Viruses become less deadly over time?

[ElliotSmith]

Viruses become less deadly/virulent over time?

 

[Astronuc]

Viruses become less deadly/virulent over time?

Not necessarily. Consider small pox, which has been around for thousands of years.

We've seen variants of SARS-Cov-2, which are less deadly/virulent, but Delta is more deadly than earlier variants, and Omicron appears to be more infections, but we are waiting to see if it as serious as Delta, or less.

In most cases, survivors develop some immunity, which can be passed on to offspring to some extent.

 

[phyzguy]

There is some evolutionary pressure for infectious diseases to become less deadly over time. If a disease kills you quickly, then you are not interacting with other people so that you can pass it on. The best case for the virus is that you go about your business spewing more virus into the environment where it can infect other people. There is also evolutionary pressure for the virus to become more infectious, so it is passed on to more people. So viruses tend to become more infectious and less deadly with time.

 

[berkeman]

Viruses become less deadly/virulent over time?

Seriously? Is the "G" key on your keyboard missing or stuck?

 

[Laroxe]

Really it's all a matter of fitness and there are a lot of things that can impact on this and of course a lot of these things are not static as both pathogen and host present moving targets for each other. It makes sense that causing severe illness and death isn't in the best interests of the pathogen, but other variables might make this irrelevant. An example might be in diseases that effect multiple species, killing one species that might be relatively unimportant might not cause much selective pressure, it's not easy to work out.

 

[Ygggdrasil]

The belief that viruses will evolve to be less virulent over time is a widely repeated myth. For example, here's an article from PolitiFact that discusses the issue in lay terms and has a list of references for further reading:

A claim that viruses and other pathogens always evolve to become less lethal is false:

• A number of factors influence the way the virulence of a virus — that is, how harmful it is to its host — affects its ability to survive and spread; in some cases, higher virulence may help a virus survive and spread.
• Many viruses have evolved to become more lethal over time.

https://www.politifact.com/factchec...s-and-other-pathogens-can-evolve-become-more/

 

[valenumr]

It's due to a theory of one Theobald Smith, circa 1880. It's not even wrong.

 

[phyzguy]

The belief that viruses will evolve to be less virulent over time is a widely repeated myth. For example, here's an article from PolitiFact that discusses the issue in lay terms and has a list of references for further reading:

For the record, I didn't say that viruses will always evolve to become less virulent over time, I said, "There is some evolutionary pressure for infectious diseases to become less deadly over time". I think this is true, why shouldn't it be?

 

[Astronuc]

"There is some evolutionary pressure for infectious diseases to become less deadly over time". I think this is true, why shouldn't it be?

Not necessarily true, if a virus resides in other hosts, e.g., swine, water fowl (as in the case of influenza), or bats and other mammals (coronavirus), where the virus could be relatively benign, then it jumps to humans where it is more lethal. In that sense, viruses are opportunistic.

African fruit bats are likely involved in the spread of Ebola virus and may even be the source animal (reservoir host). Scientists continue to search for conclusive evidence of the bat’s role in transmission of Ebola. 1 The most recent Ebola virus to be detected, Bombali virus, was identified in samples from bats collected in Sierra Leone.2

https://www.cdc.gov/vhf/ebola/history/summaries.html

As long as there are other hosts to sustain a virus, it could survive and mutate to become more deadly or less deadly. Humans would have to be immunized against such viruses.

 

[jim mcnamara]

About virulence changes:
Some virus pandemics remain awful in terms of fatalities, others become less awful.

Example of how we keep getting new viruses:

Covid is very likely the result of zoonosis.
Interspecies spillover bats->humans

Influenza can come from wild ducks->domestic ducks->pigs->humans, a chain over spillovers.
Zoonotic H5N1 avian influenza:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3321902/

Virulence of new flu strains varies due to previous exposures and immunity to similar antigens.

Extreme example: 50 million people died in 1918-19 from an H1N1 strain. One cause was that the most recent prior pandemic of H1N1 dated back to 1882-4. So young people died in droves. No immunity. Older people had lower fatality rates than did much younger members of the population. The opposite of what has been the case for Covid -- up to now.

