In discussions on the H1N1 influenza strain, there were mentions of its fitness and how it was inappropriately measured. These things could have been fleshed out somewhere, but I can’t find any explanations.
It would be nice if viral fitness is defined, and how it can be quantitatively assessed, within the context of the H1N1 influenza strain (or other viruses).
Differential reproduction, which will be very context-dependent.
Care to add some flesh?
This recent paper may also be useful:
It is critical also to distinguish fitness from virulence.
Sure; sorry, I’ve been out hiking.
One example: serially passaging a virus in cultured cells increases its fitness in that environment, while decreasing its fitness in vivo.
If one hits a sweet spot at which in vivo infections still occur but with no symptoms, maybe with greatly reduced transmission (decreased in vivo) fitness, one has created a live vaccine.
It’s not easy.
…although there are evidences that viral fitness and virulence are positively correlated.
https://www.sciencedirect.com/science/article/pii/S0042682210002734
There is also evidence of negative correlation between viral fitness and virulence.
https://jvi.asm.org/content/86/22/12228
There is no expectation that there will always be a positive correlation between fitness and virulence which is why @swamidass was correct when he said that we should distinguish between them.
It is easy to see reasons why there can be a correlation. Increased reproduction within the host is likely to simultaneously cause more severe disease, but also increase the number of infectious agents in droplets of transmission for example, which can then mean increased transmissibility.
But that doesn’t make it identical with fitness, and there are complications that can undermine what might initially seem to be well-grounded inferences. For example, if the severity of disease also increases severity of symptoms, it can inadvertently cause hosts to become better at detecting other infectious hosts, leading to a net reduction in transmissions. That means we also need to consider the difference between within-host and between-host fitness. It’s technically possible that a within-host increase in reproduction is so large it generally kills the host before they get to transmit, leading to the virus mutant’s own extinction.
So, it’s complicated, and there must be some relationship between different factors such as virulence, within-host reproductive rate, and transmissibility, where a virus has to trade off adaptations to successfully persist in some population in the long term.
That’s just not true.
Of note, it seems Sanford/Carter measured fitness of flu using a measure of virulence…oops…
Viral fitness, in an absolute sense, is measured in terms of doubling time. Carter and Sanford didn’t do anything to measure H1N1 fitness. Carter said so in an email when I asked him.
Edit (my apologies to the people who liked before the edit, I hope this does not change your opinion):
There are also well-worn ways to measure relative fitness involving growing a reference strain and the strain in question for the same amount of time under the exact same conditions, and then allowing them to infect the same host cell population, and documenting their respective population sizes after some amount of time. Carter and Sanford also did not do this.
As far as I’m concerned, this is a closed issue. They made claims related to viral fitness. They did not measure, or even attempt to measure, viral fitness, neither absolute nor relative. So there is no basis for their claims. Fin.
Sure. As John Mercer stated before your post, viral fitness is defined as…
While all environments are subject to some degree of dynamic, nothing in the animal kingdom approaches disease in terms of pace of change. Within a span of weeks, the same virulent virus can go from a steeply climbing rate of reproduction to falling off a cliff, just due to the near extermination of the infected host population. So fitness always has to be contextually defined. Same thing goes for contact between populations which have adapted to a virus, such as smallpox, with another which is immunologically naïve. That can be devastating to the newly exposed people, but the virus itself may be exactly the same. There, both virulence or fitness are contextual, not inherent traits of the virus.
The mode of transmission also influences the relationship between virulence and fitness. Rabies, aside from recent history making novel medical interventions, is 100% fatal once symptoms present, but unlike the common cold is not given to respiratory transmission. The fitness and virulence of rabies is not positively correlated for transmission. The same can be said for STDs, exhibiting symptoms hardly enhances transmission.
It appears that nature just does not operate by some fundamental principle that the more virulent the virus, the more fit. If the language we use to describe nature fits awkwardly, then we must qualify our language and refine our concepts accordingly. In the case of fitness and contagious disease, that means identifying and stipulating the many associated particulars.
What would be the reference and sample strains with regards to H1N1?
Is this metric of viral fitness always inappropriate or are there situations where it can be valid?
Thanks for this.
So virulence is just one factor influencing the fitness of viruses, but can it be used alone as a means of evaluating viral fitness?
This is wrong. We have to look to see if there is a correlation or not.
Just like in the Lenski LTEE. Makes sense.
Interesting.
Okay, so viral fitness is defined the same ways as for organisms, but I am guessing the specifics differ.
For example, a relatively more fit rat species will produce more offspring using sexually reproduction. What is the virus equivalent?
Fitness means differential reproduction, while virulence refers to the severity of disease due to a pathogen.
It’s a category error, because virulence/morbidity is not a measure of fitness. Apples and oranges.