> if you’re not regularly exposed to the organism in question, the antibodies fade faster, sometimes much faster than in communities where the organism is endemic.

Do you have a recent reference for this? My impression is that that was a good working hypothesis, but it hasn’t held up very well to data - in particular, I think that measles vaccine immunity holds up well even in regions where measles is essentially eradicated.

TL;DR: rapidly expanding populations have faster adaptive evolution, and that’s what is seen in humans.

> Human populations have increased vastly in numbers during the past 50,000 years or more (1). In theory, more people means more new adaptive mutations (2). Hence, human population growth should have increased in the rate of adaptive substitutions: an acceleration of new positively selected alleles. … In such a transient, large population, size increases the rate and effectiveness of adaptive responses. For example, natural insect populations often produce effective monogenic resistance to pesticides, whereas small laboratory populations under similar selection develop less effective polygenic adaptations (5). Chemostat experiments on Escherichia coli show a continued response to selection (6), with continuous and repeatable responses in large populations but variable and episodic responses in small populations (7). These results are explained by a model in which smaller population size limits the rate of adaptive evolution (8). A population that suddenly increases in size has the potential for rapid adaptive change. The best analogy to recent human evolution may be the rapid evolution of domesticates such as maize (9, 10).

—Recent acceleration of human adaptive evolution

The author of that paper has a blog post giving more background and explanation: Our new paper on why human evolution accelerated. His summary there:

> Our evolution has recently accelerated by around 100-fold. And that's exactly what we would expect from the enormous growth of our population.

Despite what everyone is going to say, this has nothing to do with antigenic drift in flu (i.e. accumulated mutations in circulating viruses) and certainly nothing to do with antigenic shift (genome segment rearrangement).

While antigenic drift is a concern and shift is a much rarer concern, the fact is that influenza vaccine immunity wanes extremely fast regardless of shift or drift. This is very well known and there are literally hundreds of publications about it; you can start with Waning of Measured Influenza Vaccine Effectiveness Over Time or Waning Vaccine Effectiveness Against Influenza-Associated Hospitalizations Among Adults, 2015-2016 to 2018-2019, United States Hospitalized Adult Influenza Vaccine Effectiveness Network or many others.

This waning with the influenza vaccine is generally much worse than most vaccines and in particular it’s much worse than tetanus vaccine. The sad truth, though, is we don’t know why immunity wanes so fast. Part of it is that the conventional inactivated influenza vaccine, which has no adjuvant, is poorly immunogenic - but that’s kind of going in circles because “poorly immunogenic” means its immunity wanes rapidly.

Even many more modern influenza vaccines, made through different approaches, are weakly immunogenic and have rapid waning of immunity. So maybe there’s something specific about influenza, that means it has adapted to be poorly immunogenic in people. If so, we don’t have a clear idea what it is.

Including adjuvants with the vaccine does help, and that’s used in the elderly.

But in a sense, it’s not a critical problem now because even if immunity didn’t wane, we’d still need to give nearly annual vaccines because of the antigenic drift problem. It’s annoying, it does mean that people vaccinated in fall are already less well protected by spring, but by summer flu has mostly gone away and mostly you need a new vaccination by fall again anyway.

If and when new vaccines against flu are introduced, with broader reactivity, that don’t need to be modified every year - then this will need to be solved too. But they’re not out yet.

Possibly HIV might have become less virulent, but you absolutely have not detected that. What you are seeing is improved treatment of HIV.

There are a handful of ambiguous and marginal studies that hint that, in some regions and some populations, HIV might be becoming slightly less virulent. Again, you personally have not seen this because you don’t live in those areas and you personally don’t have the opportunity to test viral blood load in tens of thousands of stage-matched, strain-matched infected people.

> In support is evidence that SPVL, and hence virulence, has declined in some African HIV subtypes, even accounting for the use of antiviral therapy, and that this reflects a trade-off between virulence and transmissibility

—The phylogenomics of evolving virus virulence

(The reference cited here is Blanquart F, et al. A transmission-virulence evolutionary trade-off explains attenuation of HIV-1 in Uganda. eLife. 2016;5:e20492.)

