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An emergent virus (or emerging virus) is a virus that is either newly appeared, notably increasing in incidence/geographic range or has the potential to increase in the near future.^[1] Emergent viruses are a leading cause of emerging infectious diseases and raise public health challenges globally, given their potential to cause outbreaks of disease which can lead to epidemics and pandemics.^[2] As well as causing disease, emergent viruses can also have severe economic implications.^[3] Recent examples include the SARS-related coronaviruses, which have caused the 2002–2004 outbreak of SARS (SARS-CoV-1) and the 2019–2023 pandemic of COVID-19 (SARS-CoV-2).^[4]^[5] Other examples include the human immunodeficiency virus, which causes HIV/AIDS; the viruses responsible for Ebola;^[6] the H5N1 influenza virus responsible for avian influenza;^[7] and H1N1/09, which caused the 2009 swine flu pandemic^[8] (an earlier emergent strain of H1N1 caused the 1918 Spanish flu pandemic).^[9] Viral emergence in humans is often a consequence of zoonosis, which involves a cross-species jump of a viral disease into humans from other animals. As zoonotic viruses exist in animal reservoirs, they are much more difficult to eradicate and can therefore establish persistent infections in human populations.^[10]

Emergent viruses should not be confused with re-emerging viruses or newly detected viruses. A re-emerging virus is generally considered to be a previously appeared virus that is experiencing a resurgence,^[1]^[11] for example measles.^[12] A newly detected virus is a previously unrecognized virus that had been circulating in the species as endemic or epidemic infections.^[13] Newly detected viruses may have escaped classification because they left no distinctive clues and/or could not be isolated or propagated in cell culture.^[14] Examples include human rhinovirus (a leading cause of common colds which was first identified in 1956),^[15] hepatitis C (eventually identified in 1989),^[16] and human metapneumovirus (first described in 2001, but thought to have been circulating since the 19th century).^[17] As the detection of such viruses is technology driven, the number reported is likely to expand.

Zoonosis

Given the rarity of spontaneous development of new virus species, the most frequent cause of emergent viruses in humans is zoonosis. This phenomenon is estimated to account for 73% of all emerging or re-emerging pathogens, with viruses playing a disproportionately large role.^[18] RNA viruses are particularly frequent, accounting for 37% of emerging and re-emerging pathogens.^[18] A broad range of animals — including wild birds, rodents, and bats — are associated with zoonotic viruses.^[19] It is not possible to predict specific zoonotic events that may be associated with a particular animal reservoir at any given time.^[20]

Zoonotic spillover can either result in self-limited 'dead-end' infections, in which no further human-to-human transmission occurs (as with the rabies virus),^[21] or in infectious cases, in which the zoonotic pathogen is able to sustain human-to-human transmission (as with the Ebola virus).^[6] If the zoonotic virus is able to maintain successful human-to-human transmission, an outbreak may occur.^[22] Some spillover events can also result in the virus adapting exclusively for human infection (as occurred with the HIV virus),^[23] in which case humans become a new reservoir for the pathogen.

A successful zoonotic 'jump' depends on human contact with an animal harboring a virus variant that is able to infect humans. In order to overcome host-range restrictions and sustain efficient human-to-human transmission, viruses originating from an animal reservoir will normally undergo mutation, genetic recombination, and reassortment.^[20] Due to their rapid replication and high mutation rates, RNA viruses are more likely to successfully adapt for invasion of a new host population.^[3]

Examples of animal sources

Bats

While bats are essential members of many ecosystems,^[24] they are also frequently implicated as frequent sources of emerging virus infections.^[25] Their immune systems have evolved in such a way as to suppress any inflammatory response to viral infections, thereby allowing them to become tolerant hosts for evolving viruses, and consequently provide major reservoirs of zoonotic viruses.^[26] They are associated with more zoonotic viruses per host species than any other mammal, and molecular studies have demonstrated that they are the natural hosts for several high-profile zoonotic viruses, including severe acute respiratory syndrome–related coronaviruses and Ebola/Marburg hemorrhagic fever filoviruses.^[27] In terms of their potential for spillover events, bats have taken over the leading role previously assigned to rodents.^[26] Viruses can be transmitted from bats via several mechanisms, including bites,^[28] aerosolization of saliva (e.g., during echolocation), and feces/urine.^[29]

Due to their distinct ecology/behavior, bats are naturally more susceptible to viral infection and transmission. Several bat species (e.g., brown bats) aggregate in crowded roosts, which promotes intra- and interspecies viral transmission. Moreover, as bats are widespread in urban areas, humans occasionally encroach on their habitats which are contaminated with guano and urine. Their ability to fly and migration patterns also means that bats are able to spread disease over a large geographic area, while also acquiring new viruses.^[30] Additionally, bats experience persistent viral infections which, together with their extreme longevity (some bat species have lifespans of 35 years), helps to maintain viruses and transmit them to other species. Other bat characteristics which contribute to their potency as viral hosts include: their food choices, torpor/hibernation habits, and susceptibility to reinfection.^[30]

Drivers of viral emergence

Viral emergence is often a consequence of both nature and human activity. In particular, ecological changes can greatly facilitate the emergence and re-emergence of zoonotic viruses.^[31] Factors such as deforestation, reforestation, habitat fragmentation, and irrigation can all impact the ways in which humans come into contact with wild animal species and consequently promote virus emergence.^[3]^[32] In particular, habitat loss of reservoir host species plays a significant role in emerging zoonoses.^[33] Additionally, climate change can affect ecosystems and vector distribution, which in turn can affect the emergence of vector-borne viruses. Other ecological changes — for example, species introduction and predator loss — can also affect virus emergence and prevalence. Some agricultural practices — for example, livestock intensification and inappropriate management/disposal of farm animal feces — are also associated with an increased risk of zoonosis.^[3]^[34]

Viruses may also emerge due to the establishment of human populations that are vulnerable to infection. For example, a virus may emerge following loss of cross-protective immunity, which may occur due to loss of a wild virus or termination of vaccination program. Well-developed countries also have higher proportions of aging citizens and obesity-related disease, thus meaning that their populations may be more immunosuppressed and therefore at risk of infection.^[3] Contrastingly, poorer nations may have immunocompromised populations due to malnutrition or chronic infection; these countries are also unlikely to have stable vaccination program.^[3] Additionally, changes in human demographics^[3] — for example, the birth and/or migration of immunologically naïve individuals — can lead to the development of a susceptible population that enables large-scale virus infection.

Other factors which can promote viral emergence include globalization; in particular, international trade and human travel/migration can result in the introduction of viruses into new areas.^[3] Moreover, as densely populated cities promote rapid pathogen transmission, uncontrolled urbanization (i.e., the increased movement and settling of individuals in urban areas) can promote viral emergence.^[35] Animal migration can also lead to the emergence of viruses, as was the case for the West Nile virus which was spread by migrating bird populations.^[36] Additionally, human practices regarding food production and consumption can also contribute to the risk of viral emergence. In particular, wet markets (i.e., live animal markets) are an ideal environment for virus transfer, due to the high density of people and wild/farmed animals present.^[29] Consumption of bushmeat is also associated with pathogen emergence.^[29]

Prevention

Control and prevention of zoonotic diseases depends on appropriate global surveillance at various levels, including identification of novel pathogens, public health surveillance (including serological surveys), and analysis of the risks of transmission.^[37] The complexity of zoonotic events around the world predicates a multidisciplinary approach to prevention.^[37] The One Health Model has been proposed as a global strategy to help prevent the emergence of zoonotic diseases in humans, including novel viral diseases.^[37] The One Health concept aims to promote the health of animals, humans, and the environment, both locally and globally, by fostering understanding and collaboration between practitioners of different interrelated disciplines, including wildlife biology, veterinary science, medicine, agriculture, ecology, microbiology, epidemiology, and biomedical engineering.^[37]^[38]

