be one of the many Firefoxes, too. Right now, so much of the drama and heightened emotions and tension are coming from people’s (well… dudes') egos about there being One True Firefox, and wanting to be the one who controls what’s in that version, as an expression of one set of values. This isn’t some blood-feud fork, there can just be a lot of different choices for different situations. Make it all work.
So, that’s the answer. I think some people want AI in Firefox, Mozilla. And some people don’t. And some people don’t know what “AI” means. And some people forgot Firefox even exists. It’s that last category I’m most concerned about, frankly. Let’s go get ‘em.
Last week, the Senate-Administration Working Group on Admissions at the University of California San Diego released their report on the state of admissions at the university, and it’s grim. For the last couple years, over one in eight new freshmen couldn’t do high school math and needed remedial instruction.
The two remedial math classes, Math 2 and Math 3B, are both quite new, and teach math typically learned in K-8 and high school, respectively. But the naming is a little confusing: Math 3B is new as of 2024, and used to be called Math 2. It was the original remedial math course, and was introduced in 2016 to deal with a small number of admitted students who weren’t prepared for college-level math courses.
Math 2 was designed by the UC San Diego Mathematics Department to remediate skills gaps in high school mathematics topics (Grades 9-11), due to the observed need to provide a 10-week on-ramp for a small number of students to our normal precalculus courses (Math 3C and Math 4C). It was first offered in 2016, and from 2016-2021 it successfully served a small number of students (usually less than 100) that needed this additional support in their first quarter at UC San Diego before entering Math 3C or 4C.
The number of admitted students needing this remedial instruction remained small until 2020, after which enrollment ballooned.
Then things got worse: beginning in 2023, Math 2 instructors started to complain that their students were missing basic math skills from K-8 instruction.
In Fall 2023, the Math 2 instructors observed a new and alarming spread of skill gaps in the Math 2 students that quarter, with many severe gaps going back to mathematics taught in middle and elementary school.
Thus Math 2 was downgraded to K-8 skills, and the original Math 2 (high school skills) rebranded to Math 3B. Both were meant to address gaps in math knowledge for students who would need math in their prospective majors.
What kind of gaps? Here are sample questions from a test prepared by the math department to assess the skills of these remedial students, each labeled by the grade level of the skill and the percentage of such students who got it correct.
We’ll come back to these in a moment, but first let’s look at an overall summary of the results. Overall, only about half of the remedial students could claim 5th grade math ability, and only 19% had 8th grade skills.
Helpfully, the math department calibrated its grade level assessments by giving the same test to five public school kids in California — bright kids, one assumes, but K-8 students nonetheless. Their performances are marked by the colored arrows in the bottom chart, which demonstrate that the median score for remedial math students admitted to UCSD in 2023 is about on par with a 5th grader. For the 2025 school year, UCSD admitted 665 such students (on top of another 256 who couldn’t do high school math).
What happened? How did the quality of admitted students fall so far, so fast? The report spends a lot of time blaming poor kids for this outcome. No, really.
In 2013, the California state legislature introduced a supplemental funding framework for California K-12 public schools, the so-called Local Control Funding Formula (LCFF). The subset of California public schools in which more than 75 percent of the school’s total enrollment is composed of students who are identified as either eligible for free or reduced-price meals, or English learners, or foster youth, are eligible for additional funding through the LCFF program. The subset of California schools that meet these eligibility requirements are referred to as LCFF+ schools, and since 2016, University of California tracks enrollment from LCFF+ High Schools. The 2016-17 state budget for the UC system included “one-time funding for 19 support services for low-income students and students from underrepresented minority groups”. The one-time funding was intended to increase the number of applications, admissions, and enrollments from LCFF+ high schools to the UC, a contract signed by then President Michael Drake. Since 2017, each fall UCOP must submit a report on what UC has done to support LCFF+ schools.
So there’s legal and political pressure increase admission from schools with predominantly poor kids, and the UC system got a sweet kickback from the state legislature in exchange for agreeing to admit more of them. And for whatever reason, UCSD ended up with more of these academic albatrosses future scholars, starting in 2022.