There’s a widely believed myth that viruses inevitably evolve to reduced virulence over time. In spite of the great confidence with which this is claimed, it is not true, there are many counterexamples, and there are 60 years worth of observation of theory (with math) demonstrating why it’s not true.

> For example, in the case of the second virus released as a biocontrol against European rabbits in Australia — rabbit haemorrhagic disease virus (RHDV) — there is evidence that virulence has increased through time … Similarly, experimental studies of plant RNA viruses have shown that high virulence does not necessarily impede host adaptation and, in the case of malaria, higher virulence was shown to provide the Plasmodium parasites with a competitive advantage within hosts.

>Theory therefore tells us that natural selection can increase or decrease pathogen virulence, depending on the particular combination between host, virus and environment

—The phylogenomics of evolving virus virulence

So there’s no particular reason to expect HIV to evolve to reduced virulence.

No one suggests raccoon dogs are the reservoir. They suggest they were an intermediate host between bats and humans, as has happened with all the other bat coronaviruses that have jumped into humans.

A very early genomic sequence of SARS-CoV-2 was posted by Chinese researchers, then removed (probably because of Chinese government pressure). However, a few western researchers grabbed the sequence before it was removed and analyzed it. As well as viral sequence, the sample had raccoon dog DNA sequences associated with it (as contaminants), implying that this extremely early virus sample came from raccoon dogs. It’s known that raccoon dogs were kept in the wet market that’s been implicated in very early COVID19 transmission, and raccoon dogs are highly susceptible to infection with SARS-CoV-2, so it’s a consistent story.

It’s unfortunate that the Chinese government are obviously trying to suppress this, because if they’d simply make available the info about this there would be less space for the silly conspiracy theories.

Here’s the WHO statement, which explains a little more and shows the level of frustration they have with the Chinese government: SAGO statement on newly released SARS-CoV-2 metagenomics data from China CDC on GISAID

> …samples collected from the environment and animals within the market in early 2020, 73/923 environmental samples tested positive for SARS-CoV-2-specific RT-qPCR, from various stalls and sewerage systems in and around the market … the presence of high levels of raccoon dog mitochondrial DNA in the metagenomics data from environmental samples identified in the new analysis, suggest that raccoon dog and other animals may have been present before the market was cleaned as part of the public health intervention…

Yes, certainly. That's why there are multiple different prion diseases in humans, such as Creutzfeldt-Jakob Disease, Gerstmann-Straussler-Scheinker Syndrome,Fatal Familial Insomnia, and Kuru.

>Although PrPC is encoded by the host genome, prions themselves encipher many phenotypic TSE variants, known as prion strains. Prion strains are TSE isolates that, after inoculation into distinct hosts, cause disease with consistent characteristics, such as incubation period, distinct patterns of PrPSc distribution and spongiosis and relative severity of the spongiform changes in the brain. The existence of such strains poses a fascinating challenge to prion research.

--Insights into prion strains and neurotoxicity

Probably not.

> Mother-to-offspring prion transmission appears to be prion-strain specific as evidence in other animal species including humans, Syrian hamsters and sheep infected with the classical bovine spongiform encephalopathy (BSE) agent show that progeny from infected females at the moment of gestation do not develop prion disease in the long-term

—Detection of CWD prions in naturally infected white-tailed deer fetuses and gestational tissues by PMCA

As that article and several others show, some prion diseases such as chronic wasting disease of deer can spread from mother to fetus, but there’s no evidence of that ever having happened in humans.

Even though “everyone knows” that mules are infertile, there are actually quite a few well documented cases of fertile mules. This page lists some older examples going back to the 19th century; some more recent (peer-reviewed) cases are listed in

• A fertile mule and hinny in China
• Key Aspects of Donkey and Mule Reproduction
• Fertile mule in China and her unusual foal
• Fertile mules
• A foal from a mule in Morocco

With dozens of instances being documented in spite of farmers actively trying to prevent mules and hinnies from breeding, it's likely that a fairly significant percentage (though of course a minority) of them are fertile.

