It’s a truism that strength of immunity depends on many factors such as antigen types and doses, organism’s replicative capacity and evasion strategies, number and types of cells involved, responder’s age and health status, to name a few. Could the type of organism influence the nature and strength of immune response? Sure but if human immunity were as a rule weaker against bacteria and fungi compared to viruses, as this question implies, that would represent a huge open sesame to the former and only humans would have emerged worse off from the ensuing bout.
Certainly, adaptations entail a trade-off but choosing to respond more weakly to entire classes of micro-organisms isn’t a trade-off, it’s more akin to signing one’s own death sentence. After all, micro-organisms mutate at a much faster rate than humans. Thus, the fact that we are still around, all >7 billion of us and counting, suggests human adaptations to evolutionary selection pressures entailed robust immunity against all types of pathogens. What that robust immunity entails differs from organism to organism, not between different classes of organisms.
In case this question implies robust immunity to mean serum antibodies that can transfer protection, this is not the exclusive purview of anti-viral immunity alone but also works against bacteria such as those that cause diphtheria (Corynebacterium diphtheriae – Wikipedia), pertussis (Bordetella pertussis – Wikipedia) and tetanus (Clostridium tetani – Wikipedia).
This answer explains why stronger immune responses to an entire class of micro-organisms such as viruses is unlikely because
- We aren’t specifically more susceptible to bacterial and fungal infections as our immune systems weaken with age.
- Not just viruses but all types of microbes from bacteria to a variety of parasites continue to impose selection pressure on us.
- No single entity within the immune system can perceive an entire organism. This implies evolution proceeds by way of incremental tweaks by human and microbe, the two parties engaged in these evolutionary trade-offs.
We Aren’t More Susceptible To Bacterial & Fungal Infections As We Age
If human immunity to virus is more robust than that to bacteria or fungi, what happens as our immune system weakens with age and Immunosenescence – Wikipedia sets in? Specifically, if ‘we develop robust immunity after viral infections, but not bacterial infections‘, do we become disproportionately more susceptible to the latter as we age, as this question implies? No, rather, the deleterious effects of immunosenescence seem to involve increased susceptibility to infectious diseases per se, not just increased susceptibility to bacteria and fungi but not viruses.
In fact, data from countries like the US suggests immunosenescence represents an equal opportunity vulnerability since it entails impaired ability to control both viruses such as Human cytomegalovirus – Wikipedia (CMV) (1, 2) as well as bacteria such as Streptococcus pneumoniae – Wikipedia (3). Even though pneumonia is common among the elderly, often the trigger remains unknown in ~50% of elderly pneumonia patients even in the US (4). Anybody’s guess if it’s a virus such as influenza or Human respiratory syncytial virus – Wikipedia (RSV), bacteria other than S. pneumoniae or fungus such as Chlamydia pneumoniae. Equal opportunity vulnerability indeed.
Major Human Pathogens Include Not Just Viruses & Bacteria But Also Other Organisms
Both human viral and bacterial pathogens, among others, continue to impose selection pressure (5, 6). Consider two textbook examples, one the bacterium, Vibrio cholerae, and the other the retrovirus, HIV. Cholera remains endemic in the Ganges Delta – Wikipedia of Bangladesh, which has the world’s lowest prevalence of blood group O, probably because it’s associated with an increased risk of severe cholera (7, 8, 9). In the case of HIV, the delta 32 mutation deletes a portion of the CCR5 – Wikipedia gene and renders homozygous carriers resistant to HIV (10, 11). Testament to the central importance of adaptive immunity, specifically T cells, is the fact that the Major histocompatibility complex – Wikipedia (MHC complex) contains more infectious disease susceptibility associations than any other portion of the human genome (5). Major human pathogens include both viruses and bacteria (see below from 5).
Other pathogens too impose selection pressure. One of the most well-known examples is malaria (see table below from 6).
No Single Entity Within The Immune System Can Perceive An Entire Organism
While this question shares no data to support its claim that ‘we develop robust immunity after viral infections, but not bacterial infections‘, it implies that some entity within the human immune system can distinguish viruses from bacteria and fungi. The overarching implication that entire classes of organisms could function as selection units for the immune system to adapt against is inaccurate and cannot be substantiated, and here’s why.
