{{Short description|Ability of the immune system to quickly and specifically recognize an antigen}} '''Immunological memory''' is the ability of the immune system to quickly and specifically recognize an antigen that the body has previously encountered and initiate a corresponding immune response. Generally, they are secondary, tertiary and other subsequent immune responses to the same antigen. The adaptive immune system and antigen-specific receptor (e.g., T-cell receptors) generation are responsible for adaptive immune memory.<ref>{{Cite journal |last=Chaplin |first=David D. |date=February 2010 |title=Overview of the immune response |journal=Journal of Allergy and Clinical Immunology |language=en |volume=125 |issue=2 |pages=S3–S23 |doi=10.1016/j.jaci.2009.12.980|pmid=20176265 |pmc=2923430 }}</ref>
After the inflammatory immune response to danger-associated antigen, some of the antigen-specific T cells and B cells persist in the body and become long-living memory T and B cells. After a second encounter with the same antigen, they recognize the antigen and mount a faster and more robust response. Immunological memory is the basis of vaccination.<ref name="janeway">{{cite book |last1= Murphy |first1= Kenneth |last2= Weaver |first2= Casey |date= 2017 |title= Janeway's Immunology|edition = 9th |url= |location=New York & London |publisher=Garland Science |pages= 473–475 |isbn= 978-0-8153-4551-0}}</ref><ref name="auto">{{cite journal|last1=Hammarlund|first1=Erika|last2=Lewis|first2=Matthew W.|last3=Hansen|first3=Scott G.|last4=Strelow|first4=Lisa I.|last5=Nelson|first5=Jay A.|last6=Sexton|first6=Gary J.|last7=Hanifin|first7=Jon M.|last8=Slifka|first8=Mark K.|title=Duration of antiviral immunity after smallpox vaccination|journal=Nature Medicine|volume=9|issue=9|date=2003|issn=1078-8956|pmid=12925846|doi=10.1038/nm917|pages=1131–1137|url=https://pubmed.ncbi.nlm.nih.gov/12925846|access-date=14 April 2026}}</ref> Emerging resources show that even the innate immune system can initiate a more efficient immune response and pathogen elimination after the previous stimulation with a pathogen, respectively with pathogen-associated molecular patterns (PAMPs) or damage-associated molecular patterns (DAMPs). Innate immune memory (also called trained immunity) is neither antigen-specific nor dependent on gene rearrangement; the different response is caused by changes in epigenetic programming and shifts in immunometabolism. Innate immune memory has been observed in invertebrates and vertebrates.<ref name=":0">{{Cite journal|last1=Crișan|first1=Tania O.|last2=Netea|first2=Mihai G.|last3=Joosten|first3=Leo A. B.|date=April 2016|title=Innate immune memory: Implications for host responses to damage-associated molecular patterns|journal=European Journal of Immunology|volume=46|issue=4|pages=817–828|doi=10.1002/eji.201545497|pmid=26970440|issn=0014-2980|doi-access=free}}</ref><ref name=":1">{{Cite journal|last1=Gourbal|first1=Benjamin|last2=Pinaud|first2=Silvain|last3=Beckers|first3=Gerold J. M.|last4=Van Der Meer|first4=Jos W. M.|last5=Conrath|first5=Uwe|last6=Netea|first6=Mihai G.|date=2018-04-17|title=Innate immune memory: An evolutionary perspective|journal=Immunological Reviews|volume=283|issue=1|pages=21–40|doi=10.1111/imr.12647|pmid=29664574|s2cid=4891922|issn=0105-2896}}</ref>
Previously acquired immune memory can be depleted ("immune amnesia") by measles in unvaccinated children, leaving them at risk of infection by other pathogens in the years after infection.<ref>{{cite journal |vauthors=Mina MJ, Kula T, Leng Y, Li M, Vries RD, Knip M, Siljander H, Rewers M, Choy DF, Wilson MS, Larman HB |display-authors=6 |date=2019-11-01 |title=Measles virus infection diminishes preexisting antibodies that offer protection from other pathogens |journal=Science |volume=366 |issue=6465 |pages=599–606 |doi=10.1126/science.aay6485 |issn=0036-8075 |pmid=31672891|pmc=8590458 |bibcode=2019Sci...366..599M |hdl=10138/307628 |s2cid=207815213 |hdl-access=free }}</ref> This weakening of the immune system increases the risk of death from other diseases.<ref name=Amnesia /><ref name="Mina 2019" />
==Adaptive immune memory==
[[File:Immune response2.svg| thumb|350px | The time course of an immune response. The formation of immunological memory causes a later reinfection to lead to a rapid increase in antibody production and effector T cell activity. The later infections can be mild or even unapparent.]]