Virulence of emergent viruses

As hosts are immunologically naïve to pathogens they have not encountered before, emergent viruses are often extremely virulent in terms of their capacity to cause disease. Their high virulence is also due to a lack of adaptation to the new host; viruses normally exert strong selection pressure on the immune systems of their natural hosts, which in turn exerts a strong selection pressure on viruses.^[39] This coevolution means that the natural host is able to manage infection. However, when the virus jumps to a new host (e.g., humans), the new host is unable to deal with infection due to a lack of coevolution, which results in mismatch between host immunoeffectors and virus immunomodulators.^{[citation needed]}

Additionally, in order to maximize transmission, viruses often naturally undergo attenuation (i.e., virulence is reduced) so that infected animals can survive long enough to infect other animals more efficiently.^[40] However, as attenuation takes time to achieve, new host populations will not initially benefit from this phenomenon. Moreover, as zoonotic viruses also naturally exist in animal reservoirs,^[10] their survival is not dependent on transmission between new hosts; this means that emergent viruses are even more unlikely to attenuate for the purpose of maximal transmission, and they remain virulent.^{[citation needed]}

Although emergent viruses are frequently highly virulent, they are limited by several host factors including: innate immunity, natural antibodies, and receptor specificity. If the host has previously been infected by a pathogen that is similar to the emergent virus, the host may also benefit from cross-protective immunity.^{[citation needed]}

Examples of emergent viruses

Influenza A

Influenza is a highly contagious respiratory infection, which affects approximately 9% of the global population and causes 300,000 to 500,000 deaths annually.^[41]^[42] Based on their core proteins, influenza viruses are classified into types A, B, C, and D.^[43]^[44] While both influenza A and B can cause epidemics in humans, influenza A also has pandemic potential and a higher mutation rate and is therefore most significant to public health.^[44]^[45]

Influenza A viruses are further classified into subtypes, based on the combinations of the surface glycoproteins hemagglutinin (HA) and neuraminidase (NA). The primary natural reservoir for most influenza A subtypes are wild aquatic birds;^[44] however, through a series of mutations, a small subset of these viruses have adapted for infection of humans (and other animals).^[46] A key determinant of whether a particular influenza A subtype can infect humans is its binding specificity. Avian influenza A preferentially binds to cell surface receptors with a terminal α2,3‐linked sialic acid, while human influenza A preferentially binds to cell surface receptors with a terminal α2,6‐linked sialic acid. Via mutation, some avian influenza A viruses have successfully altered their binding specificity from α2,3‐ to α2,6‐linked sialic acid.^[47] However, in order to emerge in humans, avian influenza A viruses must also adapt their RNA polymerases for function in mammalian cells,^[48] as well as mutating for stability in the acidic respiratory tract of humans.^[49]

Following adaptation and host switch, influenza A viruses have the potential to cause epidemics and pandemics in humans. Minor changes in HA and NA structure (antigenic drift) occur frequently, which enables the virus to cause repetitive outbreaks (i.e., seasonal influenza) by evading immune recognition.^[43] Major changes in HA and NA structure (antigenic shift), which are caused by genetic reassortment between different influenza A subtypes (e.g., between human and animal subtypes), can instead cause large regional/global pandemics.^[43] Due to the emergence of antigenically different influenza A strains in humans, four influenza pandemics occurred in the 20th century alone.^[50]

Additionally, although animal influenza A viruses (e.g., swine influenza) are distinct from human influenza viruses, they can still cause zoonotic infection in humans. These infections are largely acquired following direct contact with infected animals or contaminated environments, but do not result in efficient human-to-human transmission; examples of this include H5N1 influenza and H7N9 influenza.^[44]

SARS-CoV-1

In 2002, a highly pathogenic SARS-CoV (severe acute respiratory syndrome coronavirus) strain emerged from a zoonotic reservoir; approximately 8,000 people were infected worldwide, and mortality rates approached 50% or more in the elderly.^[51] As SARS-CoV-1 is most contagious post-symptoms, the introduction of strict public health measures effectively halted the epidemic.^[51] The natural reservoir host for SARS-CoV-1 is thought to be horseshoe bats, although the virus has also been identified in several small carnivores (e.g., palm civets and racoon dogs). The emergence of SARS-CoV-1 is believed to have been facilitated by Chinese wet markets, in which civets positive for the virus acted as intermediate hosts and passed SARS-CoV-1 onto humans (and other species).^[51]^[52] However, more recent analysis suggests that SARS-CoV-1 may have directly jumped from bats to humans, with subsequent cross-transmission between humans and civets.^[51]

In order to infect cells, SARS-CoV-1 uses the spike surface glycoprotein to recognize and bind to host ACE-2, which it uses as a cellular entry receptor;^[51] the development of this characteristic was crucial in enabling SARS-CoV-1 to 'jump' from bats to other species.

MERS-CoV

First reported in 2012, MERS-CoV (Middle East respiratory syndrome coronavirus) marks the second known introduction of a highly pathogenic coronavirus from a zoonotic reservoir into humans. The case mortality rate of this emergent virus is approximately 35%, with 80% of all cases reported by Saudi Arabia.^[53] Although MERS-CoV is likely to have originated in bats,^[54] dromedary camels have been implicated as probable intermediate hosts. MERS-CoV is believed to have been circulating in these mammals for over 20 years,^[54] and it is thought that novel camel farming practices drove the spillover of MERS-CoV into humans.^[55] Studies have shown that humans can be infected with MERS-CoV via direct or indirect contact within infected dromedary camels, while human-to-human transmission is limited.^[53]

MERS-CoV gains cellular entry by using a spike surface protein to bind to the host DPP4 surface receptor; the core subdomain of this spike surface protein shares similarities with that of SARS-CoV, but its receptor binding subdomain (RBSD) significantly differs.^[54]

Bluetongue disease

Bluetongue disease is a non-contagious vector-borne disease caused by bluetongue virus, which affects species of ruminants (particularly sheep).^[56] Climate change has been implicated in the emergence and global spread of this disease, due to its impact on vector distribution. The natural vector of the bluetongue virus is the African midge C. imicola, which is normally limited to Africa and subtropical Asia. However, global warming has extended the geographic range of C. imicola, so that it now overlaps with a different vector (C. pulcaris or C. obsoletus) with a much more northward geographic range. This change enabled the bluetongue virus to jump vector, thus causing the northward spread of bluetongue disease into Europe.^[57]

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External links

"Emerging Viruses". MicrobiologyBytes. 2007. Archived from the original on 2007-02-24.
"National Center for Emerging and Zoonotic Infectious Diseases (NCEZID)". 19 November 2021.

[Holland-1] Holland DJ (February 1998). "Emerging viruses". Current Opinion in Pediatrics. 10 (1): 34–40. doi:10.1097/00008480-199802000-00007. PMID 9529635.

[Devaux2012-2] Devaux CA (February 2012). "Emerging and re-emerging viruses: A global challenge illustrated by Chikungunya virus outbreaks". World Journal of Virology. 1 (1): 11–22. doi:10.5501/wjv.v1.i1.11. PMC 3782263. PMID 24175207.

[Lindahl-3] ^ ^a ^b ^c ^d ^e ^f ^g ^h Lindahl JF, Grace D (2015). "The consequences of human actions on risks for infectious diseases: a review". Infection Ecology & Epidemiology. 5 (1): 30048. Bibcode:2015InfEE...530048L. doi:10.3402/iee.v5.30048. PMC 4663196. PMID 26615822.

[Morens2020-4] Morens DM, Fauci AS (September 2020). "Emerging pandemic diseases: how we got to COVID-19". Cell. 182 (5): 1077–1092. doi:10.1016/j.cell.2020.08.021. PMC 7428724. PMID 32846157.

[Zheng2020-5] Zheng J (2020). "SARS-CoV-2: an Emerging Coronavirus that Causes a Global Threat". International Journal of Biological Sciences. 16 (10): 1678–1685. doi:10.7150/ijbs.45053. PMC 7098030. PMID 32226285.

