Would antibodies then be a thing within the cell part of the immune system, like some kind of an organelle?
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You make some good points! Having skin types impact the chance of infection is a good idea, and being able to choose just a toxin type before evolving a circulatory system and an actual immune system is a really good idea, maybe with the caveat of needing to choose one that doesnโt also damage your cells.
Iโm not sure if microbes should have a dedicated mish, the waya I envisioned it only your organism is able to get infected, it would definetly be cool but it would need a lot of optimization as calculating the microbes infecting every evolved creature and how they respond to them would need a lot of computing power.
I also donโt know if the way a player acts should impact their chance of getting infected, the way i thought it it wasnโt the player getting a disease but more the species as a whole having to respond to common diseases that evolve along side them, maybe the type of food the specie eats and their behaviour could impact the chance? I dont think it would be necessary but it would be cool. This is also why i think they shouldnโt kill the player but more so debuff the species as a whole, itโs more realistic and also because in a gameplay prospective it just wouldnโt be fun for the player to randomly die.
Finally i donโt really get how my system is overly complicated, in my mind it was basically as simple as an immune system could be made in this game, which is also why you pointed out some additions it might need, if anything with your comment I realize it might have been a bit too simple and general. I also donโt really get how it would impact the CPU, it would only need the autoevo to calculate at maximum nine different interactions, which it can already do tens of times over right now for the microbe stage.
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Speaking of the toxin thing, would you first unlock if from having reached enough of a debuff since toxins arenโt the easiest things to unlock currently?
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Death from infection is unlikely, even with average immunity. As I said, immunity will affect the population of your species and the likelihood of infected individuals appearing. I donโt really like the idea of โโ"simply affecting your bodyโs efficiency"; it sounds as if every individual in your species is sick.
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I mean it would increase the fitness of the overall species indeed.
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I think we just have to agree to disagree, there would need to be selective pressure for an immune system to evolve, so if not all most of your species would have to be infected for there to be enough pressure, which is why I think it affecting your species chance of survival makes the most sense, it also isnโt too unrealistic, many parasites and diseases in the wild infect most of all organisms of a species, just at the top of my head certain populations of koala have a 90% rate of infection with a chlamydia strand. Finally I think simulating reates of infection between members of your species would definetly be cool, but it would add a whole level of calculations the system needs to do that i donโt think is worth it.
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Would interspecies diseases like rabies also be allowed to exist?
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In multicellular organisms, innate immunity represents the oldest and most immediate line of defense. It does not rely on clonal selection or somatic gene rearrangement, but instead uses a set of germline-encoded receptors and effector mechanisms to mount a rapid, relatively coarse response to invading pathogens. From an evolutionary perspective, innate-like immune mechanisms are found in insects, worms, and even plants, whereas true adaptive immunityโcomprising B and T lymphocytes with highly diverse antigen receptors and long-lasting immunological memoryโappears only in jawed vertebrates. This indicates that innate immunity predates adaptive immunity in evolutionary time. At the level of an individual infection, innate immunity also responds first: once pathogens breach physical and chemical barriers such as skin and mucosal surfaces, neutrophils, macrophages, dendritic cells, and natural killer cells are activated within minutes to hours, whereas adaptive responses typically take several days to develop in secondary lymphoid organs through antigen presentation and clonal expansion.
Within innate immunity, pattern recognition receptors (PRRs) function as the primary โsensorsโ and โswitchesโ of host defense. Rather than recognizing unique antigens from individual strains, PRRs detect conserved molecular structures shared by broad classes of microbes, known as pathogen-associated molecular patterns (PAMPs), such as lipopolysaccharide in Gram-negative bacteria, fragments of peptidoglycan, flagellin, or viral double-stranded RNA and unmethylated CpG DNA. PRRs also sense danger-associated molecular patterns (DAMPs) released from stressed or dying host cells, including extracellular ATP, uric acid crystals, and self-nucleic acids, thereby responding to endogenous danger signals as well. These receptors are widely expressed on macrophages, dendritic cells, neutrophils, and epithelial cells, and their genes are fixed in the germline rather than diversified by V(D)J recombination, allowing them to recognize danger and initiate signaling within a very short time after pathogen entry.