=== Development of adaptive immune memory ===
Immunological memory occurs after a primary immune response against the antigen. Immunological memory is thus created by each individual after a previous initial exposure to a potentially dangerous agent. The course of secondary immune response is similar to the primary immune response. After the memory B cell recognizes the antigen, it presents the peptide in the MHC class II complex to nearby effector T cells. That leads to activation of these cells and rapid proliferation of cells. After the primary immune response has disappeared, the effector cells of the immune response are eliminated.<ref>Sprent, Jonathan, and Susan R. Webb. "Intrathymic and extrathymic clonal deletion of T cells." Current opinion in immunology 7.2 (1995): 196-205.</ref>
However, antibodies that were previously produced in the body persist and represent the humoral component of immunological memory and serve as an important defense against subsequent infections. In addition to the formed antibodies in the body, there remains a small number of memory T and B cells that make up the cellular component of the immunological memory. They stay in blood circulation in a resting state, and at the subsequent encounter with the same antigen, these cells are able to respond immediately and eliminate the antigen. Memory cells have a long life and last up to several decades in the body.<ref>Crotty, Shane, et al. "Cutting edge: long-term B cell memory in humans after smallpox vaccination." The Journal of Immunology 171.10 (2003): 4969-4973.</ref><ref name="auto" />
Immunity to chickenpox, measles, and some other diseases lasts a lifetime. Immunity to many diseases eventually wears off. The immune system's response to a few diseases, such as dengue, counterproductively worsens the next infection (antibody-dependent enhancement).<ref> {{Cite web |last=Yong |first=Ed |date=2020-08-05 |title=Immunology Is Where Intuition Goes to Die |url=https://www.theatlantic.com/health/archive/2020/08/covid-19-immunity-is-the-pandemics-central-mystery/614956/ |access-date=2025-02-24 |website=The Atlantic |language=en}} </ref>
As of 2019, researchers are still trying to find out why some vaccines produce lifelong immunity, while the effectiveness of other vaccines drops to zero in less than 30 years (for mumps) or less than six months (for H3N2 influenza).<ref> {{Cite web |title=How long do vaccines last? The surprising answers may help protect people longer |url=https://www.science.org/content/article/how-long-do-vaccines-last-surprising-answers-may-help-protect-people-longer |access-date=2025-02-24 |website=www.science.org |language=en}} </ref>
===Evolution of adaptive immune memory===
The evolutionary invention of memory T and B cells is widespread; however, the conditions required to develop this costly adaptation are specific. First, to evolve immune memory, the initial molecular machinery cost must be high and will entail losses in other host characteristics. Second, middling- or long-lived organisms are more likely to evolve such an apparatus. The cost of this adaptation increases if the host has a middling lifespan, as the immune memory must be effective earlier in life.<ref>{{Cite journal|last1=Best|first1=Alex|last2=Hoyle|first2=Andy|date=2013-06-06|title=The evolution of costly acquired immune memory|journal=Ecology and Evolution|volume=3|issue=7|pages=2223–2232|doi=10.1002/ece3.611| pmc=3728959|pmid=23919164|issn=2045-7758|doi-access=free|bibcode=2013EcoEv...3.2223B }}</ref>
Furthermore, research models show that the environment plays an essential role in the diversity of memory cells in a population. Comparing the influence of multiple infections to a specific disease as opposed to disease diversity of an environment provides evidence that memory cell pools accrue diversity based on the number of individual pathogens exposed, even at the cost of efficiency when encountering more common pathogens. Individuals living in isolated environments, such as islands, have a less diverse population of memory cells, which are, however, present with sturdier immune responses. That indicates that the environment plays a large role in the evolution of memory cell populations.<ref>{{Cite journal|last1=Graw|first1=Frederik|last2=Magnus|first2=Carsten|last3=Regoes|first3=Roland R|date=2010|title=Theoretical analysis of the evolution of immune memory|journal=BMC Evolutionary Biology|volume=10|issue=1|page=380|doi=10.1186/1471-2148-10-380|pmid=21143840|pmc=3018457|issn=1471-2148|doi-access=free|bibcode=2010BMCEE..10..380G }}</ref>