There are several cases of plants with odd numbers of chromosomes, such as Homeria flavescens (2n = 9). These plants can generally (always?) reproduce through self-compatibility and autogamy, which reduces the issues of odd chromosome numbers.

There are a number of species in which the males have odd chromosome counts, such as the Indian muntjac (6 chromosomes in the female, 7 in the male).

It’s complicated.

On the one hand, chickenpox vaccination means that there will eventually be fewer elderly people who carry chickenpox virus in their nerves, who are susceptible to virus reactivating and causing shingles.

On the other hand, it’s possible that for today’s older adults (who are too old to have been vaccinated as children) who still carry the virus, they’re exposed to less chickenpox in the environment (because fewer children are infected) so they have less immune boosting and the virus may be better able to reactivate. And in fact there has been a gradual increase in shingles for many years now, in many countries; especially in people between 30-60, i.e. those who probably didn't get chicken pox vaccine as children and who aren't old enough to get the shingles vaccine.

On the third hand, there’s apparently something else that may be increasing shingles incidence, other than vaccination. The increasing frequency started before the childhood vaccine was available, and doesn't parallel vaccine usage in general; so while it's possible that's one cause, it's not likely to be the only cause. Other explanations are basically handwaving, "better identification", or "unknown risk factors".

>One theory is that childhood varicella zoster virus vaccination has decreased the circulation of wild-type varicella virus [19, 20]. Without this exposure, the general population receives less exogenous immune boosting against varicella, increasing the risk of virus reactivation [19, 20]. However, studies have shown that the incidence of HZ has been increasing in the United States since before varicella vaccination introduction and is similar in countries with and without varicella vaccination [7, 21, 22]. Enhanced awareness of HZ by patients and healthcare practitioners, increased surveillance, and improved electronic health record coding practices are other potential drivers of the increasing number of HZ cases among middle-aged adults.

--Herpes Zoster and Postherpetic Neuralgia: Changing Incidence Rates From 1994 to 2018 in the United States

Also see

• Modelling varicella vaccination – What does a lack of surge in herpes zoster incidence tell us about exogenous boosting?
• The impact of the varicella vaccination program on herpes zoster epidemiology in the United States: a review

This is why r/AskScience doesn’t allow AI-generated answers, and bans people who provide them.

Maybe.

In sheep and pigs, there’s a complex scenario (“polar overdominance”) in which only heterozygotes with a particular mutation show the phenotype:

> A single nucleotide polymorphism in the DLK1-DIO3 imprinted gene cluster alters gene expression … muscle hypertrophy only occurs in heterozygous animals that inherit a normal maternal allele and the callipyge SNP on the paternal allele (+/C).

—New insights into polar overdominance in callipyge sheep

The details of how this works don’t seem to be well understood and I’m not going to try to summarize the complicated tentative explanations. In sheep and pigs, the muscular hypertrophy phenotype is at least somewhat desirable, but in humans there may be a similar mutation that, in heterozygotes, is associated with severe obesity.

> In a study sample of 1025 French and German trio families comprised of both parents and extremely obese offspring we found a single nucleotide polymorphism (rs1802710) associated with child and adolescent obesity. Analysis of the allelic transmission pattern indicated the existence of polar overdominance, an unusual mode of non-mendelian inheritance in humans previously known from the callipyge mutation in sheep.

—Preferential reciprocal transfer of paternal/maternal DLK1 alleles to obese children: first evidence of polar overdominance in humans

You’ll find that actual evolutionary biologists use “designed” all the time. If your main exposure to evolution is via media popularizers, you might avoid the word, but scientists are adult enough to understand its use.

This is a great question.