UC campuses have participated unevenly in these changes to LCFF+ admissions and enrollments. In 2021, UC Riverside and UC Merced admitted the largest numbers of LCFF+ students, while Riverside and Irvine enrolled the most. Beginning in 2022, however, UC San Diego took the lead, with enrollment jumping from 894 in 2021 to roughly 1,800 in each of the following three years (2022-2024). By comparison, most other campuses saw only modest increases. UC Berkeley remained below 1,000, and UCLA below 1,100 LCFF+ enrollments.
For those not in the know, Riverside and Merced are the two down-market UC schools, admitting 76% and 91% of applicants respectively (compared to UCLA’s 9%). You won’t catch anyone wringing their hands about Riverside’s math skills, certainly not writing long mystified reports asking where it all went wrong. Their function in the system, the UCSD report seems to tacitly imply, is to absorb that kind of student so that the rest of the UC doesn’t have to deal with them. So what changed? Why did those students suddenly start getting into prestigious UCSD, traditionally the third-pickiest UC school, around 2021?
Oh.
So without standardized testing, how does the UC decide whom to admit? By a complex process they call “Holistic Review” or HR. The report dedicates 6 pages of dense, unbroken text to explaining this process without once describing what factors are included beyond high school GPA.
The process of our Holistic Review for first-year applicants can be divided into two stages. In the first stage, readers score each application with consideration of a range of factors derived from BOARS guidance.
There you have it, “a range of factors.” (BOARS apparently stands for Board of Admissions and Relations with Schools). They do mention that they have various statistical corrections to deal with grade inflation and inconsistent grading practices when appraising high school GPA, but otherwise that’s all you get, “a range of factors.” Or “a variety of other factors”, as below.
Beyond these highly quantitative factors, holistic readers are trained to look out for a variety of other factors that all conform within the BOARS list of approved considerations in admission and use the PIQs (a series of short essays) and activities lists to determine more about the student’s background, potential, and life experiences.
Every UC school, barred from using standardized test scores in admission, does something similar. So why is it that UCSD seems to be, uniquely among the elite UC schools, admitting so many dummies? Here I can only speculate, but my honest guess is that the UCSD admissions staff and administrators who oversee the program have a particular, shall we say, soft spot for certain kinds of “life experiences” that some students may have been wisely coached to include in their applications. But that’s just speculation.
More importantly, having recognized the magnitude and severity of the problem, what are they going to do about it? Remember, they cannot use standardized test scores in their admission process. Briefly: they recommend using a new model they invent called the Math Placement Outcome (MPO), which looks at applicants’ math grades and makes various adjustments for the student’s school. The big issue with this idea, which they do note, to their credit, is that a relatively meager difference in math grades separates students who can’t do algebra versus those headed straight into calculus. Specifically, 3.65 v. 3.84.
Recall that this average high school math GPA of 3.65 among Math 2 enrollees corresponds to approximately a 5th grade level of math skills. Can the MPO find a signal in the 0.19 grade points that separate an A- in calculus from a being unable to name a triangle? Good luck!
It’s important to cut through the cope and HR-speak and discuss what these results actually mean. What does it mean that a quarter of remedial admits got this question wrong?
For some of the questions, such as simplifying complex expressions involving fractions, or expanding the square of an algebraic expression, you can will yourself to believe that an otherwise smart kid has been badly served by their math instruction, or has simply forgotten how to do that kind of problem in the years since being taught. But being unable to fill in a “3” in the box for the problem above? That points to a deeper deficit that can’t be described as a “gap” in understanding. There’s no trick to remember here, just an elementary level of symbolic reasoning and the ability to count. A student who can’t do this problem simply isn’t very bright, and is extremely unlikely to succeed in university courses absent radical dumbing-down and thumbs on the scale at every turn. That the university admitted about 200 such students last year should indict the entire admissions process.
The UCSD freshmen taking Math 2 are not to blame for their situation. They haven’t done anything wrong and shouldn’t be the subject of our anger or ridicule. There will always be a left-hand side of the bell curve, and somebody has to land there — in fact, half of all kids do. They’re not worse people because they’re less bright, and in fact they have every chance to achieve as much wealth and happiness as their brighter peers (IQ is correlated with income, but surprisingly weakly).