=== Memory B cells ===
{{Main|Memory B cell}} Memory B cells are plasma cells that are able to produce antibodies for a long time. Unlike the naive B cells involved in the primary immune response, the memory B cell response is slightly different. The memory B cell has already undergone clonal expansion, differentiation and affinity maturation, so it is able to divide multiple times faster and produce antibodies with much higher affinity (especially IgG).<ref name="janeway" />
In contrast, the naive plasma cell is fully differentiated and cannot be further stimulated by antigen to divide or increase antibody production. Memory B cell activity in secondary lymphatic organs is highest during the first 2 weeks after infection. Subsequently, after 2 to 4 weeks, its response declines. After the germinal center reaction, the memory plasma cells are located in the bone marrow, which is the main site of antibody production within the immunological memory.<ref name="Slifka_1995">Slifka, Mark K., Mehrdad Matloubian, and Rafi Ahmed (1995). "Bone marrow is a major site of long-term antibody production after acute viral infection." ''Journal of Virology'', '''69(3)''', 1895–1902.</ref>
=== Memory T cells ===
{{Main|Memory T cell}} Memory T cells can be both CD4+ and CD8+. These memory T cells do not require further antigen stimulation to proliferate; therefore, they do not need a signal via MHC.<ref>Kassiotis, George, et al. "Impairment of immunological memory in the absence of MHC despite survival of memory T cells." Nature immunology 3.3 (2002): 244.</ref> Memory T cells can be divided into two functionally distinct groups based on the expression of the CCR7 chemokine receptor. This chemokine indicates the direction of migration into secondary lymphatic organs. Those memory T cells that do not express CCR7 (these are CCR7-) have receptors to migrate to the site of inflammation in the tissue and represent an immediate effector cell population. These cells were named memory effector T cells (T<sub>EM</sub>). After repeated stimulation they produce large amounts of IFN-γ, IL-4 and IL-5. In contrast, CCR7+ memory T cells lack proinflammatory and cytotoxic functions but express receptors for lymph node migration. These cells were named central memory T cells (T<sub>CM</sub>). They effectively stimulate dendritic cells, and after repeated stimulation, they are able to differentiate into CCR7- effector memory T cells. Both populations of these memory cells originate from naive T cells and remain in the body for several years after initial immunization.<ref>Sallusto, Federica, et al. "Two subsets of memory T lymphocytes with distinct homing potentials and effector functions." Nature 401.6754 (1999): 708.</ref>
Experimental techniques used to study these cells include measuring antigen-stimulated cell proliferation and cytokine release, staining with peptide-MHC multimers, or using an activation-induced marker (AIM) assay.<ref>{{Cite journal |last1=Poloni |first1=Chad |last2=Schonhofer |first2=Cole |last3=Ivison |first3=Sabine |last4=Levings |first4=Megan K. |last5=Steiner |first5=Theodore S. |last6=Cook |first6=Laura |date=2023-02-24 |title=T-cell activation-induced marker assays in health and disease |journal=Immunology and Cell Biology |volume=101 |issue=6 |pages=491–503 |doi=10.1111/imcb.12636 |issn=1440-1711 |pmid=36825901|doi-access=free |pmc=10952637 }}</ref>
==Innate immune memory==