In 2009 there was another H1N1 outbreak, and public health people were afraid of a repeat of 1918.
https://www.cdc.gov/flu/pandemic-resources/2009-h1n1-pandemic.html

As mentioned, Variola (small pox) never became less virulent over thousands of years. Infected persons died at a rate of 3 out of 10 and the disease slowly moved to become worldwide.

CDC history:
https://www.cdc.gov/smallpox/history/history.html

Example of Coronavirus quasispecies that apparently became tame: Coronavirus colds.
https://www.cdc.gov/coronavirus/general-information.html

As far as Omicron goes, it first appeared that some of the changes seemed similar to Coronavirus cold viruses, like someone had a cold, caught Covid and then the virus assimilated some of the cold strain's RNA.
There is no direct evidence of this, just some genomic assays. Which cannot rule out chance changes.

I have seen no further report than this opinion piece - it is not a peer reviewed science report
https://www.forbes.com/sites/williamhaseltine/2021/12/02/omicron-origins/?sh=5bd6e0b41bc1

If you know of a more standard paper please post a link.

 

[haruspex]

There is some evolutionary pressure for infectious diseases to become less deadly over time

If a pathogen new to the species kills the victim nearly as quickly as it renders the victim infectious then to persist it must evolve in one or more of three ways:
- kill more slowly (in which case the victim may well fight it off rather than die)
- become infectious faster
- become more readily transmitted
The omicron variant has certainly gone the third route, so no particular reason to suppose it is also less deadly. But it would certainly be no disadvantage to the virus to be less deadly, so we can hope that one of its mutations has that side effect.

Wrt the data from South Africa, it is hard to know yet what that implies. There may be many in SA who had an earlier variant, undiagnosed, and thereby acquired some degree of immunity to $\omicron$.

 

[Laroxe]

If a pathogen new to the species kills the victim nearly as quickly as it renders the victim infectious then to persist it must evolve in one or more of three ways:
- kill more slowly (in which case the victim may well fight it off rather than die)
- become infectious faster
- become more readily transmitted
The omicron variant has certainly gone the third route, so no particular reason to suppose it is also less deadly. But it would certainly be no disadvantage to the virus to be less deadly, so we can hope that one of its mutations has that side effect.

Wrt the data from South Africa, it is hard to know yet what that implies. There may be many in SA who had an earlier variant, undiagnosed, and thereby acquired some degree of immunity to $\omicron$.

Again its all down to the effects changes have on fitness. If you consider diseases like cholera, which spreads by faecal contamination, changes that make symptoms like diarrhoea worse, actually increase the chances of spread potentially increasing the organisms fitness.
It is thought that HIV is becoming less severe but working out why can be difficult, this virus is a genetic mess and there are all sorts of possible selective pressures. This is a report which explains some of the thinking
https://www.bbc.co.uk/news/health-30254697
its based on this study: https://www.pnas.org/content/111/50/E5393
The data we have on Ebola which appears to clearly limit its own spread because of its severity really doesn't help at all, even just looking at a single strain, the Zaire ebolavirus shows a case fatality rate that ranges from 39% to 89% and this appears unrelated to the available medical resources. There is also no clear direction for these rates over time.
It appears that we are now starting to see some evidence that Omicron is indeed less severe, it apparently multiplies quickly in the upper respiratory tract leading to increased shedding of the virus but it doesn't colonise the lower resp. tract as effectively though this still needs confirming. However its been decided in England that despite the rapid increase in infections no further restrictions will be imposed, its not going to be stopped and it might provide additional immunity with relatively little risk. A little Christmas hope.

 

[Ygggdrasil]

Researchers recently identified a new, more virulent strain of HIV. It is associated with higher viral loads among those infected and faster decline in T-cell counts. Luckily, the new variant seems to have a similar susceptibility to most antiretroviral drugs used to treat HIV infection:

A highly virulent variant of HIV-1 circulating in the Netherlands
https://www.science.org/doi/10.1126/science.abk1688

Abstract:

We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV—CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences—is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence.