But they don’t belong in college, and they can’t be in college without radically changing what college is, what it’s for. This shouldn’t be controversial, and in most other universities, it’s not. Lots of colleges went test-free during covid and admitted whomever their hearts whispered they should, and in every case the result was a disaster, an unmanageable wave of unqualified freshmen who looked good on paper (or tugged at the heart strings just right) but couldn’t do the work. Nearly every university learned their lesson quickly and reversed course. California is uniquely stubborn in this respect, but now there are legal headwinds suggesting the UC schools will be brought to heel as well.
I find myself torn between sympathy for bright California high school kids being denied admission to give a spot to more sympathetic kids who can’t handle algebra on the one hand; and the fervent desire to see California maximally pursue these destructive policies as an object lesson to the rest of the country on the other. But what I know for sure is that things can’t go on like this forever, and so they won’t. If a university degree is to mean anything at all, then it must exclude those who can’t fill in the box.
Whether that happens before or after the UC system implodes is anyone’s guess. I’m rooting for you, UCSD.
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If you live in this one tiny county in California, you might be more likely to die from Sin Nombre Virus than in a car crash.
In the same way that “why does the frozen spinach I want to buy cost much more than it used to?” engages with a vast interconnected web of economies and monetary policies and farmers and supply chains, asking “what’s up with this rare disease people sometimes get in my part of the world?” is actually a question about the entire ecosystem, plus how organisms even work.
The reason you have to think about the natural world when you do biosecurity is that the vast majority of human diseases come from animals. What we think of as diseases to humans is a two-dimensional slice of a giant, rotating, obscure shape of many dimensions – a whole world of diseases, little communities of microbes and macrobes interacting and evolving and getting sick and occasionally passing their diseases around between them. Communities of parasites built on communities of hosts, all colliding constantly. This is the large scale of biosecurity. Nothing in infectious disease research makes sense without it. Any question about human health or symptomology or individual risk or what have you is a tiny speck on the shore of this ocean.
Occasionally, one of those parasites reaches out of the host community it’s adapted to, and finds a foothold in another host. And so the sphere gets a little bigger, a little more interconnected.
Today we’ll be looking at a single slice of the grand pageant, about this size – one virus in one part of the world, that sometimes slips from its home and finds its way into a human animal.
Sin Nombre Virus
Sin Nombre Virus was first characterized in 1993 in New Mexico. Since then, there haven’t been many identified infections, but every now and then, cases crop up. Even in the medically well-equipped United States, Sin Nombre virus has maintained an astonishing 40% mortality rate.
Here’s a map of hantavirus infections in the US by state, since its discovery. We can see that it’s far-reaching, but it clearly has a geographic localization.
So if you live in California, your risk is even comparatively low. But out of curiosity, let’s look closer at a map of SNV infections in California counties.
Huh, what’s the deal with that one county? Note that this is a total case map, not a per capita case map, and that county doesn’t have any large cities. In fact, it’s the 4th least populated out of California’s 58 counties. So the risk is even higher than that map makes it look!
But it’s pretty unlikely that any given blogger would live in that county, isn’t it?
Ha ha, what a funny idea. Anyway, I happened to take an interest in this rare, hyperdeadly disease.
The virus without a name
Most current reporting describes the disease we’re looking at today with the more general name of hantavirus – which it is, but there are multiple human diseases in the hantavirus family.
They’re split into the Old World and New World hantavirus. The Old World hantaviruses cause hantavirus hemorrhagic fever with renal syndrome (HFRS) in Eurasia.
The New World hantaviruses include our subject of interest today as well as the related Andes virus in South America (plus a few other, even rarer North American viruses we’ll discuss later). Andes virus has similar symptoms and is about as deadly as Sin Nombre Virus, but it sees more cases every year – 100-200 versus North America’s “dozens” – and it shows occasional person-to-person spread. We’ll come back to that, but for now, I’m focusing on the most common North American hantavirus because it’s the one that’s in my own backyard. …Potentially literally.
The North American hantavirus we’re discussing today is more specifically known as Sin Nombre virus. Why is it called that?