Many invertebrates such as species of freshwater snails, copepod crustaceans, and tapeworms have been observed activating innate immune memory to instigate a more efficient immune response to second encounter with specific pathogens, despite missing an adaptive branch of the immune system.<ref name=":0" /> ''RAG1''-deficient mice without functional T and B cells were able to survive the administration of a lethal dose of ''Candida albicans'' when exposed previously to a much smaller amount, showing that vertebrates also retain this ability.<ref name=":1" /> Despite not having the ability to manufacture antibodies like the adaptive immune system, the innate immune system has immune memory properties as well. Innate immune memory—trained immunity—is defined as a long-term functional reprogramming of innate immune cells evoked by exogenous or endogenous insults and leading to an altered response towards a second challenge after returning to a non-activated state.<ref name=":3">{{Cite journal |last1=Netea |first1=Mihai G. |last2=Domínguez-Andrés |first2=Jorge |last3=Barreiro |first3=Luis B. |last4=Chavakis |first4=Triantafyllos |last5=Divangahi |first5=Maziar |last6=Fuchs |first6=Elaine |last7=Joosten |first7=Leo A. B. |last8=van der Meer |first8=Jos W. M. |last9=Mhlanga |first9=Musa M. |last10=Mulder |first10=Willem J. M. |last11=Riksen |first11=Niels P. |last12=Schlitzer |first12=Andreas |last13=Schultze |first13=Joachim L. |last14=Stabell Benn |first14=Christine |last15=Sun |first15=Joseph C. |date=June 2020 |title=Defining trained immunity and its role in health and disease |journal=Nature Reviews Immunology |language=en |volume=20 |issue=6 |pages=375–388 |doi=10.1038/s41577-020-0285-6 |pmid=32132681 |pmc=7186935 |issn=1474-1741}}</ref>
When innate immune cells receive an activation signal, for example, through recognition of PAMPs with pattern recognition receptors (PRRs), they start the expression of proinflammatory genes, initiate an inflammatory response, and undergo epigenetic reprogramming. After the second stimulation, the transcription activation is faster and more robust.<ref name=":2">{{Cite journal |last1=Fanucchi |first1=Stephanie |last2=Domínguez-Andrés |first2=Jorge |last3=Joosten |first3=Leo A. B. |last4=Netea |first4=Mihai G. |last5=Mhlanga |first5=Musa M. |date=2021-01-12 |title=The Intersection of Epigenetics and Metabolism in Trained Immunity |journal=Immunity |language=English |volume=54 |issue=1 |pages=32–43 |doi=10.1016/j.immuni.2020.10.011 |issn=1074-7613 |pmid=33220235|s2cid=227124221 |doi-access=free |hdl=2066/229964 |hdl-access=free }}</ref> Immunological memory was reported in monocytes, macrophages, natural killer cells, and innate lymphoid cells 1, 2, and 3 cells.<ref>{{Cite journal |last1=Hartung |first1=Franziska |last2=Esser-von Bieren |first2=Julia |date=2022-09-05 |title=Trained immunity in type 2 immune responses |journal=Mucosal Immunology |volume=15 |issue=6 |language=en |pages=1158–1169 |doi=10.1038/s41385-022-00557-0 |pmid=36065058 |pmc=9705254 |issn=1935-3456}}</ref><ref name=":2" /> Concomitantly, some nonimmune cells, for example, epithelial stem cells on barrier tissues, or fibroblasts, change their epigenetic state and respond differently after priming insult.<ref>{{Cite journal |last1=Ordovas-Montanes |first1=Jose |last2=Beyaz |first2=Semir |last3=Rakoff-Nahoum |first3=Seth |last4=Shalek |first4=Alex K. |date=May 2020 |title=Distribution and storage of inflammatory memory in barrier tissues |journal=Nature Reviews Immunology |language=en |volume=20 |issue=5 |pages=308–320 |doi=10.1038/s41577-019-0263-z |pmid=32015472 |pmc=7547402 |issn=1474-1741}}</ref>
=== Mechanism of innate immune memory ===
At the steady state, unstimulated cells have reduced biosynthetic activities and more condensed chromatin with reduced gene transcription. The interaction of exogenous PAMPs (β-glucan, muramyl peptide) or endogenous DAMPs (oxidized LDL, uric acid) with PRR initiates a cellular response. Triggered Intracellular signaling cascades lead to the upregulation of metabolic pathways such as glycolysis, the Krebs cycle, and fatty acid metabolism. An increase in metabolic activity provides cells with energy and building blocks, which are needed for the production of signaling molecules such as cytokines and chemokines.<ref name=":2" />