Popular press summary: https://www.nature.com/articles/d41586-022-00317-x

The findings, published in Science on 3 February1, serve as a reminder that viruses do not always evolve to become less virulent over time. Reports that infections with the Omicron variant of SARS-CoV-2 tend to cause mild COVID-19 symptoms have fuelled the narrative that the virus is becoming less deadly. “This is not how it works,” says Emma Hodcroft, a molecular epidemiologist at the University of Bern. Although HIV and SARS-CoV-2 are different in many ways, “it’s not a given that SARS-CoV-2 will become milder”, Hodcroft says.

Relevant perspective piece published along side the research article in Science:

When viruses become more virulent
https://www.science.org/doi/10.1126/science.abn4887

The evolution of virulence—the degree to which a pathogen sickens, kills, or otherwise reduces its host’s fitness—depends on the biology of infection and transmission (1). A more virulent virus may be less transmissible because in killing its host, it reduces the opportunity for transmission. But virulence and transmissibility can be intrinsically linked, so that to maintain or increase infectiousness, a virus must be virulent. On page 540 of this issue, Wymant et al. (2) describe the emergence of a more virulent and transmissible variant of HIV that has spread to 102 known cases, mostly in the Netherlands, over the past decade. This finding raises questions about the selective pressures and molecular mechanisms that drive increased virulence and transmission.

The full article is worth a read and concludes with some thoughts on the relevance of this issue to the COVID-19 pandemic.

 

[Laroxe]

While virulence and transmissibility are important their involvement in evolution is only because of their possible effect on fitness and there are a large number of variables that might influence this, some of which may not even be recognised. I'm not even convinced that comparing HIV to Covid 19 is in any way useful and I think there are some serious problems the these speculations.
HIV is a bit of a mess really, its an RNA virus with hardly any error checking for its genetic material when it reproduces so despite high viral loads early in the course of infection, most are unviable, infection requires a high inoculum but once established, the high error rate means that HIV is a veritable variant factory. People develop their own variant profile. Its also described as a lentivirus as following the initial acute infection the virus tends to remain inactive in infected cells until that cell is activated, usually by other infections.
I really don't know how they have established their views about transmissibility or virulence, we have a good idea about how its transmitted and the fact it requires particular conditions and behaviours can be very limiting.
Current treatment guidelines are to begin treatment as soon as possible after diagnosis and as the drugs used in treatment remain effective they can't really have any data about progression over time, something else which can be highly variable over time. They say this variant arose some 30 years ago and they don't provide evidence of increased rates of infection or in fact increased mortality.
Of course, to predict the likely evolution of a pathogen, we would really need a detailed knowledge of all the possible variables that might act as selective pressures and these pressures are unlikely to be consistent. There are some indicators that can help based on similar viruses that cause similar pathologies in similar animals and the research does provide more reliable information than augers of the past.

 

[jim mcnamara]

Virulence is a messy way to view pathogens. So an an extreme example of hosts reacting to 100% virulence is here:
https://virologyj.biomedcentral.com/articles/10.1186/s12985-019-1244-3

Mimivirus and other giant viruses that attack amoebas have elicited major changes in the host amoebae. Note that if an amoeba becomes infected its ultimate fate is sealed. Meaning that all successfully 'attackable' amoebic genomes are going extinct in the long term.

The point is that this scenario is for a very virulent pathogen. Virulence defined as the death rate post infection.

Which is 100% deaths in most of the interactions of virus vs. amoebae

So let's look at an example of a host under extreme selection pressure with 100% virulence and death from infection:

Emiliana huxleyi (an amoeba) has become like the Cheshire Cat, and puts on a disappearing act. It forms an impervious calcite shell - virus-proof - in the diploid stage. The haploid stage is very resistant to viral infection. What you cannot see you cannot infect, I guess.