[Holmes2016-6] Holmes EC, Dudas G, Rambaut A, Andersen KG (October 2016). "The evolution of Ebola virus: Insights from the 2013-2016 epidemic". Nature. 538 (7624): 193–200. Bibcode:2016Natur.538..193H. doi:10.1038/nature19790. PMC 5580494. PMID 27734858.

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@@ Line 1: / Line 1: @@
 {{Short description|Classification of species of viruses}}
 {{cs1 config|name-list-style=vanc}}
-An '''emergent virus''' (or '''emerging virus''') is a [[virus]] that is either newly [[Viral evolution|appeared]], notably increasing in [[incidence (epidemiology)|incidence]]/[[geographic range limit|geographic range]] or has the potential to increase in the near future.<ref name="Holland">{{cite journal | vauthors = Holland DJ | title = Emerging viruses | journal = Current Opinion in Pediatrics | volume = 10 | issue = 1 | pages = 34–40 | date = February 1998 | pmid = 9529635 | doi = 10.1097/00008480-199802000-00007 }}</ref> Emergent viruses are a leading cause of [[emerging infectious disease]]s and raise [[public health]] challenges globally, given their potential to cause [[disease outbreak|outbreak]]s of disease which can lead to [[epidemic]]s and [[pandemic]]s.<ref name="Devaux2012">{{cite journal | vauthors = Devaux CA | title = Emerging and re-emerging viruses: A global challenge illustrated by Chikungunya virus outbreaks | journal = World Journal of Virology | volume = 1 | issue = 1 | pages = 11–22 | date = February 2012 | pmid = 24175207 | pmc = 3782263 | doi = 10.5501/wjv.v1.i1.11 | doi-access = free }}</ref> As well as causing [[disease]], emergent viruses can also have severe [[economy|economic]] implications.<ref name=Lindahl/> Recent examples include the [[SARS-related coronavirus]]es, which have caused the [[2002-2004 SARS outbreak|2002-2004 outbreak]] of [[severe acute respiratory syndrome|SARS]] ([[severe acute respiratory syndrome coronavirus|SARS-CoV-1]]) and the [[COVID-19 pandemic|2019–21 pandemic]] of [[coronavirus disease 2019|COVID-19]] ([[severe acute respiratory syndrome coronavirus 2|SARS-CoV-2]]).<ref name=Morens2020>{{cite journal |vauthors=Morens DM, Fauci AS |title=Emerging pandemic diseases: how we got to COVID-19 |journal=Cell |volume=182 |issue=5 |pages=1077–1092 |date=September 2020 |pmid=32846157 |pmc=7428724 |doi=10.1016/j.cell.2020.08.021 }}</ref><ref name="Zheng2020">{{cite journal | vauthors = Zheng J | title = SARS-CoV-2: an Emerging Coronavirus that Causes a Global Threat | journal = International Journal of Biological Sciences | volume = 16 | issue = 10 | pages = 1678–1685 | date = 2020 | pmid = 32226285 | pmc = 7098030 | doi = 10.7150/ijbs.45053 }}</ref> Other examples include the [[human immunodeficiency virus]] which causes [[HIV/AIDS]]; the viruses responsible for [[Ebola]];<ref name="Holmes2016">{{cite journal | vauthors = Holmes EC, Dudas G, Rambaut A, Andersen KG | title = The evolution of Ebola virus: Insights from the 2013-2016 epidemic | journal = Nature | volume = 538 | issue = 7624 | pages = 193–200 | date = October 2016 | pmid = 27734858 | pmc = 5580494 | doi = 10.1038/nature19790 | bibcode = 2016Natur.538..193H }}</ref> the [[H5N1]] influenza virus responsible for [[avian flu]];<ref name="Wei2016">{{cite journal | vauthors = Wei P, Cai Z, Hua J, Yu W, Chen J, Kang K, Qiu C, Ye L, Hu J, Ji K | display-authors = 6 | title = Pains and Gains from China's Experiences with Emerging Epidemics: From SARS to H7N9 | journal = BioMed Research International | volume = 2016 | pages = 5717108 | date = 2016 | pmid = 27525272 | pmc = 4971293 | doi = 10.1155/2016/5717108 | doi-access = free }}</ref> and [[H1N1/09]], which caused the [[2009 swine flu]] pandemic<ref name="Smith2009">{{cite journal | vauthors = Smith GJ, Vijaykrishna D, Bahl J, Lycett SJ, Worobey M, Pybus OG, Ma SK, Cheung CL, Raghwani J, Bhatt S, Peiris JS, Guan Y, Rambaut A | display-authors = 6 | title = Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic | journal = Nature | volume = 459 | issue = 7250 | pages = 1122–5 | date = June 2009 | pmid = 19516283 | doi = 10.1038/nature08182 | doi-access = free | bibcode = 2009Natur.459.1122S }}</ref> (an earlier emergent [[Viral strain|strain]] of [[H1N1]] caused the 1918 [[Spanish flu]] pandemic).<ref name="Taubenberger2006">{{cite journal | vauthors = Taubenberger JK, Morens DM | title = 1918 Influenza: the mother of all pandemics | journal = Emerging Infectious Diseases | volume = 12 | issue = 1 | pages = 15–22 | date = January 2006 | pmid = 16494711 | pmc = 3291398 | doi = 10.3201/eid1201.050979 }}</ref> Viral emergence in humans is often a consequence of [[zoonosis]], which involves a [[Cross-species transmission|cross-species jump]] of a [[viral disease]] into humans from other animals. As zoonotic viruses exist in [[Natural reservoir|animal reservoir]]s, they are much more difficult to [[eradication of infectious diseases|eradicate]] and can therefore establish persistent infections in human populations.<ref name="Eidson">{{cite web | vauthors = Eidson M |title=Zoonotic disease |url=https://www.britannica.com/science/zoonotic-disease |publisher=Britannica |access-date=16 April 2020}}</ref>
+An '''emergent virus''' (or '''emerging virus''') is a [[virus]] that is either newly [[Viral evolution|appeared]], notably increasing in [[incidence (epidemiology)|incidence]]/[[Marginal distribution (biology)|geographic range]] or has the potential to increase in the near future.<ref name="Holland">{{cite journal | vauthors = Holland DJ | title = Emerging viruses | journal = Current Opinion in Pediatrics | volume = 10 | issue = 1 | pages = 34–40 | date = February 1998 | pmid = 9529635 | doi = 10.1097/00008480-199802000-00007 }}</ref> Emergent viruses are a leading cause of [[emerging infectious disease]]s and raise [[public health]] challenges globally, given their potential to cause [[disease outbreak|outbreak]]s of disease which can lead to [[epidemic]]s and [[pandemic]]s.<ref name="Devaux2012">{{cite journal | vauthors = Devaux CA | title = Emerging and re-emerging viruses: A global challenge illustrated by Chikungunya virus outbreaks | journal = World Journal of Virology | volume = 1 | issue = 1 | pages = 11–22 | date = February 2012 | pmid = 24175207 | pmc = 3782263 | doi = 10.5501/wjv.v1.i1.11 | doi-access = free }}</ref> As well as causing [[disease]], emergent viruses can also have severe [[economy|economic]] implications.<ref name=Lindahl/> Recent examples include the [[SARS-related coronavirus]]es, which have caused the [[2002–2004 SARS outbreak|2002–2004 outbreak]] of [[SARS]] ([[SARS-CoV-1]]) and the [[COVID-19 pandemic|2019–2023 pandemic]] of [[COVID-19]] ([[SARS-CoV-2]]).