Signal transduction changes the epigenetic marks and increases chromatin accessibility, to allow binding of transcription factors and the start of transcription of genes connected with inflammation. There is an interplay between metabolism and epigenetic changes because some metabolites such as fumarate and acetyl-CoA can activate or inhibit enzymes involved in chromatin remodeling.<ref name=":3" /> After the stimulus let up, there is no need for immune factors production, and their expression in immune cells is terminated. Several epigenetic modifications created during stimulation remain. Characteristic epigenetic rewiring in trained cells is the accumulation of H3K4me3 on immune gene promoters and the increase of H3K4me1 and H3K27ac on enhancers. Additionally, cellular metabolism does not return to the state before stimulation, and trained cells remain in a prepared state. This status can last from weeks to several months and can be transmitted to daughter cells. Secondary stimulation induces a new response, which is faster and stronger.<ref name=":3" /><ref name=":2" />
=== Evolution of innate immune memory ===
Immune memory brings a major evolutionary advantage when the organism faces repeated infections. Inflammation is very costly, and increased effectivity of response accelerates pathogen elimination and prevents damage to the host's own tissue. Classical adaptive immune memory evolved in jawed vertebrates and in jawless fish (lamprey), which is approximately just 1% of living organisms. Some form of immune memory is, therefore, reported in other species. In plants and invertebrates, faster kinetics, increased magnitude of immune response, and an improved survival rate can be seen after secondary infection encounters. Immune memory is common for the vast majority of biodiversity on Earth.<ref>{{Cite journal |last1=Netea |first1=Mihai G. |last2=Schlitzer |first2=Andreas |last3=Placek |first3=Katarzyna |last4=Joosten |first4=Leo A. B. |last5=Schultze |first5=Joachim L. |date=2019-01-09 |title=Innate and Adaptive Immune Memory: an Evolutionary Continuum in the Host's Response to Pathogens |journal=Cell Host & Microbe |language=English |volume=25 |issue=1 |pages=13–26 |doi=10.1016/j.chom.2018.12.006 |issn=1931-3128 |pmid=30629914|s2cid=58623144 |doi-access=free }}</ref>
It has been proposed that immune memory in innate and adaptive immunity represents an evolutionary continuum in which a more robust immune response evolved first, mediated by epigenetic reprogramming. In contrast, specificity through antigen-specific receptors evolved later in some vertebrates.<ref>{{Cite journal |last1=Divangahi |first1=Maziar |last2=Aaby |first2=Peter |last3=Khader |first3=Shabaana Abdul |last4=Barreiro |first4=Luis B. |last5=Bekkering |first5=Siroon |last6=Chavakis |first6=Triantafyllos |last7=van Crevel |first7=Reinout |last8=Curtis |first8=Nigel |last9=DiNardo |first9=Andrew R. |last10=Dominguez-Andres |first10=Jorge |last11=Duivenvoorden |first11=Raphael |last12=Fanucchi |first12=Stephanie |last13=Fayad |first13=Zahi |last14=Fuchs |first14=Elaine |last15=Hamon |first15=Melanie |date=January 2021 |title=Trained immunity, tolerance, priming and differentiation: distinct immunological processes |journal=Nature Immunology |language=en |volume=22 |issue=1 |pages=2–6 |doi=10.1038/s41590-020-00845-6 |pmid=33293712 |pmc=8020292 |issn=1529-2916}}</ref>
==Evolutionary mechanisms leading to the development of immunological memory==
The emergence of the adaptive immune system is rooted in the deep history of evolution dating back roughly 500 million years. Investigations and recent studies found that two major events led to the emergence of the same.<ref name="originandevolution">{{cite journal |doi=10.1038/nrg2703 |title=Origin and evolution of the adaptive immune system: Genetic events and selective pressures |date=2010 |last1=Flajnik |first1=Martin F. |last2=Kasahara |first2=Masanori |journal=Nature Reviews Genetics |volume=11 |issue=1 |pages=47–59 |pmid=19997068 |pmc=3805090 }}</ref> These two macroevolutionary events were the origin of RAG and two whole rounds of genome duplication (WGD).The early origins and evidence for emergence of features resembling AIS dates to the era where jawed and jawless vertebrates diverged phylogenetically. Early investigations around the 1970s led to the discovery of unique inverted repeat flanking signal sequences while groups studied the RAG genome.