It was discovered in 1994 after a lot of people got sick in the Four Corners region of New Mexico. Local Native communities actually had stories about odd numbers of people getting suddenly sick and dying during years where the pine nut harvest was good, and indeed, 1994 was a good pine nut mast year. Because of abundant nuts to eat, the mouse population exploded and came into a lot of contact with humans, and enough people got sick and died that USAMRIID and the CDC investigated. And they found a virus at the root.
Ongoing practice at the time was to name newly-discovered viruses after geographic locations nearby the site of origin. But this was already facing pushback – who wants to take a vacation to the scenic Ebola River? On top of that, the area and early cases were heavily Native American communities, and before the disease was shown to NOT be communicable, Native groups were facing racism and shunning over this mystery disease.
The Four Corners region didn’t want it to be the Four Corners virus; the nearby Muetro Canyon was proposed but rejected because the Navajo community didn’t want more stigma (and also Muerto Canyon was named after a massacre against the Navajo), and back and forth, and eventually they just called it the virus without a name, AKASin Nombre virus.
I have some thoughts on infectious disease naming that are too long for the current margin to contain, but I will say that I think this is the kind of cool infectious disease naming schema that you can pull off once.
Mice
This is the western deer mouse, Peromyscus sonoriensis. Sin Nombre virus lives here.
The worst part of biosecurity is having to look at something like this and be like “this thing is the enemy.” Okay, maybe that’s not the worst part.
This is a pretty common strategy of infectious viruses – playing the slow, long game. Humans have a few: cytomegalovirus, herpes simplex virus (especially HSV-1), Human T-cell lymphotropic virus type 1… viruses that lots of people have for their entire lives, and have no idea that they have.
Compare also things like the common cold or human papillomaviruses that cause warts – shorter lifespan and some chance of symptoms but also not much, really. The immune system eventually clears these out in most cases without help, but they have time and means to spread, and they circulate among us and periodically annoy us, but mostly, they don’t kill us.
The deer mouse is not the same thing as the house mouse Mus musculus, which you’re probably more familiar with. But let’s take a minute here.
There’s mice and then there’s mice
We all know Mus musculus – it’s the common house mouse, which has spread worldwide alongside people. If humans build a town, the house mouse will soon follow. There are a lot of less-common related species of mice, like the adorable African pygmy mouse (Mus minutoides).
But Peromyscus sonoriensis isn’t either of these. Technically speaking, is it a rat or a mouse?
Well, what a great question. It’s neither.
Huh, you might think. Mice are on there twice? If you know your way around a phylogenetic tree, you may wonder: maybe the common ancestor was more like a mouse, and it’s rats that are doing something weird?
Ha. Haha. Hahahaha. No. The real situation is more complicated than you could possibly believe.
Rats and mice have evolved multiple times, with some incredibly weird variations in the mean time.
This is the distance between the western deer mouse and the house mouse:
Despite all of this genetic distance, hice mice and deer mice occupy extremely similar niches. Where the western deer mouse is native, it’s completely comfortable cozying up to human dwellings and making its nests inside our big, fancy, warm, dry, food-filled nests.
And deer mice that are widely regarded as the vectors of Sin Nombre virus – the host species that it’s evolved to circulate in. In New Mexico, two studies (one statewide, one in an area where a human was infected) found that about 35% of deer mice had the virus at any given time. Eyeballing it, this lines up pretty well with a “disease circulating stably among the mouse population that rarely spontaneously spills into humans” situation.
…But wait, are deer mice really the only carriers? That second study also found replicating, viable Sin Nombre virus in other local rodents – including the house mouse, mus musculus! The sample sizes weren’t huge, but 3 out of the 9 captured had it!
Note, however, that they only found house mice at one of the sites. There were many more deer mice than house mice. But still, 3/9!
What I don’t know, and what I don’t think anyone knows, is the degree to which hantavirus actively circulates among these other rodents. Are they just getting it incidentally from neighboring deer mice, or do they pass the virus around between themselves too? Is Sin Nombre virus just as at home in them as it is in western deer mice?