<ref name=Morens2020>{{cite journal |vauthors=Morens DM, Fauci AS |title=Emerging pandemic diseases: how we got to COVID-19 |journal=Cell |volume=182 |issue=5 |pages=1077–1092 |date=September 2020 |pmid=32846157 |pmc=7428724 |doi=10.1016/j.cell.2020.08.021 }}</ref><ref name="Zheng2020">{{cite journal | vauthors = Zheng J | title = SARS-CoV-2: an Emerging Coronavirus that Causes a Global Threat | journal = International Journal of Biological Sciences | volume = 16 | issue = 10 | pages = 1678–1685 | date = 2020 | pmid = 32226285 | pmc = 7098030 | doi = 10.7150/ijbs.45053 }}</ref> Other examples include the [[HIV|human immunodeficiency virus]], which causes [[HIV/AIDS]]; the viruses responsible for [[Ebola]];<ref name="Holmes2016">{{cite journal | vauthors = Holmes EC, Dudas G, Rambaut A, Andersen KG | title = The evolution of Ebola virus: Insights from the 2013-2016 epidemic | journal = Nature | volume = 538 | issue = 7624 | pages = 193–200 | date = October 2016 | pmid = 27734858 | pmc = 5580494 | doi = 10.1038/nature19790 | bibcode = 2016Natur.538..193H }}</ref> the [[Influenza A virus subtype H5N1|H5N1]] influenza virus responsible for [[avian influenza]];<ref name="Wei2016">{{cite journal | vauthors = Wei P, Cai Z, Hua J, Yu W, Chen J, Kang K, Qiu C, Ye L, Hu J, Ji K | display-authors = 6 | title = Pains and Gains from China's Experiences with Emerging Epidemics: From SARS to H7N9 | journal = BioMed Research International | volume = 2016 | pages = 5717108 | date = 2016 | pmid = 27525272 | pmc = 4971293 | doi = 10.1155/2016/5717108 | doi-access = free }}</ref> and [[Pandemic H1N1/09 virus|H1N1/09]], which caused the [[2009 swine flu pandemic]]<ref name="Smith2009">{{cite journal | vauthors = Smith GJ, Vijaykrishna D, Bahl J, Lycett SJ, Worobey M, Pybus OG, Ma SK, Cheung CL, Raghwani J, Bhatt S, Peiris JS, Guan Y, Rambaut A | display-authors = 6 | title = Origins and evolutionary genomics of the 2009 swine-origin H1N1 influenza A epidemic | journal = Nature | volume = 459 | issue = 7250 | pages = 1122–5 | date = June 2009 | pmid = 19516283 | doi = 10.1038/nature08182 | doi-access = free | bibcode = 2009Natur.459.1122S }}</ref> (an earlier emergent [[Viral strain|strain]] of [[Influenza A virus subtype H1N1|H1N1]] caused the 1918 [[Spanish flu]] pandemic).<ref name="Taubenberger2006">{{cite journal | vauthors = Taubenberger JK, Morens DM | title = 1918 Influenza: the mother of all pandemics | journal = Emerging Infectious Diseases | volume = 12 | issue = 1 | pages = 15–22 | date = January 2006 | pmid = 16494711 | pmc = 3291398 | doi = 10.3201/eid1201.050979 }}</ref> Viral emergence in humans is often a consequence of [[zoonosis]], which involves a [[Cross-species transmission|cross-species jump]] of a [[viral disease]] into humans from other animals. As zoonotic viruses exist in [[Natural reservoir|animal reservoir]]s, they are much more difficult to [[eradication of infectious diseases|eradicate]] and can therefore establish persistent infections in human populations.<ref name="Eidson">{{cite web | vauthors = Eidson M |title=Zoonotic disease |url=https://www.britannica.com/science/zoonotic-disease |publisher=Britannica |access-date=16 April 2020}}</ref>
-Emergent viruses should not be confused with re-emerging viruses or newly detected viruses. A re-emerging virus is generally considered to be a previously appeared virus that is experiencing a resurgence,<ref name="Holland"/><ref name="Porta2008">{{cite book |editor=Miquel Porta |title=A Dictionary of Epidemiology |url=https://books.google.com/books?id=3Dr8dyuzvTkC |year=2008 |publisher=Oxford University Press, USA |isbn=978-0-19-971815-3 |pages = 78}}</ref> for example [[measles]].<ref name=Fraser-bell2019>{{cite journal | vauthors = Fraser-Bell C |title=Global Re-emergence of Measles - 2019 update |journal=Global Biosecurity |date=2019 |volume=1 |issue=3 |doi=10.31646/gbio.43 |language=en |issn=2652-0036|doi-access=free }}</ref> A newly detected virus is a previously unrecognized virus that had been circulating in the species as [[endemic (epidemiology)|endemic]] or [[epidemic]] infections.<ref name="Woolhouse2">{{cite journal | vauthors = Woolhouse M, Scott F, Hudson Z, Howey R, Chase-Topping M | title = Human viruses: discovery and emergence | journal = Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences | volume = 367 | issue = 1604 | pages = 2864–71 | date = October 2012 | pmid = 22966141 | pmc = 3427559 | doi = 10.1098/rstb.2011.0354 }}</ref> Newly detected viruses may have escaped [[Virus classification|classification]] because they left no distinctive [[Disease surveillance|clues]], and/or could not be isolated or propagated in [[Viral culture|cell culture]].<ref name="Leland">{{cite journal | vauthors = Leland DS, Ginocchio CC | title = Role of cell culture for virus detection in the age of technology | journal = Clinical Microbiology Reviews | volume = 20 | issue = 1 | pages = 49–78 | date = January 2007 | pmid = 17223623 | pmc = 1797634 | doi = 10.1128/CMR.00002-06 }}</ref> Examples include [[rhinovirus|human rhinovirus]] (a leading cause of common colds which was first identified in 1956),<ref name=Kennedy2012>{{cite journal | vauthors = Kennedy JL, Turner RB, Braciale T, Heymann PW, Borish L | title = Pathogenesis of rhinovirus infection | journal = Current Opinion in Virology | volume = 2 | issue = 3 | pages = 287–93 | date = June 2012 | pmid = 22542099 | pmc = 3378761 | doi = 10.1016/j.coviro.2012.03.008 }}</ref> [[hepatitis C]] (eventually identified in 1989),<ref name=Houghton>{{cite journal | vauthors = Houghton M | title = The long and winding road leading to the identification of the hepatitis C virus | journal = Journal of Hepatology | volume = 51 | issue = 5 | pages = 939–48 | date = November 2009 | pmid = 19781804 | doi = 10.1016/j.jhep.2009.08.004 | url = http://www.journal-of-hepatology.eu/article/S0168-8278%2809%2900535-2/fulltext | author-link = Michael Houghton (virologist) | doi-access = free }}</ref>  and [[human metapneumovirus]] (first described in 2001, but thought to have been circulating since the 19th century).<ref>{{cite journal | vauthors = de Graaf M, Osterhaus AD, Fouchier RA, Holmes EC | title = Evolutionary dynamics of human and avian metapneumoviruses | journal = The Journal of General Virology | volume = 89 | issue = Pt 12 | pages = 2933–2942 | date = December 2008 | pmid = 19008378 | doi = 10.1099/vir.0.2008/006957-0 | doi-access = free }}</ref> As the detection of such viruses is technology driven, the number reported is likely to expand.
+Emergent viruses should not be confused with re-emerging viruses or newly detected viruses. A re-emerging virus is generally considered to be a previously appeared virus that is experiencing a resurgence,<ref name="Holland"/><ref name="Porta2008">{{cite book |editor=Miquel Porta |title=A Dictionary of Epidemiology |url=https://books.google.com/books?id=3Dr8dyuzvTkC |year=2008 |publisher=Oxford University Press, USA |isbn=978-0-19-971815-3 |pages = 78}}</ref> for example [[measles]].<ref name=Fraser-bell2019>{{cite journal | vauthors = Fraser-Bell C |title=Global Re-emergence of Measles - 2019 update |journal=Global Biosecurity |date=2019 |volume=1 |issue=3 |doi=10.31646/gbio.43 |language=en |issn=2652-0036|doi-access=free }}</ref> A newly detected virus is a previously unrecognized virus that had been circulating in the species as [[endemic (epidemiology)|endemic]] or epidemic infections.<ref name="Woolhouse2">{{cite journal | vauthors = Woolhouse M, Scott F, Hudson Z, Howey R, Chase-Topping M | title = Human viruses: discovery and emergence | journal = Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences | volume = 367 | issue = 1604 | pages = 2864–71 | date = October 2012 | pmid = 22966141 | pmc = 3427559 | doi = 10.1098/rstb.2011.0354 }}</ref> Newly detected viruses may have escaped [[Virus classification|classification]] because they left no distinctive [[Disease surveillance|clues]] and/or could not be isolated or propagated in [[Viral culture|cell culture]].