 

[Andrew Wright]

You could argue that social isolation during experience of Covid symptoms would cause all viruses that make humans cough have an increased survival pressure not to produce symptoms. Perhaps viruses can learn to "hide"? In fact I read somewhere that Coronavirus evolved a very sophisticated relationship with bats where it produced almost no symptoms. Bats have developed this kind of compromise with many viruses (I think)

 

[Andrew Wright]

I can provide a counter argument to the original suggestion that there is survival pressure for a virus to keep the host alive so the virus can reproduce.

Surely there would be viruses that spread more easily during and after the decay of the host? Humans treat their dead with more attention than most animals rotting in the wild.

 

[Laroxe]

I can provide a counter argument to the original suggestion that there is survival pressure for a virus to keep the host alive so the virus can reproduce.

Surely there would be viruses that spread more easily during and after the decay of the host? Humans treat their dead with more attention than most animals rotting in the wild.

Because viruses do not have their own metabolic machinery, they require their host cells to be alive and metabolically active, this means that most do not survive for very long after death. The few that can survive for significant periods, e.g. smallpox, do so in a non-reproductive state and require a living host to become active. Whether the death of the host acts as a selective pressure really depends on a whole range of factors, for a virus that is easily transmitted from people who are infectious for a period of time when there is a reasonable population of non-immune hosts, eventual deaths would be pretty irrelevant. So the selective pressure is really whether the virus has the time to infect others, ideally over a period in which they are asymptomatic and so remain active and social. You have to remember that disease is the product of an interaction between a virus and the host, viruses tend to specialise and can only infect specific target cells. The immune system of bats appears to tolerate the presence of quite a few viruses, controlling their reproduction while avoiding disease, the exact mechanism of this is still not clearly understood, but even bats have their own viral diseases that can be fatal.
Bacteria on the other hand love a dead body, particularly one of the same species, this is one of the reasons that humans do pay attention to dead bodies, some pathogens can live for quite some time and many of the bacteria responsible for putrefaction are very dangerous. Even animals will avoid dead bodies after a period of time, with only a few species that specialise as scavengers able to tolerate the bacterial load and toxins produced. It's even suggested that we have a behavioural immune system, we find the smell of putrefying flesh highly aversive and use smell and taste to detect evidence of spoilt foods.

 

[jsgruszynski]

Viruses become less deadly/virulent over time?

When the virus is highly lethal, yes - because it's "kills the golden goose" of a viable host population to quickly and too effectively. So those mutations that survive will tend to "let the host have a chance" by favoring less lethal alleles because that preserves reproductive options at all. The ideal situation is one where the host isn't greatly harmed yet the virus is free to multiple. The classic example is the common cold and influenza.

In the case of coronaviruses (and most cold viruses like rhino and adeno), the virus high mutability is in large part to already favor this less lethal scenario. This is also why vaccine claims against coronaviruses should always be treated with extreme skepticism and doubt - they mutate far too quickly to make vaccines viable because by the time an epidemic growth occurs, there's already the next mutated versions within the epidemic population - it's already too late for a vaccine. This is why a successful one has never been created and probably never will be.

 

[Laroxe]

When the virus is highly lethal, yes - because it's "kills the golden goose" of a viable host population to quickly and too effectively. So those mutations that survive will tend to "let the host have a chance" by favoring less lethal alleles because that preserves reproductive options at all. The ideal situation is one where the host isn't greatly harmed yet the virus is free to multiple. The classic example is the common cold and influenza.

In the case of coronaviruses (and most cold viruses like rhino and adeno), the virus high mutability is in large part to already favor this less lethal scenario. This is also why vaccine claims against coronaviruses should always be treated with extreme skepticism and doubt - they mutate far too quickly to make vaccines viable because by the time an epidemic growth occurs, there's already the next mutated versions within the epidemic population - it's already too late for a vaccine. This is why a successful one has never been created and probably never will be.