The literature is very clear that deer mice are the ones associated with Sin Nombre virus infection. For instance:
The most common hantavirus that causes HPS [that virus being SNV] in the U.S. is spread by the deer mouse.
But “common house mice (Mus musculus), which are prevalent in urban and suburban communities, do not carry hantavirus,” said Charles Chiu, MD, PhD, professor of laboratory medicine in the division of infectious diseases at the University of California, San Francisco.
(Sidenote: this article also quotes one of those New Mexico survey articles I mentioned above, saying that it “found less than 9% of deer mice had the virus.” The study did report that 10/113 deer mice had antibodies to SNV, but it also found that 37/113 of the deer mice had SNV DNA in their system. This is weird, because viral DNA is a sign of an active infection – it’s made by a virus! – but the immune response can linger for a long time after infection, so we’d really expect more mice to have antibodies to SNV than to have SNV DNA. The study does mention that this trend held up across all rodents studied, so maybe this just has to do with the sensitivity of their antibody assay.)
And there are a lot of cases where people got sick, in which the victims knew they’d come into contact with material contaminated by deer mice.
But there are also cases of infection where nobody saw a mouse, and the presence of any mice at all just has to be intuited. Is it possible that Mus musculus is responsible for some Sin Nombre cases in humans?
The public health literature is pretty unanimous about the deer mouse thing, so I’m going to proceed assuming that’s effectively the only way any human gets Sin Nombre virus, but I don’t understand why they’ve ruled out other mice too.
Human
The adventures of a dead-end host
Sin Nombre virus is a transient inside human beings – it’s not adapted here, it doesn’t stay here. We know this because when we isolate the virus from infected humans, it doesn’t easily reinfect deer mice. This suggests that small mutations have to occur to make the virus able to replicate in humans – ones that make it less viable within mice.
[…] which implies that humans are truly dead-end hosts of SNV. Thus, virus evolution is primarily, if not exclusively, occurring in the natural rodent reservoirs.
But SNV can infect humans, and a virus has to replicate to make its host sick. How does it do that?
Well, it’s almost always inhaled from mouse-contaminated material. Then the virus somehow gets into the blood stream.
Once it’s there, Sin Nombre virus replicates inside a variety of human cells, but especially likes endothelial cells and macrophages.
Endothelial cells are the guys that line our blood vessels. They grow everywhere the blood vessels grow, which is to say, all over
Macrophages are a kind of immune cell that devours pathogens. The SNVs are captured by the macrophages, and as with all of their prey, are moved into a lysosome – a cellular chamber that turns into an acid bath, designed to inactivate complex biomolecules (and pathogens they’re attached to) trapped within. But the SNV particles escape into the cell membrane just as the acidification starts.
Replicating inside immune cells is a pretty common strategy for viruses. Sure, the immune cells try to spot and destroy pathogens, but they also end up capturing and moving pathogens around a lot, which can be a big boon if the pathogen has a way to just not get killed by the cell.
Some macrophages roam the bloodstream, but others are concentrated in outposts around the body. Some are in the lungs.
As far as I can tell, Sin Nombre Virus probably gets into the lungs, then infects the alveolar macrophages (and possibly other lung-based immune cells), and then escapes from those into the blood stream where it might infect other endothelial cells. They might also manage to get through tears or thin spots in the alveolar-capillary membrane and get straight into the blood – that’s just a guess.
Replicating in endothelial cells seems kind of overpowered for a virus, right? Like, we have a gazillion of ‘em and they’re all over the body and once you’re next to the bloodstream, it’s an easy highway for a virus to get from one part of the body to a totally different part of the body. to spread from one part of the body to a totally different part of the body – and if you mounted an inflammation or severe immune response, that seems like that would kill the entire host easily and quickly.
And indeed, Sin Nombre Virus does kill its host quite effectively. Ebola, another famously lethal disease, also replicates in endothelial cells. Covid seems to be able to sometimes (in addition to its main habitat in the respiratory tract, an interesting similarity between it and Sin Nombre Virus.)
So is replication in endothelial cells a sure sign that a disease will wreck havoc on the human body?