<ref name="originandevolution" /> These so-called RAG transposons invaded regions of genome which may have been involved in AIS.<ref>{{Cite journal |last1=Flajnik |first1=Martin F. |last2=Kasahara |first2=Masanori |date=January 2001 |title=Origin and evolution of the adaptive immune system: genetic events and selective pressures |journal=Nature Reviews Genetics |language=en |volume=11 |issue=1 |pages=47–59 |doi=10.1038/nrg2703 |pmid=19997068 |issn=1471-0056|pmc=3805090 }}</ref> Culmination of several works and review suggests that these disruptions could have been selected for a rearrangement to maintain genomic integrity which ultimately led to mechanisms like RAG diversifications in AIS. This discovery led to the hypothesis that there was an invasion event of a regulatory element-like region because these repeats resembled a remnant transposable element.<ref name="originandevolution" /> This invasion was argued to be necessary for the emergence of BCR and TCR-dependent immunity as we see now in all gnathostomes .According to recent scientific findings around 450-500mya the vertebrate genome went through two rounds of whole genome duplication. This is usually referred to as the "2R hypothesis". Such intense genomic events lead to gene sub-functionalization, neofunctionalization or in many cases lead to loss of functions. Ohno, 40 years ago proposed that the evolutionary events which led to whole genome duplication was key for the emergence of the diversity we see in adaptive immunity and memory.<ref name="originandevolution" /> Further works illustrate that newer genic regions which arose because of this duplication event, are major contributors to today's adaptive immune systems which control immunological memory in gnathostomes. Okada's work on investigating ohnologues that arose from WGD is clear proof of the same, that today AIS systems are remnants of the WGD events.<ref>{{Cite journal |last1=Harper |first1=A. |last2=Baudouin Gonzalez |first2=L. |last3=Schönauer |first3=A. |last4=Janssen |first4=R. |last5=Seiter |first5=M. |last6=Holzem |first6=M. |last7=Arif |first7=S. |last8=McGregor |first8=A. P. |last9=Sumner-Rooney |first9=L. |date=September 6, 2021 |title=Widespread retention of ohnologs in key developmental gene families following whole-genome duplication in arachnopulmonates |journal=G3 |volume=11 |issue=12 |article-number=jkab299 |doi=10.1093/g3journal/jkab299 |pmid=34849767 |pmc=8664421 }}</ref>
== Measles and immune amnesia ==
The measles virus can deplete previously acquired immune memory by killing cells that make antibodies, thus weakening the immune system and increasing the risk of death from other diseases.<ref name=Amnesia /><ref name="Mina 2019">{{cite journal | vauthors = Mina MJ, Kula T, Leng Y, Li M, de Vries RD, Knip M, Siljander H, Rewers M, Choy DF, Wilson MS, Larman HB, Nelson AN, Griffin DE, de Swart RL, Elledge SJ | title = Measles virus infection diminishes preexisting antibodies that offer protection from other pathogens | journal = Science | volume = 366 | issue = 6465 | pages = 599–606 | date = 1 November 2019 | pmid = 31672891 | doi = 10.1126/science.aay6485 | pmc = 8590458 | issn = 0036-8075 | bibcode = 2019Sci...366..599M | hdl = 10138/307628 | doi-access = free | title-link = doi}}</ref><ref name=Nature /> Suppression of the immune system by measles lasts about two years and has been epidemiologically implicated in up to 90% of childhood deaths in third world countries, and historically may have caused rather more deaths in the United States, the UK and Denmark than were directly caused by measles.