B and T lymphocytes are unique in vertebrates because they’re designed to physically chop out and re-link chunks of their chromosomes, as part of the development of antibodies and T cell receptors (V(D)J recombination in Wikipedia). A super simplified sketch

Original chromosome:

—-A—————-B—————

Rearranged chromosome:

—-A-B—————

This is driven by Recombination-activating genes, which look for specific DNA sequences (“A” and “B” in my ludicrously simplified sketch above), cut the chromosome at those signals, and re-attach the broken ends.

So far, so good. But evolution is stupid, and this process happens simultaneously on multiple chromosomes, because antibodies and TcR have multiple chains and those chains are encoded on different chromosomes.

So what’s supposed to happen is:

Antibody heavy chain, chromosome 1: —-A—————-B————— > —-A-B—————

Antibody light chain, chromosome 2: —-a—————-b————— > —-a-b—————

The question is, Why doesn’t RAG hop across the chromosomes and do this:

—-A—————-B————— \ —-A-b—————

—-a—————-b————— / —-a-B—————

Or some other weird combinations that would lead to splicing, chopping, and/or discarding chromosomes?

The answer is (1) RAG needs to see a particular chromosome loop structure that’s formed when the single chromosome is being spliced (Chromosomal Loop Domains Direct the Recombination of Antigen Receptor Genes, but (2) RAG fucks up all the time and that’s one reason lymphomas are such a common tumor (though chromosomal translocations are not the only reason for this).

> Memory B cells acquired, on average, 18 off-target mutations genome-wide for every on-target IGHV mutation during the germinal centre reaction. Structural variation was 16-fold higher in lymphocytes than in stem cells, with around 15% of deletions being attributable to off-target recombinase-activating gene activity

—Diverse mutational landscapes in human lymphocytes

> Canonical chromosomal translocations juxtaposing antigen receptor genes and oncogenes are a hallmark of many lymphoid malignancies. These translocations frequently form through the joining of DNA ends from double-strand breaks (DSBs) generated by the recombinase activating gene (RAG)-1 and -2 proteins at lymphocyte antigen receptor loci and breakpoint targets near oncogenes.

—Aberrantly resolved RAG-mediated DNA breaks in Atm-deficient lymphocytes target chromosomal breakpoints in cis

> inappropriate RAG activity throughout the genome has been implicated in a large variety of human and mouse lymphomas. Mechanisms by which RAG can provoke or perpetuate lymphoma include deregulation of certain genes by translocation to antigen receptor regulatory regions, the formation of chimeric oncogenes, inactivation of tumor suppressor or micro-RNA loci, or activation of oncogenes.

—Recombination Activating Genes (RAG) in Lymphoma Development

It doesn’t change the original question much, but there are actually quite a few well documented cases of fertile mules. This page lists some older examples going back to the 19th century; some more recent (peer-reviewed) cases are listed in

• A fertile mule and hinny in China
• Key Aspects of Donkey and Mule Reproduction
• Fertile mule in China and her unusual foal
• Fertile mules
• A foal from a mule in Morocco

With dozens of instances being documented in spite of farmers actively trying to prevent mules and hinnies from breeding, it's likely that a fairly significant percentage (though of course a minority) of them are fertile.

Others have given great answers. I wanted to point out that the “Red Queen hypothesis” (Wikipedia link) is relevant here. In Lenski’s experiment, conditions were intentionally kept pretty much constant, but in the real world

> species must constantly adapt, evolve, and proliferate in order to survive while pitted against ever-evolving opposing species.… the effective environment of any homogeneous group of organisms deteriorates at a stochastically constant rate. …the evolutionary progress (= increase in fitness) of one species deteriorates the fitness of coexisting species, but because coexisting species evolve as well, no one species gains a long-term increase in fitness

Other people have answered correctly but the details are interesting (and I’m sitting in an airport waiting for my plane to arrive so I have time).

In the big picture, people generally produce “the same” antibodies in that almost everybody tends to target the same places on a pathogen protein. For example, H1N1 influenza viruses have 6-7 places that antibodies preferentially bind to, and different people all target those same places. They’re called “immunodominant” sites, and immunodubdominant sites are less well targeted.