PRRs can be classified into several major families according to their localization and structure. Membrane-bound PRRs such as Toll-like receptors (TLRs) are expressed on the plasma membrane and endosomal membranes, where they sense bacterial cell wall components and viral nucleic acids, respectively. Cytosolic PRRs, including NOD-like receptors (NLRs), RIG-I-like receptors (RLRs), and the cGASโSTING pathway, detect bacterial fragments, viral RNA, or aberrant DNA in the cytoplasm and can assemble inflammasomes that activate caspase-1 and promote the maturation of IL-1ฮฒ and IL-18. In addition, soluble pattern recognition moleculesโsuch as complement components, mannose-binding lectin, and C-reactive proteinโbind to microbial surfaces in the circulation and facilitate opsonization and clearance. Once engaged by PAMPs or DAMPs, PRRs trigger the production of inflammatory cytokines and type I interferons, enhance phagocytic and microbicidal functions, and upregulate MHC and costimulatory molecules while secreting polarizing cytokines that shape subsequent T cell responses. Thus, pattern recognition receptors form the molecular basis of the rapid innate detection of danger and serve as essential hubs linking innate and adaptive immunity.
Although the ontogeny of immune cells, particularly lymphocytes, is highly complex, the evolution of host defense can be schematically viewed as a stepwise progression from cell-intrinsic immunity in single-celled organisms, to innate immunity in multicellular animals, and finally to lymphocyte-based adaptive immunity in vertebrates.
This simplified view emphasizes that sophisticated adaptive responses emerged on top of pre-existing innate and cell-intrinsic defense mechanisms, rather than replacing them.
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Welcome to the forum @Sillywolf !
Your summary does seem to be accurate to the evolution of immunity across various organisms, though I am afraid the developers of Thrive may have more important tasks to do than develop an ultra-complex infection and immunity system into the game. Still a good suggestion nevertheless that could perhaps be simplified to be more acceptable from development time standpoint.
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As a person who has taken Immunology, it is always great to see other people who also appreciate its complexities.
Wait, was that summary written by ChatGPT? Not saying you did. AI writing is so rampant, it is hard to believe what people write anymore.
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Welcome to the forum, @Sillywolf.
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Thanks for asking, and I really appreciate you being honest about your concerns with AI writing.
To be transparent, I did use AI as a tool when putting that summary together. Iโm an undergraduate biology major and currently taking immunology, and the points in that post reflect what Iโve been learning in class and from recent review articles. I didnโt just copy whatever the AI generated โ I went through the content myself, compared it with my course notes and understanding, and asked it to provide references and DOIs so I could double-check the scientific details.
I honestly didnโt realize you felt this strongly about using AI as a learning aid, and Iโm really sorry if that came across as misleading or disrespectful in any way โ that was never my intention.
For transparency, the main reviews I relied on were:Li D, Wu M. Pattern recognition receptors in health and diseases. Signal Transduct Target Ther. 2021;6(1):291. doi:10.1038/s41392-021-00687-0.Chen R, Zou J, Chen J, Zhong X, Kang R, Tang D. Pattern recognition receptors: function, regulation and therapeutic potential. Signal Transduct Target Ther. 2025;10(1):216. doi:10.1038/s41392-025-02264-1.
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Is Janewayโs Immunobiology used as a textbook for the course? It was the textbook used for my Immunology course.
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No, itโs not used as our course textbook, but I bought the Chinese translation and Iโm using it as a reference book.
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A lot of people would love to have scientifically accurate and complicated immune system, including myself (since I have a Bachelorโs in Molecular Cell Biology). Unfortunately, the developers cannot make it too complicated, as not everyone who will play the game may have the educational background to understand all the science if it is too in-depth. There is a possibility a โsuper-scientificโ mode/mod may be developed for the game eventually.
Also, feel free to make a thread on the โIntroductionsโ topics sections.
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Janewayโs Immunobiology is an excellent textbook. I also really like Scott F. Gilbert & Michael J. F. Barresiโs Developmental Biology, Robert F. Weaverโs Molecular Biology, and R. A. Weinbergโs The Biology of Cancer โ theyโre all fantastic as well.
But in my experience, another really important way to learn is to actually read the original research papers. I feel like working through primary literature can sometimes help you make progress even faster.
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Yes. This is why I actually really like my Graduate courses in Nutritional Biochemistry and Metabolism. I have to actively read papers and sort out information from them. People donโt realize how much in-depth science in Biochemistry, Microbiology, Genetics, Metabolimics, Anatomy and Physiology, Immunology, Histology, and other fields one has to know in order to properly understand what is going on with Nutrition at the molecular to the organismal level.
This is an example of a paper I had to read:
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Exactly! I often feel that the different subfields of biology, and the related disciplines around them, are like one huge web. Every part is closely or indirectly connected to the others, and Iโm constantly struck by how similar and beautifully intricate they are, both on the macro and the micro level.
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This connectability is ought to be taken into account when we get to the stages with the immune system in question.
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