Well, no. Dengue fever replicates in endothelial cells, and most of its hosts are asymptomatic or mildly symptomatic. Its fatality rate is literally one in a million. And moreover, cytomegalovirus is an endothelial replicator. Like we talked about before, cytomegalovirus of those viruses that’s almost a commensal – most people have symptomless cytomegalovirus infections. (It can cause disease in unborn fetuses, infants, and the immunocompromised, and seems to contribute to cancer risks down the line – it’s not great – but, again, most people have it.)
Also, lots of viruses attack tissues that are essential and would be bad to call the full attention of the immune system to – herpes viruses (another near-commensal genre of virus that most infected carry without any symptoms whatsoever) infect nerve cells, for instance. Lots of viruses infect the lungs, which are famously important, and some of them kill you and some of them are no big deal.
So I think a general lesson here is that the driver of virulence here has more to do with the rate of growth / level of viruses active at once and the degree to which they activate the immune system, not the infected tissue.
Do a bunch of people within the regions where it is have indications of asymptomatic or past infections?
This is a great question. After all, mice have it quietly, and people seem to have the capacity to carry or fight off a lot of infections quietly without notable symptoms. Are we sure this isn’t the case for hantavirus?
Well, so far as I know, nobody has checked.
Wait, can we talk about the actual disease?
Yeah, fine I guess.
According to the CDC, the early symptoms of Sin Nombre virus disease in humans – AKA hantavirus pulmonary syndrome (HPS) or hantavirus cardiopulmonary syndrome (HCPS) – emerge 1-8 weeks after acquiring the virus. They start out, like a lot of fucked up viral diseases, with generic symptoms:
Muscle aches
Fever and chills
Malaise
Headaches
Abdominal pain
Though “aches” might be a standout. University of Colorado Health (Colorado has a lot of SNV cases) reports that severe muscle aches, especially in the back and lower extremities, are a common hallmark of HCPS cases. (Hey, I got severe leg pain when I got shigellosis on purpose too – shigellosis, much like Sin Nombre virus, is an infectious disease that notably does not target the legs. What’s up with that?)
4-10 days after this, the cardiopulmonary stage of disease begins, AKA “the part that kills you”:
Coughing
Shortness of breath
Fluid buildup in lungs/chest
Tachycardia
Arrythmia
Cardogenic shock
Respiratory failure
HCPS has a 40% death rate. Deaths occur 24-48 hours after the start of the cardiopulmonary phase. There is no vaccine or known effective antiviral.
Buying time
If you get HCPS and reach the cardiopulmonary stage, the thing that will save your life is a medical technology called extracorporeal membrane oxygenation (ECMO). An ECMO device draws large volumes of blood out of the body via inserted tubes (called cannulae), runs the blood through an artificial lung (called a membrane oxygenator) to remove carbon dioxide and reoxygenate the blood cells, and puts the blood back in the body.
HCPS seems to be one of those diseases where the body can rally and fight off the disease, if it has enough time. I attended an online lecture delivered by clinician Dr. Greg Mertz and this is the sense I got: SNV doesn’t permanently damage the heart and lungs, it just overwhelms them. If ECMO takes over while the heart and lungs are out of commission and keeps plenty of oxygenated blood in the system, the immune system can finish the job and the heart and lungs can go back to work afterward.
If you go to a hospital with symptoms and they make a presumptive diagnosis of HCPS, you can opt into having the ECMO cannulae inserted in advance – they won’t start ECMO until you go into shock (because your heart/lungs fail), but if you do go into shock, they’ll be able to start re-oxygenating your blood immediately. At this point, doing this changes your odds of survival from 50% to 80%.
(I see that in my notes from that talk, I also wrote “Do not go into shock”, as it leads to “DEATH V FAST.” So if you get to decide at some point whether or not to go into cardiac shock in general, try not to.)
So if you think you’ve been exposed to SNV and 1-9 weeks later you start experiencing arrhythmia and shortness of breath, proceed straight to a hospital with an ECMO device.
ECMO devices are not extremely common. You can find out which hospitals near you have ECMO devices on the Extracorporeal Life Support Organization website. If you happen to be reading in Mono County, your nearest ECMO is probably in Reno Renown Regional Medical Center.