<ref name="pmid25954009" >{{cite journal |title=Long-term measles-induced immunomodulation increases overall childhood infectious disease mortality |journal=Science |date=May 2015 |doi=10.1126/science.aaa3662 |pmid=25954009 |pmc=4823017 |bibcode=2015Sci...348..694M |vauthors=Mina MJ, Metcalf CJ, de Swart RL, Osterhaus AD, Grenfell BT |volume=348 |issue=6235 |pages=694–9 | doi-access = free | title-link = doi }}</ref><ref>{{cite web | last=Bakalar | first=Nicholas | title=Measles May Increase Susceptibility to Other Infections | website=The New York Times | date=7 May 2015 | url=https://archive.nytimes.com/well.blogs.nytimes.com/2015/05/07/measles-may-increase-susceptibility-to-other-infections/ |access-date=7 June 2015 |archive-date=10 May 2015 |archive-url=https://web.archive.org/web/20150510032648/http://well.blogs.nytimes.com/2015/05/07/measles-may-increase-susceptibility-to-other-infections/ |url-status=live }}</ref> Although the measles vaccine contains an attenuated strain, it does not deplete immune memory.<ref name="Mina 2019" />
Complications of measles are relatively common. Some are caused directly by the virus, while others are caused by viral suppression of the immune system. This phenomenon, known as "immune amnesia", increases the risk of secondary bacterial infections;<ref name=Rot2016>{{cite journal | vauthors = Rota PA, Moss WJ, Takeda M, de Swart RL, Thompson KM, Goodson JL | title = Measles | journal = Nature Reviews. Disease Primers | volume = 2 | article-number = 16049 | date = July 2016 | pmid = 27411684 | doi = 10.1038/nrdp.2016.49 | doi-access = free | title-link = doi }}</ref><ref>{{cite journal |vauthors=Griffin DE |date=July 2010 |title=Measles virus-induced suppression of immune responses |journal=Immunological Reviews |volume=236 |pages=176–89 |doi=10.1111/j.1600-065X.2010.00925.x |pmc=2908915 |pmid=20636817}}</ref><ref name="Amnesia">{{cite web |last=Griffin |first=Ashley Hagen |date=18 May 2019 |title=Measles and Immune Amnesia |url=https://asm.org/Articles/2019/May/Measles-and-Immune-Amnesia |url-status=live |archive-url=https://archive.today/20200118042959/https://asm.org/Articles/2019/May/Measles-and-Immune-Amnesia |archive-date=18 January 2020 |access-date=18 January 2020 |website=asm.org |publisher=American Society for Microbiology}}</ref><ref name="Mina 2019" /> two months after recovery there is an 11–73% decrease in the number of antibodies against other bacteria and viruses.<ref name="Nature">{{cite journal|title=Measles erases immune 'memory' for other diseases|url=https://www.nature.com/articles/d41586-019-03324-7|journal=Nature|access-date=3 November 2019|date=31 October 2019|doi=10.1038/d41586-019-03324-7|last=Guglielmi|first=Giorgia|pmid=33122832|s2cid=208489179|archive-date=2 November 2019|archive-url=https://web.archive.org/web/20191102065033/https://www.nature.com/articles/d41586-019-03324-7|url-status=live|url-access=subscription}}</ref> Population studies from prior to the introduction of the measles vaccine suggest that immune amnesia typically lasts 2–3 years. Primate studies suggest that immune amnesia in measles is effected by replacement of memory lymphocytes with ones that are specific to measles virus, since they are destroyed after being infected by the virus. This creates lasting immunity to measles re-infection, but decreases immunity to other pathogens.<ref name="Amnesia" /> Complications may be directly related to the virus - e.g. viral pneumonia or viral laryngotracheobronchitis (croup) - or related to the damage measles virus causes to tissues and the immune system. The most serious direct complications include acute encephalitis,<ref>{{cite journal |vauthors=Fisher DL, Defres S, Solomon T |date=March 2015 |title=Measles-induced encephalitis |journal=QJM |volume=108 |issue=3 |pages=177–82 |doi=10.1093/qjmed/hcu113 |pmid=24865261 | doi-access = free | title-link = doi }}</ref> corneal ulceration (leading to corneal scarring);<ref>{{cite journal |vauthors=Semba RD, Bloem MW |date=March 2004 |title=Measles blindness |journal=Survey of Ophthalmology |volume=49 |issue=2 |pages=243–55 |doi=10.1016/j.survophthal.2003.12.005 |pmid=14998696}}</ref> and subacute sclerosing panencephalitis, a progressive and fatal inflammation of the brain that occurs in about 1 in 600 unvaccinated infants under 15 months. Common secondary infections include infectious diarrhea, bacterial pneumonia, and otitis media.<ref name="Rot2016" />
==See also==
* Immunity (medical) * Seroconversion * Serostatus * Virgin soil epidemic
==References== {{Reflist}}
Category:Immune system