(Because this is biology, nothing is ever 100%, so there are occasionally people who don’t target one or a few sites well, or people who are particularly good at targeting sites that are normally subdominant. Studying these people and understanding why they do this is an active area of research.)

So that’s the big picture, but if you drill down and look at the actual protein sequence of the antibodies that are doing the binding, they are not typically the same. Other comments have pointed to somatic hypermutation as a cause of this, but even ignoring SHM, most people have very different sets of responding antibodies. Antibodies are originally generated randomly, and it turns out that there are many ways to find very similar solutions - there may be billions of ways to get an antibody that binds to H1N1 immunodominant site “Sa”, say.

So if you compare the sequences of antibodies that are apparently doing the same thing - even between identical twins infected with the same virus at the same time - you won’t find much overlap.

But, drilling down yet another level, you will find some some overlap. We call the overlapping sequences, that are shared between different people, “public” sequences, and those that are not shared “private”.

The ability to sequence antibodies in this way is fairly new, with tech that really started to become widespread in the last ten years, so we are still trying to get a handle on the ratio of public to private sequences. If you look at two people, they may share no sequences; if you look at 100, you may find a couple dozen clusters that various people share; if you look at a thousand, who knows? It’s starting to seem that a significant percentage of antibodies are kind of public - someone else out there has something like it; but most are not widely public - it might only be shared among say 5% of the population.

Again, this is an area of very active research, with groups trying to understand the significance and potential uses of public vs private sequences.

H5N1 is more versatile than the vast majority of viruses. There are lots of viruses and H5N1 certainly isn't unique, but it is unusual.

H5N1 is among a fairly small number of viruses that have a very clear and obvious potential to cause human outbreaks, and for that reason public health groups have tracked it closely since it emerged in the 1990s.

Many of the other viruses in that category (obvious human pandemic potential) are also influenza viruses (H7N9, various swine influenza viruses), but there are many others - you've probably heard of Ebola, Monkeypox, and Zika, for example, but there are a dozen or two others including Nipah, Marburg, Lassa fever, MERS-CoV, and so on.

(Bat coronaviruses were also on that list since the early 2000s when SARS, and COVID proved the virologists right.)

Prevalence of diagnosed dental fluorosis is increasing (though in spite of the loaded phrasing in the question it's generally not an actual health risk) and there are probably at least three reasons:

1. Misdiagnosis
2. Improved diagnosis
3. Increased fluoride exposure.

The fluorosis that's increasing is, to a large extent, mild and very mild fluorosis (Current Guidance for Fluoride Intake: Is It Appropriate?; Dental Fluorosis: Chemistry and Biology). That means that the symptoms are not as dramatic as the classic severe fluorosis, and because there are many other disorders that look like mild fluorosis, there's a fair bit of misdiagnosis:

>Thus, misdiagnosis of non-fluoride-induced enamel defects may occur frequently. Reports of unexpectedly high population prevalence and individual cases of fluorosis, where such diagnoses are irreconcilable with the identified fluoride history, highlight the necessity for a more precise definition and diagnosis of dental fluorosis.

--Dental Fluorosis: the Risk of Misdiagnosis—a Review

Because there's increasing awareness of fluorosis it's also more likely to be correctly diagnosed today than it was 20 or 40 years ago, meaning that even if there was no increased prevalence there would still be increased diagnosis.

Finally, even taking away those factors, there is a genuine increase in mild fluorosis, and the reason is probably just what you'd think - Because adding fluoride is so effective and so beneficial, fluoride has been increasingly added to more and more products. When water fluoridation was introduced, the assumption was that people wouldn't be getting fluoride from other sources. Today, since that's obviously no longer true, there's movement toward revising water fluoridation guidelines, but since the current levels are clearly still safe as well as effective, the moves to reducing fluoride levels are cautious so that the baby isn't thrown out with the bathwater.