…But if you’re one of the 12,000 residents of Mono County, then yeah, probably. Mono County has had an unusually high 3 HCPS deaths from hantavirus this year, so you have a 0.025% chance of dying from HCPS.
You might actually be more likely to die from hantavirus as in a car crash (0.012% chance in any given year.)
(Sidenote: Naively, I’d expect Mono County residents to have a 0.000004% of dying by being struck by lightning like anyone else, but if you actually look into it, Florida specifically and the southeast generally have a really disproportionate number of lightning strike deaths. We should probably stop rhetorically treating getting struck by lightning as an entirely random act of god and start thinking of it as a physical event with contributing factors like everything else.)
Questions
Why is the geographic range of hantavirus infection so limited?
Let’s go back to that map of USA state-level infections.
So mostly, that makes sense. But how are there ANY cases in the east half of the state?
SNV’s weird siblings
Those other HCPS cases on the east coast? Well, they’re not (or at least, not only) people who happened to travel from the West Coast, and they’re not (or at least, not only) far-ranging western deer mice.
Those are the work of other, rarer hantaviruses, carried by other rodents, spilling over occasionally into other humans in the same way, causing HCPS, and with about the same fatality rate.
Each of these is really rare, even rarer than SNV. But that’s odd in and of itself, right? Like, do all of these host species just interact less often with humans than deer mice in the Western US? Are the viruses less common in their hosts, or even less transmissible than SNV? The answers might be out there, but I don’t know that they are.
I ’m also curious about the California county-level breakdown: why Mono County? (And note that this is raw cases, not cases per capita – Mono County has a tiny population.) Is it because there are more deer mice? Or is hantavirus localized to certain populations of deer mice?
Well, here’s this other data on seroprevalance of hantavirus among captured mice in various counties. Sure enough, Mono County has the highest seroprevalance, at 31%, but apparently 25% of tested mice in Santa Barbara County also had SNV, and Santa Barbara has a lot of people in it!
So why does Santa Barbara see very few human cases, while Mono County has a lot?
Here’s my guess at why: it has to do with the houses, and it has to do with mice. Mono County has a lot of barns, sheds, and vacation houses that are left empty part of the year. The classic situation where a person gets SNV is cleaning out a shed or outbuilding that’s been inhabited by mice, kicking up a lot of mousy dust and particles, and inhaling SNV. A shed or a building that’s left for the summer or winter is a nicer place to build a shelter than under a bush, but it’s still not that cozy – it might not have food inside so the mouse still has to forage a lot, and it might get very cold or very dry. There might not be many other buildings nearby. A region-adapted, mostly-wild deer mouse, is going to have a better go in an outbuilding then the urban Mus musculus – and indeed, every mouse I’ve seen or caught around my home has been a deer mouse.
Santa Barbara County is much more urban and has a warmer climate. I bet the mice that people encounter there are almost all Mus musculus. I bet all the Santa Barbara deer mice live in the wild, outcompeted in cities by the larger and more urbanized mus musculus.
And the deer mice are god’s chosen carriers of SNV, and the Mus musculus aren’t. It’s just a deer mouse disease. So it’s much more likely to crop up where people interact with deer mice, and they do so a lot more in these rural, more-wild environments.
It’s an apparent puzzle that makes a lot of sense once you just ignore the human health angle for a second. SNV is a deer mouse disease that circulates among deer mice. Think about which mice want to live where. Humans, as is often the case, are providers and users of nests, and otherwise, are only relevant incidentally.
But wait, can we check this?
If my model is correct, areas that have high SNV caseloads will:
Be mostly rural (probably without major cities?)
Have extreme climates
Have a lot of outbuildings, plus homes that are inhabited seasonally
It would also be interesting if they’re clearly geographically clustered – like if specifically one part of the world is a hantavirus hotbed.
Yeah, let’s look at some other states that get a lot of SNV cases. I don’t expect to get great data at anything lower than the county level. Colorado and New Mexico both get more SNV cases than California, and have county level data.
I tried to look into this further, and ran into kind of a dead end. Or maybe I’m just wrong.
The counties with the highest rates include La Plata and Weld counties in Colorado, and Mckinley county in New Mexico, which is such a standout that it dwarfs the others.