<ref name="Leland">{{cite journal | vauthors = Leland DS, Ginocchio CC | title = Role of cell culture for virus detection in the age of technology | journal = Clinical Microbiology Reviews | volume = 20 | issue = 1 | pages = 49–78 | date = January 2007 | pmid = 17223623 | pmc = 1797634 | doi = 10.1128/CMR.00002-06 }}</ref> Examples include [[rhinovirus|human rhinovirus]] (a leading cause of common colds which was first identified in 1956),<ref name=Kennedy2012>{{cite journal | vauthors = Kennedy JL, Turner RB, Braciale T, Heymann PW, Borish L | title = Pathogenesis of rhinovirus infection | journal = Current Opinion in Virology | volume = 2 | issue = 3 | pages = 287–93 | date = June 2012 | pmid = 22542099 | pmc = 3378761 | doi = 10.1016/j.coviro.2012.03.008 }}</ref> [[hepatitis C]] (eventually identified in 1989),<ref name=Houghton>{{cite journal | vauthors = Houghton M | title = The long and winding road leading to the identification of the hepatitis C virus | journal = Journal of Hepatology | volume = 51 | issue = 5 | pages = 939–48 | date = November 2009 | pmid = 19781804 | doi = 10.1016/j.jhep.2009.08.004 | url = http://www.journal-of-hepatology.eu/article/S0168-8278%2809%2900535-2/fulltext | author-link = Michael Houghton (virologist) | doi-access = free }}</ref>  and [[human metapneumovirus]] (first described in 2001, but thought to have been circulating since the 19th century).<ref>{{cite journal | vauthors = de Graaf M, Osterhaus AD, Fouchier RA, Holmes EC | title = Evolutionary dynamics of human and avian metapneumoviruses | journal = The Journal of General Virology | volume = 89 | issue = Pt 12 | pages = 2933–2942 | date = December 2008 | pmid = 19008378 | doi = 10.1099/vir.0.2008/006957-0 | doi-access = free }}</ref> As the detection of such viruses is technology driven, the number reported is likely to expand.
 ==Zoonosis==
 {{See also|Zoonosis}}
-Given the rarity of spontaneous development of new virus species, the most frequent cause of emergent viruses in humans is [[zoonosis]]. This phenomenon is estimated to account for 73% of all [[Emerging infectious disease|emerging or re-emerging pathogens]], with viruses playing a disproportionately large role.<ref name="Woolhouse"/> [[RNA virus]]es are particularly frequent, accounting for 37% of emerging and re-emerging pathogens.<ref name="Woolhouse">{{cite journal | vauthors = Woolhouse ME, Gowtage-Sequeria S | title = Host range and emerging and reemerging pathogens | journal = Emerging Infectious Diseases | volume = 11 | issue = 12 | pages = 1842–7 | date = December 2005 | pmid = 16485468 | pmc = 3367654 | doi = 10.3201/eid1112.050997 | author-link = Mark Woolhouse }}</ref> A broad range of animals - including wild birds, rodents and bats - are associated with zoonotic viruses.<ref name="Kruse">{{cite journal | vauthors = Kruse H, kirkemo AM, Handeland K | title = Wildlife as source of zoonotic infections | journal = Emerging Infectious Diseases | volume = 10 | issue = 12 | pages = 2067–72 | date = December 2004 | pmid = 15663840 | pmc = 3323390 | doi = 10.3201/eid1012.040707 }}</ref> It is not possible to predict specific zoonotic events that may be associated with a particular animal reservoir at any given time.<ref name="Domingo"/>
+Given the rarity of spontaneous development of new virus species, the most frequent cause of emergent viruses in humans is [[zoonosis]]. This phenomenon is estimated to account for 73% of all [[Emerging infectious disease|emerging or re-emerging pathogens]], with viruses playing a disproportionately large role.<ref name="Woolhouse"/> [[RNA virus]]es are particularly frequent, accounting for 37% of emerging and re-emerging pathogens.<ref name="Woolhouse">{{cite journal | vauthors = Woolhouse ME, Gowtage-Sequeria S | title = Host range and emerging and reemerging pathogens | journal = Emerging Infectious Diseases | volume = 11 | issue = 12 | pages = 1842–7 | date = December 2005 | pmid = 16485468 | pmc = 3367654 | doi = 10.3201/eid1112.050997 | author-link = Mark Woolhouse }}</ref> A broad range of animals '''—''' including wild birds, rodents, and bats '''—''' are associated with zoonotic viruses.<ref name="Kruse">{{cite journal | vauthors = Kruse H, kirkemo AM, Handeland K | title = Wildlife as source of zoonotic infections | journal = Emerging Infectious Diseases | volume = 10 | issue = 12 | pages = 2067–72 | date = December 2004 | pmid = 15663840 | pmc = 3323390 | doi = 10.3201/eid1012.040707 }}</ref> It is not possible to predict specific zoonotic events that may be associated with a particular animal reservoir at any given time.<ref name="Domingo"/>
-[[Spillover infection|Zoonotic spillover]] can either result in self-limited 'dead-end' infections, in which no further human-human transmission occurs (as with the [[rabies|rabies virus]]),<ref name="Baum">{{cite journal | vauthors = Baum SG | title = Zoonoses-with friends like this, who needs enemies? | journal = Transactions of the American Clinical and Climatological Association | volume = 119 | pages = 39–51; discussion 51–2 | year = 2008 | pmid = 18596867 | pmc = 2394705 }}</ref> or in infectious cases, in which the zoonotic pathogen is able to sustain human-human transmission (as with the [[Ebola|Ebola virus]]).<ref name=Holmes2016/> If the zoonotic virus is able to maintain successful human-human transmission, an [[Disease outbreak|outbreak]] may occur.<ref name=Parrish>{{cite journal | vauthors = Parrish CR, Holmes EC, Morens DM, Park EC, Burke DS, Calisher CH, Laughlin CA, Saif LJ, Daszak P | display-authors = 6 | title = Cross-species virus transmission and the emergence of new epidemic diseases | journal = Microbiology and Molecular Biology Reviews | volume = 72 | issue = 3 | pages = 457–70 | date = September 2008 | pmid = 18772285 | pmc = 2546865 | doi = 10.1128/MMBR.00004-08 }}</ref> Some spillover events can also result in the virus adapting exclusively for human infection (as occurred with the [[HIV|HIV virus]]),<ref name="AIDS">{{cite web |last1=THE AIDS INSTITUTE |title=Where did HIV come from? |url=https://www.theaidsinstitute.org/education/aids-101/where-did-hiv-come-0 |website=THE AIDS INSTITUTE |access-date=16 April 2020}}</ref> in which case humans become a new reservoir for the pathogen.
+[[Spillover infection|Zoonotic spillover]] can either result in self-limited 'dead-end' infections, in which no further human-to-human transmission occurs (as with the [[rabies|rabies virus]]),<ref name="Baum">{{cite journal | vauthors = Baum SG | title = Zoonoses-with friends like this, who needs enemies? | journal = Transactions of the American Clinical and Climatological Association | volume = 119 | pages = 39–51; discussion 51–2 | year = 2008 | pmid = 18596867 | pmc = 2394705 }}</ref> or in infectious cases, in which the zoonotic pathogen is able to sustain human-to-human transmission (as with the [[Zaire ebolavirus|Ebola virus]]).<ref name=Holmes2016/> If the zoonotic virus is able to maintain successful human-to-human transmission, an [[Disease outbreak|outbreak]] may occur.<ref name=Parrish>{{cite journal | vauthors = Parrish CR, Holmes EC, Morens DM, Park EC, Burke DS, Calisher CH, Laughlin CA, Saif LJ, Daszak P | display-authors = 6 | title = Cross-species virus transmission and the emergence of new epidemic diseases | journal = Microbiology and Molecular Biology Reviews | volume = 72 | issue = 3 | pages = 457–70 | date = September 2008 | pmid = 18772285 | pmc = 2546865 | doi = 10.1128/MMBR.00004-08 }}</ref> Some spillover events can also result in the virus adapting exclusively for human infection (as occurred with the [[HIV|HIV virus]]),<ref name="AIDS">{{cite web |last1=THE AIDS INSTITUTE |title=Where did HIV come from? |url=https://www.theaidsinstitute.org/education/aids-101/where-did-hiv-come-0 |website=THE AIDS INSTITUTE |access-date=16 April 2020}}</ref> in which case humans become a new reservoir for the pathogen.