>In the present review, we discuss the appropriateness of the current guidance for fluoride intake, in light of the windows of susceptibility to caries and fluorosis, the modern trends of fluoride intake from multiple sources, individual variations in fluoride metabolism, and recent epidemiological data. ... An "optimal" range of fluoride intake is, however, desirable at the population level to guide programs of community fluoridation, but further research is necessary to provide additional support for future decisions on guidance in this area.

--Review of Fluoride Intake and Appropriateness of Current Guidelines

Post-vaccination monitoring is active and aggressive (especially in the Scandinavian countries where the link was made). Unfortunately viral surveillance, while a part of normal public health, is underfunded and understaffed, but hey, what could go wrong?

“The article”? There are literally hundreds of them. This is a very well known phenomenon.

Unsurprisingly, the virus infection is much more likely to cause narcolepsy than was the vaccine, so vaccination against H1N1 protects against narcolepsy overall. But since this only happened with a single vaccine, it was replaced by the other vaccines.

For anti-vax loons reading this, I’ll point out that the hysterical anti-vax voices didn’t find this out, it was discovered very rapidly by the usual surveillance that public health groups routinely conduct. Vaccine-associated effects are routinely detected even when they only occur at a 1 in 20,000 incidence (or much lower, as we saw with the J&J COVID vaccine, where adverse effects were rapidly identified at the 1 in 200,000 level). And even though the vaccine overall was protective and beneficial, when these very rare events were detected the vaccine was immediately pulled from use.

Probably not.

In 2017 there was a flurry of media reports claiming that infection with the pandemic H1N1 virus ("H1N1pdm09") might cause diabetes. These were all based on an unpublished presentation, not a paper and not peer-reviewed, from a Norwegian group.

The group subsequently published a more complete study, which was inconclusive:

>Overall, we could not demonstrate a clear association between clinically reported pandemic influenza infection and incident type 1 diabetes.

--Pandemic influenza and subsequent risk of type 1 diabetes: a nationwide cohort study

To help explain what "inconclusive" means, similar studies were able to conclusively link a 1 in 20,000 risk of narcolepsy to a specific vaccine. So presumably if there's any risk it's lower than 1 in 20,000; more likely it’s zero.

As far as I know, no subsequent studies have found any link.

Some diseases could be eradicated if they were eliminated from every person. But many diseases have reservoirs in the environment (tetanus, Legionella, histoplasmosis) or in animals (West Nile, monkeypox, Ebola, MERS). Other diseases arise more or less spontaneously due to e.g. mutation (feline infectious peritonitis -- I can't offhand think of a human example) or recombination with related animal viruses (SARS, SARS-CoV-2). Since these diseases don't depend on remaining in the affected population, they wouldn't be eliminated by clearing them from that population.

>if we were lucky enough to get to a point where nobody would be infected by smallpox, would that mean the end of smallpox

That's exactly what happened, but there was nothing "lucky" about it - it was the result of a decades-long enormous vaccination and eradication effort by every country on Earth,

It’s debated whether domestic dogs are species or subspecies. The arguments are arcane and extremely tedious. Since it’s pretty much irrelevant to the question here (are there five thousand species since humans appeared, or five thousand and one?) I’m not interested in this semantic argument.

Yes, hundreds of them. Mankind dates back maybe 200,000 years, if you limit it to Homo sapiens, and there are many species far younger than that:

>Haplochromine cichlid fishes of Africa’s Lake Victoria region encompass >700 diverse species that all evolved in the last 150,000 years.

--Ancient hybridization fuels rapid cichlid fish adaptive radiations

So there's hundreds of new species far younger than humans, in a single lake.

Glaciation (including the most recent Ice Age, which is of course more recent than humans) has also led to lots of speciation, as populations became isolated and diverged. For example:

>Pleistocene glacial cycles resulted in a burst of species diversification... By sampling across the geographic range of the five kiwi species, we discovered many cryptic lineages, bringing the total number of kiwi taxa that currently exist to 11 and the number that existed just before human arrival to 16 or 17. We found that 80% of kiwi diversification events date to the major glacial advances of the Middle and Late Pleistocene.

--Explosive ice age diversification of kiwi