La Plata County has a population of 55,638 with the largest city (Durango) at 10,000. It has some parks and overlaps a national forest, no major ski areas.
Weld County has several cities and a population of 329,000. (It contains parts of some large cities that are on the border so it’s hard to break down for sure, but a lot of people live here.) Okay, not looking great. It’s fairly flat with some mountains, and mostly farming country.
Mckinley county has one city of 20,000 and no other cities, but a lot of smaller towns and census-designated places and such. Its total population is 73,000, which is pretty big! I can’t find indications that it has a lot in the way of seasonal dwellings – there aren’t many ski resorts. The county does seem to be pretty dispersed, housingwise, which might imply more outbuildings.
So, uh, none of this actually cleanly supports my mode, but it’s not necessarily evidence against it either. We might just need data on which kinds of mice are common in human dwellings in these areas, and how common mice are overall.
What makes Andes virus infectious interpersonally, and SNV not?
It seems like ANDV builds up in the salivary glands of humans, and saliva is its mode of transmission. SNV doesn’t do that.
SNV collects in the lungs and heart. ANDV collects in the heart, lungs, and salivary glands, and tests studies have indicated virus in fluids from both of these. It seems to spread via saliva, droplets, and aerosols. Sex and close contact are major risk factors. Otherwise, ANDV has a similar features and fatality rate to SNV.
Saliva also seems to be how deer mice spread SNV and ANDV among each other – both of them show up in the salivary glands of their host mice, but only ANDV inhabits human salivary glands.
(If we could somehow prove that ANDV could spread from the lungs, well, that would suggest some new mechanism also in play – but that seems hard to test, given that the mouth is, you know, between the lungs and the rest of the world.)
That said, I actually don’t understand why ANDV isn’t airborne, or otherwise transmitted from the lungs. The mousy particles that infect humans seem to be from kicked up dust and such, so there’s reason to think it could be aerosolized – maybe the virus particles don’t escape the lungs very well?
That’s all the things I know about Sin Nombre virus, plus some things I don’t. Let me know if you have the answers. In the mean time, don’t die of cardiopulmonary shock. I, for one, am doing my best out here.
Erin Patterson used death cap mushrooms in a beef Wellington she served to members of her extended family in 2023, killing three of her four lunch guests in a triple homicide that shocked Australia. For Vittles, Aaron Timms asks, “What were the specific historical conjunctures that led Patterson to choose, for her victims, death by duxelles?”
Patterson’s escapades took place against the backdrop of a nation suddenly mad for foraging – or at least dead keen on the idea of a trained professional doing it for them. Death caps are not, I probably don’t need to point out, the type of thing Australians usually like to harvest for their own consumption. But thanks to the species identification tool on iNaturalist – a photo-based, user-sourced biodiversity platform that includes more than 300 million observations of plants and other organisms worldwide – they’re relatively easy to identify. Indeed, Patterson relied on iNaturalist to scout her noxious haul, diverting users’ cautionary tagging of death caps on the platform towards a far darker end.
I learned many surprising lessons from my 20 months as editor-in-chief of Deadspin, the skeptical, irreverent, hilarious, trailblazing sports outlet that entertained, offended, and educated audiences in roughly equal measure.
I learned from a cease-and-desist letter that Jacuzzi is a trademarked brand, and that the hotel room in which a world-famous soccer star was alleged to have raped a woman contained a mere “spa” or “hot tub.” I learned from inhaling Chartbeat that our very dumbest stories and our very smartest stories would always be our biggest traffic drivers. I learned from our general counsel more than I ever wanted to know about the precise limits of fair use. I learned from my coworkers — all of them brilliant and entirely deranged — that there is no limit to how hard I can laugh in a soul-suckingly bland Times Square cubicle farm. Even knowing how it all ended, I’d still take the job 100 times out of 100.
The most consequential lessons I learned, though, were about the ways in which I had misunderstood “free market” capitalism, and about what that meant for the industry that gave me my career. Those are the lessons I haven’t stopped agonizing over six years later, the ones that led to my first book but also caused scores of sleepless nights.
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