-A successful zoonotic 'jump' depends on human contact with an animal harbouring a virus variant that is able to infect humans. In order to overcome host-range restrictions and sustain efficient human-human transmission, viruses originating from an animal reservoir will normally undergo [[mutation]], [[genetic recombination]] and [[reassortment]].<ref name="Domingo">{{cite journal | vauthors = Domingo E | title = Mechanisms of viral emergence | journal = Veterinary Research | volume = 41 | issue = 6 | pages = 38 | year = 2010 | pmid = 20167200 | pmc = 2831534 | doi = 10.1051/vetres/2010010 }}</ref> Due to their rapid replication and high mutation rates, RNA viruses are more likely to successfully adapt for invasion of a new host population.<ref name="Lindahl">{{cite journal | vauthors = Lindahl JF, Grace D | title = The consequences of human actions on risks for infectious diseases: a review | journal = Infection Ecology & Epidemiology | volume = 5 | pages = 30048 | date = 2015 | issue = 1 | pmid = 26615822 | pmc = 4663196 | doi = 10.3402/iee.v5.30048 | bibcode = 2015InfEE...530048L }}</ref>
+A successful zoonotic 'jump' depends on human contact with an animal harboring a virus variant that is able to infect humans. In order to overcome host-range restrictions and sustain efficient human-to-human transmission, viruses originating from an animal reservoir will normally undergo [[mutation]], [[genetic recombination]], and [[reassortment]].<ref name="Domingo">{{cite journal | vauthors = Domingo E | title = Mechanisms of viral emergence | journal = Veterinary Research | volume = 41 | issue = 6 | pages = 38 | year = 2010 | pmid = 20167200 | pmc = 2831534 | doi = 10.1051/vetres/2010010 }}</ref> Due to their rapid replication and high mutation rates, RNA viruses are more likely to successfully adapt for invasion of a new host population.<ref name="Lindahl">{{cite journal | vauthors = Lindahl JF, Grace D | title = The consequences of human actions on risks for infectious diseases: a review | journal = Infection Ecology & Epidemiology | volume = 5 | pages = 30048 | date = 2015 | issue = 1 | pmid = 26615822 | pmc = 4663196 | doi = 10.3402/iee.v5.30048 | bibcode = 2015InfEE...530048L }}</ref>
 ===Examples of animal sources===
@@ Line 17: / Line 17: @@
 [[File: Wikipedia-Bats-001-v01.jpg| 260px|thumb|upright=0.4|left|alt=Different bat species.|Different bat species]]
-While [[bat]]s are essential members of many ecosystems,<ref name="NSF">{{cite web |last1=National Science Foundation |title=The Night Life: Why We Need Bats All the Time-Not Just on Halloween |url=https://www.nsf.gov/discoveries/disc_summ.jsp?cntn_id=125883 |website=National Science Foundation |access-date=14 April 2020}}</ref> they are also frequently implicated as frequent sources of emerging virus infections.<ref name="Shi2013">{{cite journal | vauthors = Shi Z | title = Emerging infectious diseases associated with bat viruses | journal = Science China Life Sciences | volume = 56 | issue = 8 | pages = 678–82 | date = August 2013 | pmid = 23917838 | pmc = 7088756 | doi = 10.1007/s11427-013-4517-x }}</ref> Their [[immune system]]s have evolved in such a way as to suppress any [[Inflammation|inflammatory response]] to viral infections, thereby allowing them to become tolerant hosts for evolving viruses, and consequently provide major reservoirs of zoonotic viruses.<ref name=Subudhi2019>{{cite journal |vauthors=Subudhi S, Rapin N, Misra V |title=Immune system modulation and viral persistence in bats: understanding viral spillover |journal=Viruses |volume=11 |issue=2 |date=2019 |page=192 |pmid=30813403 |pmc=6410205 |doi=10.3390/v11020192 |doi-access=free }}</ref> They are associated with more zoonotic viruses per host species than any other mammal, and molecular studies have demonstrated that they are the natural hosts for several high-profile zoonotic viruses, including [[severe acute respiratory syndrome-related coronavirus]]es and [[Ebola]]/[[Marburg virus disease|Marburg]] hemorrhagic fever filoviruses.<ref name="O'Shea">{{cite journal | vauthors = O'Shea TJ, Cryan PM, Cunningham AA, Fooks AR, Hayman DT, Luis AD, Peel AJ, Plowright RK, Wood JL | display-authors = 6 | title = Bat flight and zoonotic viruses | journal = Emerging Infectious Diseases | volume = 20 | issue = 5 | pages = 741–5 | date = May 2014 | pmid = 24750692 | pmc = 4012789 | doi = 10.3201/eid2005.130539 }}</ref> In terms of their potential for spillover events, bats have taken over the leading role previously assigned to rodents.<ref name=Subudhi2019/> Viruses can be transmitted from bats via several mechanisms, including bites,<ref name="Wang2019">{{cite journal | vauthors = Wang LF, Anderson DE | title = Viruses in bats and potential spillover to animals and humans | journal = Current Opinion in Virology | volume = 34 | pages = 79–89 | date = February 2019 | pmid = 30665189 | pmc = 7102861 | doi = 10.1016/j.coviro.2018.12.007 }}</ref> aerosolization of saliva (e.g. during [[animal echolocation|echolocation]]), and faeces/urine.<ref name="Kuzmin">{{cite journal | vauthors = Kuzmin IV, Bozick B, Guagliardo SA, Kunkel R, Shak JR, Tong S, Rupprecht CE | title = Bats, emerging infectious diseases, and the rabies paradigm revisited | journal = Emerging Health Threats Journal | volume = 4 | pages = 7159 | date = June 2011 | pmid = 24149032 | pmc = 3168224 | doi = 10.3402/ehtj.v4i0.7159 }}</ref>
+While [[bat]]s are essential members of many ecosystems,<ref name="NSF">{{cite web |last1=National Science Foundation |title=The Night Life: Why We Need Bats All the Time-Not Just on Halloween |url=https://www.nsf.gov/discoveries/disc_summ.jsp?cntn_id=125883 |website=National Science Foundation |access-date=14 April 2020}}</ref> they are also frequently implicated as frequent sources of emerging virus infections.<ref name="Shi2013">{{cite journal | vauthors = Shi Z | title = Emerging infectious diseases associated with bat viruses | journal = Science China Life Sciences | volume = 56 | issue = 8 | pages = 678–82 | date = August 2013 | pmid = 23917838 | pmc = 7088756 | doi = 10.1007/s11427-013-4517-x }}</ref> Their [[immune system]]s have evolved in such a way as to suppress any [[Inflammation|inflammatory response]] to viral infections, thereby allowing them to become tolerant hosts for evolving viruses, and consequently provide major reservoirs of zoonotic viruses.<ref name=Subudhi2019>{{cite journal |vauthors=Subudhi S, Rapin N, Misra V |title=Immune system modulation and viral persistence in bats: understanding viral spillover |journal=Viruses |volume=11 |issue=2 |date=2019 |page=192 |pmid=30813403 |pmc=6410205 |doi=10.3390/v11020192 |doi-access=free }}</ref> They are associated with more zoonotic viruses per host species than any other mammal, and molecular studies have demonstrated that they are the natural hosts for several high-profile zoonotic viruses, including [[SARS-related coronavirus|severe acute respiratory syndrome'''–'''related coronaviruses]] and [[Ebola]]/[[Marburg virus disease|Marburg]] hemorrhagic fever filoviruses.