Different cells in the immune system express different kinds of receptors of varying specificity and sensitivity. Those of the Innate immune system – Wikipedia (dendritic cells, macrophages, neutrophils, mast cells, NK cells, Innate lymphoid cells, gamma-delta T cells, etc.) are germline-encoded meaning they stay unchanged within the lifespan of an individual while only those of the Adaptive immune system – Wikipedia (T and B cells) are somatically rearranged, meaning they are derived de novo during the lifespan of each individual. Though this feature vastly expands their range to the order of 10^12 unique receptors each per individual as an estimate, what T and B cell receptors bind are hardly the sizes capable of distinguishing a virus from bacterium or fungus or even host cell-derived material for that matter.
- A B cell’s antigen is estimated in the range of 25 to 30 amino acids in length while CD4 and CD8 T cell receptors recognize even smaller peptides ranging in length a mere 15-20 to 8-10 amino acids, respectively.
- Binding larger molecules of varying sizes, derived not just from microbes but also the body’s own breakdown products including dead and dying cells, obviously germ-line encoded receptors too lack the capacity to discern their source.
Thus, no single cell of the immune system can directly differentiate a virus from bacterium or fungus or even allergen for that matter. Instead, different immune cells recognize and bind different bits and pieces of their targets. Thus, be the source of physiological disruption virus, bacteria, fungus, archaea, protist or helminth and so on, varied responses of all these immune cells and their products to varying bits and pieces need to be in sync to neutralize and/or eliminate the source of their individual targets, typically a whole organism.
The beauty as also the mystery of the human immune system is that this process occurs by rote in a healthy body even as no single element within the system can ‘see’ the entirety of the disruptor that sets the process in motion in the first place. This is also why on the one hand, Autoimmunity – Wikipedia, i.e., sustained and deleterious immune attack on one’s own cells and tissues, occurs when the immune system’s not functioning optimally, and why on the other, Cancer immunotherapy – Wikipedia can even be considered a realistic treatment option for tumors. Regardless the trigger, a common set of rules learned over evolutionary time guide the initiation, maintenance, termination and yes, even strength of immune responses, even as no single entity within this system can discern that trigger in its entirety.
1. Pawelec, Graham, et al. “The impact of CMV infection on survival in older humans.” Current opinion in immunology 24.4 (2012): 507-511. https://www.researchgate.net/pro…
2. Weltevrede, Marlies, et al. “Cytomegalovirus persistence and T-cell immunosenescence in people aged fifty and older: a systematic review.” Experimental gerontology 77 (2016): 87-95.
3. Janssens, Jean-Paul, and Karl-Heinz Krause. “Pneumonia in the very old.” The Lancet infectious diseases 4.2 (2004): 112-124. http://www.pneumonologia.gr/arti…
4. Kaplan, Vladimir, et al. “Hospitalized community-acquired pneumonia in the elderly: age-and sex-related patterns of care and outcome in the United States.” American journal of respiratory and critical care medicine 165.6 (2002): 766-772. https://www.researchgate.net/pro…
5. Karlsson, Elinor K., Dominic P. Kwiatkowski, and Pardis C. Sabeti. “Natural selection and infectious disease in human populations.” Nature Reviews Genetics 15.6 (2014): 379-393. Natural selection and infectious disease in human populations
6. Quach, Hélène, and Lluis Quintana-Murci. “Living in an adaptive world: Genomic dissection of the genus Homo and its immune response.” Journal of Experimental Medicine 214.4 (2017): 877-894. http://jem.rupress.org/content/j…
7. Barua, D., and A. S. Paguio. “ABO blood groups and cholera.” Annals of human biology 4.5 (1977): 489-492.
8. Glass, Roger I., et al. “Predisposition for cholera of individuals with o blood group possible evolutionary significance.” American journal of epidemiology 121.6 (1985): 791-796.
9. Harris, Jason B., and Regina C. LaRocque. “Cholera and ABO Blood Group: Understanding an Ancient Association.” The American Journal of Tropical Medicine and Hygiene 95.2 (2016): 263-264. https://pdfs.semanticscholar.org…
10. Liu, Rong, et al. “Homozygous defect in HIV-1 coreceptor accounts for resistance of some multiply-exposed individuals to HIV-1 infection.” Cell 86.3 (1996): 367-377. https://www.researchgate.net/pro…
11. Dean, Michael, et al. “Genetic restriction of HIV-1 infection and progression to AIDS by a deletion allele of the CKR5 structual gene.” Science 273.5283 (1996): 1856.