Editing Herd immunity (section)

===Evolutionary pressure and serotype replacement===
Herd immunity itself acts as an [[evolutionary pressure]] on pathogens, influencing [[viral evolution]] by encouraging the production of novel strains, referred to as escape mutants, that are able to evade herd immunity and infect previously immune individuals.<ref name=pmid24175217>{{Cite journal|pmid=24175217|pmc=3782273|year=2012|last1=Rodpothong|first1=P|title=Viral evolution and transmission effectiveness|journal=World Journal of Virology|volume=1|issue=5|pages=131–34|last2=Auewarakul|first2=P|doi=10.5501/wjv.v1.i5.131 |doi-access=free }}</ref><ref name=pmid23330954>{{Cite journal|pmid=23330954|year=2013|last1=Corti|first1=D|title=Broadly neutralizing antiviral antibodies|journal=Annual Review of Immunology|volume=31|pages=705–42|last2=Lanzavecchia|first2=A|doi=10.1146/annurev-immunol-032712-095916}}</ref> The evolution of new strains is known as [[serotype]] replacement, or serotype shifting, as the [[prevalence]] of a specific serotype declines due to high levels of immunity, allowing other serotypes to replace it.<ref name="pmid21492929">{{Cite journal|last1=Weinberger|first1=D. M.|last2=Malley|first2=R|last3=Lipsitch|first3=M|year=2011|title=Serotype replacement in disease after pneumococcal vaccination|journal=The Lancet|volume=378|issue=9807|pages=1962–73|doi=10.1016/S0140-6736(10)62225-8|pmc=3256741|pmid=21492929}}</ref><ref name="pmid22903767">{{Cite journal|last1=McEllistrem|first1=M. C.|last2=Nahm|first2=M. H.|year=2012|title=Novel pneumococcal serotypes 6C and 6D: Anomaly or harbinger|journal=Clinical Infectious Diseases|volume=55|issue=10|pages=1379–86|doi=10.1093/cid/cis691|pmc=3478140|pmid=22903767}}</ref>

At the molecular level, viruses escape from herd immunity through [[antigenic drift]], which is when [[mutation]]s accumulate in the portion of the [[Virus#Genome|viral genome]] that encodes for the virus's surface [[antigen]], typically a protein of the virus [[capsid]], producing a change in the viral [[epitope]].<ref name=pmid21310617>{{cite journal|vauthors=Bull RA, White PA|title=Mechanisms of GII.4 norovirus evolution|journal=Trends in Microbiology|volume=19|issue=5|pages=233–40|date=May 2011|pmid=21310617|doi=10.1016/j.tim.2011.01.002}}</ref><ref name=pmid24232370>{{cite journal|vauthors=Ramani S, Atmar RL, Estes MK|title=Epidemiology of human noroviruses and updates on vaccine development|journal=Current Opinion in Gastroenterology|volume=30|issue=1|pages=25–33|date=January 2014|pmid=24232370|pmc=3955997|doi=10.1097/MOG.0000000000000022}}</ref> Alternatively, the reassortment of separate viral genome segments, or [[antigenic shift]], which is more common when there are more strains in circulation, can also produce new [[serotype]]s.<ref name=pmid24175217/><ref name=pmid23124938>{{Cite book|pmid=23124938|year=2013|vauthors=Pleschka S|title=Swine Influenza|volume=370|pages=1–20|doi=10.1007/82_2012_272|chapter=Overview of Influenza Viruses|series=Current Topics in Microbiology and Immunology|isbn=978-3642368707}}</ref> When either of these occur, [[memory T cell]]s no longer recognize the virus, so people are not immune to the dominant circulating strain.<ref name=pmid24232370/><ref name=pmid23124938/> For both influenza and [[norovirus]], epidemics temporarily induce herd immunity until a new dominant strain emerges, causing successive waves of epidemics.<ref name=pmid21310617/><ref name=pmid23124938/> As this evolution poses a challenge to herd immunity, [[Neutralizing antibody#Broadly neutralizing antibodies|broadly neutralizing antibodies]] and "universal" vaccines that can provide protection beyond a specific serotype are in development.<ref name=pmid23330954/><ref>{{cite journal|vauthors=Han T, Marasco WA|title=Structural basis of influenza virus neutralization|journal=Annals of the New York Academy of Sciences|volume=1217|issue=1|pages=178–90|date=January 2011|pmid=21251008|pmc=3062959|doi=10.1111/j.1749-6632.2010.05829.x|bibcode=2011NYASA1217..178H}}</ref><ref>{{cite journal|vauthors=Reperant LA, Rimmelzwaan GF, Osterhaus AD|title=Advances in influenza vaccination|journal=F1000Prime Reports|volume=6|pages=47|year=2014|pmid=24991424|pmc=4047948|doi=10.12703/p6-47 |doi-access=free }}</ref>

Initial vaccines against ''[[Streptococcus pneumoniae]]'' significantly reduced nasopharyngeal carriage of vaccine serotypes (VTs), including [[Antimicrobial resistance|antibiotic-resistant]] types,<ref name=pmid22862432/><ref>{{cite journal|vauthors=Dagan R|title=Impact of pneumococcal conjugate vaccine on infections caused by antibiotic-resistant Streptococcus pneumoniae|journal=Clinical Microbiology and Infection|volume=15|issue=Suppl 3|pages=16–20|date=April 2009|pmid=19366365|doi=10.1111/j.1469-0691.2009.02726.x|doi-access=free}}</ref> only to be entirely offset by increased carriage of non-vaccine serotypes (NVTs).<ref name=pmid22862432/><ref name=pmid21492929/><ref name=pmid22903767/> This did not result in a proportionate increase in disease incidence though, since NVTs were less invasive than VTs.<ref name=pmid21492929/> Since then, [[pneumococcal vaccine]]s that provide protection from the emerging serotypes have been introduced and have successfully countered their emergence.<ref name=pmid22862432/> The possibility of future shifting remains, so further strategies to deal with this include expansion of VT coverage and the development of vaccines that use either [[Inactivated vaccine|killed whole-cells]], which have more surface antigens, or proteins present in multiple serotypes.<ref name=pmid22862432/><ref>{{cite journal|vauthors=Lynch JP, Zhanel GG|title=Streptococcus pneumoniae: epidemiology and risk factors, evolution of antimicrobial resistance, and impact of vaccines|journal=Current Opinion in Pulmonary Medicine|volume=16|issue=3|pages=217–25|date=May 2010|pmid=20375783|doi=10.1097/MCP.0b013e3283385653|s2cid=205784538}}</ref>