<ref name="O'Shea">{{cite journal | vauthors = O'Shea TJ, Cryan PM, Cunningham AA, Fooks AR, Hayman DT, Luis AD, Peel AJ, Plowright RK, Wood JL | display-authors = 6 | title = Bat flight and zoonotic viruses | journal = Emerging Infectious Diseases | volume = 20 | issue = 5 | pages = 741–5 | date = May 2014 | pmid = 24750692 | pmc = 4012789 | doi = 10.3201/eid2005.130539 }}</ref> In terms of their potential for spillover events, bats have taken over the leading role previously assigned to rodents.<ref name=Subudhi2019/> Viruses can be transmitted from bats via several mechanisms, including bites,<ref name="Wang2019">{{cite journal | vauthors = Wang LF, Anderson DE | title = Viruses in bats and potential spillover to animals and humans | journal = Current Opinion in Virology | volume = 34 | pages = 79–89 | date = February 2019 | pmid = 30665189 | pmc = 7102861 | doi = 10.1016/j.coviro.2018.12.007 }}</ref> aerosolization of saliva (e.g., during [[animal echolocation|echolocation]]), and feces/urine.<ref name="Kuzmin">{{cite journal | vauthors = Kuzmin IV, Bozick B, Guagliardo SA, Kunkel R, Shak JR, Tong S, Rupprecht CE | title = Bats, emerging infectious diseases, and the rabies paradigm revisited | journal = Emerging Health Threats Journal | volume = 4 | pages = 7159 | date = June 2011 | pmid = 24149032 | pmc = 3168224 | doi = 10.3402/ehtj.v4i0.7159 }}</ref>
-Due to their distinct [[ecology]]/behaviour, bats are naturally more susceptible to viral infection and transmission. Several bat species (e.g. brown bats) aggregate in crowded roosts, which promotes intra- and interspecies viral transmission. Moreover, as bats are widespread in urban areas, humans occasionally encroach on their habitats which are contaminated with [[guano]] and urine. Their ability to fly and [[migration (ecology)|migration patterns]] also means that bats are able to spread disease over a large geographic area, while also acquiring new viruses.<ref name=Calisher/> Additionally, bats experience persistent viral infections which, together with their extreme longevity (some bat species have lifespans of 35 years), helps to maintain viruses and transmit them to other species. Other bat characteristics which contribute to their potency as viral hosts include: their food choices, [[torpor]]/[[hibernation]] habits, and susceptibility to reinfection.<ref name="Calisher">{{cite journal|author1-link=Charles Calisher | vauthors = Calisher CH, Childs JE, Field HE, Holmes KV, Schountz T | title = Bats: important reservoir hosts of emerging viruses | journal = Clinical Microbiology Reviews | volume = 19 | issue = 3 | pages = 531–45 | date = July 2006 | pmid = 16847084 | pmc = 1539106 | doi = 10.1128/CMR.00017-06 }}</ref>
+Due to their distinct [[ecology]]/behavior, bats are naturally more susceptible to viral infection and transmission. Several bat species (e.g., brown bats) aggregate in crowded roosts, which promotes intra- and interspecies viral transmission. Moreover, as bats are widespread in urban areas, humans occasionally encroach on their habitats which are contaminated with [[guano]] and urine. Their ability to fly and [[migration (ecology)|migration patterns]] also means that bats are able to spread disease over a large geographic area, while also acquiring new viruses.<ref name=Calisher/> Additionally, bats experience persistent viral infections which, together with their extreme longevity (some bat species have lifespans of 35 years), helps to maintain viruses and transmit them to other species. Other bat characteristics which contribute to their potency as viral hosts include: their food choices, [[torpor]]/[[hibernation]] habits, and susceptibility to reinfection.<ref name="Calisher">{{cite journal|author1-link=Charles Calisher | vauthors = Calisher CH, Childs JE, Field HE, Holmes KV, Schountz T | title = Bats: important reservoir hosts of emerging viruses | journal = Clinical Microbiology Reviews | volume = 19 | issue = 3 | pages = 531–45 | date = July 2006 | pmid = 16847084 | pmc = 1539106 | doi = 10.1128/CMR.00017-06 }}</ref>
 ==Drivers of viral emergence==
 {{See also | Infection#Emerging diseases}}
-Viral emergence is often a consequence of both [[Infection#Emerging diseases|nature and human activity]]. In particular, [[Ecological succession|ecological change]]s can greatly facilitate the emergence and re-emergence of zoonotic viruses.<ref name=Woolhouse2007>{{cite journal | vauthors = Woolhouse M, Gaunt E | s2cid = 19213392 | title = Ecological origins of novel human pathogens | journal = Critical Reviews in Microbiology | volume = 33 | issue = 4 | pages = 231–42 | date = 2007 | pmid = 18033594 | doi = 10.1080/10408410701647560 }}</ref> Factors such as [[deforestation]], [[reforestation]], [[habitat fragmentation]] and [[irrigation]] can all impact the ways in which humans come into contact with wild animal species, and consequently promote virus emergence.<ref name=Lindahl/><ref name="Nava">{{cite journal | vauthors = Nava A, Shimabukuro JS, Chmura AA, Luz SL | title = The Impact of Global Environmental Changes on Infectious Disease Emergence with a Focus on Risks for Brazil | journal = ILAR Journal | volume = 58 | issue = 3 | pages = 393–400 | date = December 2017 | pmid = 29253158 | doi = 10.1093/ilar/ilx034 | doi-access = free }}</ref> In particular, habitat loss of reservoir host species plays a significant role in emerging [[zoonoses]].<ref>{{Citation |last=von Csefalvay |first=Chris |title=Host-vector and multihost systems |date=2023 |url=https://linkinghub.elsevier.com/retrieve/pii/B978032395389400013X |work=Computational Modeling of Infectious Disease |pages=121–149 |publisher=Elsevier |language=en |doi=10.1016/b978-0-32-395389-4.00013-x |isbn=978-0-323-95389-4 |access-date=2023-03-02}}</ref> Additionally, [[climate change (general concept)|climate change]] can affect [[ecosystem]]s and [[Vector (epidemiology)|vector]] distribution, which in turn can affect the emergence of vector-borne viruses. Other [[ecology|ecological changes]] - for example, species introduction and predator loss - can also affect virus emergence and prevalence. Some [[agriculture|agricultural]] practices, for example livestock intensification and inappropriate management/disposal of farm animal faeces, are also associated with an increased risk of zoonosis.<ref name=Lindahl/><ref name="Penakalapati">{{cite journal | vauthors = Penakalapati G, Swarthout J, Delahoy MJ, McAliley L, Wodnik B, Levy K, Freeman MC | title = Exposure to Animal Feces and Human Health: A Systematic Review and Proposed Research Priorities | journal = Environmental Science & Technology | volume = 51 | issue = 20 | pages = 11537–11552 | date = October 2017 | pmid = 28926696 | pmc = 5647569 | doi = 10.1021/acs.est.7b02811 | bibcode = 2017EnST...5111537P }}</ref>