I'm not sure why you say there isn't a successful vaccine, there are several, and I think you might be misunderstanding immunity.
Its true that RNA viruses tend to have a high reproductive error rate so mutations are frequent, in fact as infection progresses every infected individual has in effect their very own variant, that's one of the reasons they can trace infections. However there are lots of potential drivers for the selection of certain variants and few viruses are very predictable, you suggest that influenza is a classic example of the selection of less pathogenic strains/variants. There are in fact frequent outbreaks of highly virulent influenza viruses, not many people would consider the 1918 pandemic as evidence of the virus becoming less virulent.
The way in which we respond to viral infections varies depending on the virus but the development of adaptive immunity is complex and generally very efficient, the first thing to remember is that our body learns to recognise and attack all of the exposed antigens on the virus surface and there are lots of them. So we produce lots of different antibodies, which can have different levels of effectiveness against a virus. Our body also learns to recognise the virus and virus infected cells for destruction, by T cells, using slightly different target proteins.
A single mutation may change one of the surface proteins but it needs multiple mutations to allow the virus to evade, at least partially, the antibody response. This became an issue when the Delta variant appeared, causing more severe disease. However, the variant with the greatest ability to evade vaccine induced antibodies was the Beta variant, which had 23 mutations, 8 of which were on the spike proteins, it had been quickly identified that it was antibodies to the spike protein that conferred the greatest protection, and high levels still conferred protection. The next issue was in how persistent the antibodies were, again this varies with the virus and in the case of Covid the answer is not very, maintaining high antibody levels is very costly in terms of our physiological resources so they tend to reduce over time. In Covid 19, like influenza antibody levels fall quite rapidly over a period of a few months, however memory B cells remain in circulation and these are activated if we encounter the virus again, it just takes longer to re-establish the high antibody levels. This does mean that infection can get established but as the response is much quicker than in non-immune individuals, people are far less likely to become seriously ill. The vaccinations have in fact been highly effective in reducing serious illness and deaths.
In each re-infection our immune system refines the antibody response, tuning it to the current variant and increasing their effectiveness. So the vaccines have been very effective in preventing serious illness or deaths, the figures are widely available. In fact, currently it appears that the ability to evade part of our antibody response seems to have conferred very little fitness advantage, in fact the beta variant has largely disappeared. In fact its difficult to identify why certain variants have become dominant, in the case of omicron it has been suggested that the rapid rate of reproduction might explain its success.
We are still finding things out about this infection and there were certainly mistakes in the initial vaccination program.

 

[jim mcnamara]

Virions make up about .04% of Earth's biomass. In terms of numbers of virions this is an astronomical number.
https://www.visualcapitalist.com/all-the-biomass-of-earth-in-one-graphic/

Virus are r selected with a vengeance - RNA viruses "deliberately" (an anthropomorphism) create errors in making new virus particles. This rate of mutations allows processes like zoonosis - transfer of diseases - between unrelated mammals to occur. It creates variants which may help to evade some immune system protection from infection. It also means that a LOT virus particles never cause any disease and degrade instead.

Search for Covid in animals:
https://www.nature.com/articles/d41586-021-00531-z
r and K selection, Northern Arizona content:
https://www2.nau.edu/lrm22/lessons/r_and_k_selection/r_and_k.html

 

[berkeman]

When the virus is highly lethal, yes - because it's "kills the golden goose" of a viable host population to quickly and too effectively. So those mutations that survive will tend to "let the host have a chance" by favoring less lethal alleles because that preserves reproductive options at all. The ideal situation is one where the host isn't greatly harmed yet the virus is free to multiple. The classic example is the common cold and influenza.

In the case of coronaviruses (and most cold viruses like rhino and adeno), the virus high mutability is in large part to already favor this less lethal scenario. This is also why vaccine claims against coronaviruses should always be treated with extreme skepticism and doubt - they mutate far too quickly to make vaccines viable because by the time an epidemic growth occurs, there's already the next mutated versions within the epidemic population - it's already too late for a vaccine. This is why a successful one has never been created and probably never will be.

This is nonsense. Check your PMs.

 

[ddouglas86]

Viruses become less deadly/virulent over time?

No, they not. We just have more knowledge, prevention, and medicine to treat them. You should ask about mental health issues, addictions etc. - this stuff is more and more deadly :D

 

[berkeman]

No, they not. We just have more knowledge, prevention, and medicine to treat them. You should ask about mental health issues, addictions etc. - this stuff is more and more deadly :D

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