+Viral emergence is often a consequence of both [[Infection#Emerging diseases|nature and human activity]]. In particular, [[Ecological succession|ecological change]]s can greatly facilitate the emergence and re-emergence of zoonotic viruses.<ref name=Woolhouse2007>{{cite journal | vauthors = Woolhouse M, Gaunt E | s2cid = 19213392 | title = Ecological origins of novel human pathogens | journal = Critical Reviews in Microbiology | volume = 33 | issue = 4 | pages = 231–42 | date = 2007 | pmid = 18033594 | doi = 10.1080/10408410701647560 }}</ref> Factors such as [[deforestation]], [[reforestation]], [[habitat fragmentation]], and [[irrigation]] can all impact the ways in which humans come into contact with wild animal species and consequently promote virus emergence.<ref name="Lindahl" /><ref name="Nava">{{cite journal | vauthors = Nava A, Shimabukuro JS, Chmura AA, Luz SL | title = The Impact of Global Environmental Changes on Infectious Disease Emergence with a Focus on Risks for Brazil | journal = ILAR Journal | volume = 58 | issue = 3 | pages = 393–400 | date = December 2017 | pmid = 29253158 | doi = 10.1093/ilar/ilx034 | doi-access = free }}</ref> In particular, habitat loss of reservoir host species plays a significant role in emerging [[Zoonosis|zoonoses]].<ref>{{Citation |last=von Csefalvay |first=Chris |title=Host-vector and multihost systems |date=2023 |url=https://linkinghub.elsevier.com/retrieve/pii/B978032395389400013X |work=Computational Modeling of Infectious Disease |pages=121–149 |publisher=Elsevier |language=en |doi=10.1016/b978-0-32-395389-4.00013-x |isbn=978-0-323-95389-4 |access-date=2023-03-02}}</ref> Additionally, [[Climate variability and change|climate change]] can affect [[ecosystem]]s and [[Disease vector|vector]] distribution, which in turn can affect the emergence of vector-borne viruses. Other [[ecology|ecological changes]] '''—''' for example, species introduction and predator loss '''—''' can also affect virus emergence and prevalence. Some [[agriculture|agricultural]] practices '''—''' for example, livestock intensification and inappropriate management/disposal of farm animal feces '''—''' are also associated with an increased risk of zoonosis.<ref name=Lindahl/><ref name="Penakalapati">{{cite journal | vauthors = Penakalapati G, Swarthout J, Delahoy MJ, McAliley L, Wodnik B, Levy K, Freeman MC | title = Exposure to Animal Feces and Human Health: A Systematic Review and Proposed Research Priorities | journal = Environmental Science & Technology | volume = 51 | issue = 20 | pages = 11537–11552 | date = October 2017 | pmid = 28926696 | pmc = 5647569 | doi = 10.1021/acs.est.7b02811 | bibcode = 2017EnST...5111537P }}</ref>
-Viruses may also emerge due to the establishment of human populations that are vulnerable to infection. For example, a virus may emerge following loss of [[cross-reactivity|cross-protective immunity]], which may occur due to loss of a wild virus or termination of [[vaccination]] programmes. Well-developed countries also have higher proportions of [[population aging|aging citizens]] and [[obesity|obesity-related disease]], thus meaning that their populations may be more immunosuppressed and therefore at risk of infection.<ref name=Lindahl/> Contrastingly, poorer nations may have immunocompromised populations due to [[malnutrition]] or chronic infection; these countries are also unlikely to have stable vaccination programmes.<ref name=Lindahl/> Additionally, changes in human [[demography|demographics]]<ref name=Lindahl/> – for example, the birth and/or migration of immunologically naïve individuals – can lead to the development of a susceptible population that enables large-scale virus infection.
+Viruses may also emerge due to the establishment of human populations that are vulnerable to infection. For example, a virus may emerge following loss of [[cross-reactivity|cross-protective immunity]], which may occur due to loss of a wild virus or termination of [[vaccination]] program. Well-developed countries also have higher proportions of [[Population ageing|aging citizens]] and [[obesity|obesity-related disease]], thus meaning that their populations may be more immunosuppressed and therefore at risk of infection.<ref name=Lindahl/> Contrastingly, poorer nations may have immunocompromised populations due to [[malnutrition]] or chronic infection; these countries are also unlikely to have stable vaccination program.<ref name=Lindahl/> Additionally, changes in human [[demography|demographics]]<ref name=Lindahl/> '''—''' for example, the birth and/or migration of immunologically naïve individuals '''—''' can lead to the development of a susceptible population that enables large-scale virus infection.
-Other factors which can promote viral emergence include [[globalisation]]; in particular, [[international trade]] and human travel/[[human migration|migration]] can result in the introduction of viruses into new areas.<ref name=Lindahl/> Moreover, as densely populated cities promote rapid pathogen transmission, uncontrolled [[urbanization]] (i.e. the increased movement and settling of individuals in [[urban area]]s) can promote viral emergence.<ref name="Neiderud">{{cite journal | vauthors = Neiderud CJ | title = How urbanization affects the epidemiology of emerging infectious diseases | journal = Infection Ecology & Epidemiology | volume = 5 | issue = 1 | pages = 27060 | date = 2015 | pmid = 26112265 | pmc = 4481042 | doi = 10.3402/iee.v5.27060 | bibcode = 2015InfEE...527060N }}</ref> [[Animal migration]] can also lead to the emergence of viruses, as was the case for the [[West Nile virus]] which was spread by migrating bird populations.<ref name="Rappole">{{cite journal | vauthors = Rappole JH, Derrickson SR, Hubálek Z | title = Migratory birds and spread of West Nile virus in the Western Hemisphere | journal = Emerging Infectious Diseases | volume = 6 | issue = 4 | pages = 319–28 | date = 2000 | pmid = 10905964 | pmc = 2640881 | doi = 10.3201/eid0604.000401 }}</ref> Additionally, human practices regarding food production and consumption can also contribute to the risk of viral emergence. In particular, [[wet market]]s (i.e. live animal markets) are an ideal environment for virus transfer, due to the high density of people and wild/farmed animals present.<ref name=Kuzmin/> Consumption of [[bushmeat]] is also associated with pathogen emergence.<ref name=Kuzmin/>
+Other factors which can promote viral emergence include [[globalization]]; in particular, [[international trade]] and human travel/[[human migration|migration]] can result in the introduction of viruses into new areas.<ref name=Lindahl/> Moreover, as densely populated cities promote rapid pathogen transmission, uncontrolled [[urbanization]] (i.e., the increased movement and settling of individuals in [[urban area]]s) can promote viral emergence.<ref name="Neiderud">{{cite journal | vauthors = Neiderud CJ | title = How urbanization affects the epidemiology of emerging infectious diseases | journal = Infection Ecology & Epidemiology | volume = 5 | issue = 1 | pages = 27060 | date = 2015 | pmid = 26112265 | pmc = 4481042 | doi = 10.3402/iee.v5.27060 | bibcode = 2015InfEE...527060N }}</ref> [[Animal migration]] can also lead to the emergence of viruses, as was the case for the [[West Nile virus]] which was spread by migrating bird populations.<ref name="Rappole">{{cite journal | vauthors = Rappole JH, Derrickson SR, Hubálek Z | title = Migratory birds and spread of West Nile virus in the Western Hemisphere | journal = Emerging Infectious Diseases | volume = 6 | issue = 4 | pages = 319–28 | date = 2000 | pmid = 10905964 | pmc = 2640881 | doi = 10.3201/eid0604.000401 }}</ref> Additionally, human practices regarding food production and consumption can also contribute to the risk of viral emergence. In particular, [[wet market]]s (i.e., live animal markets) are an ideal environment for virus transfer, due to the high density of people and wild/farmed animals present.<ref name=Kuzmin/> Consumption of [[bushmeat]] is also associated with pathogen emergence.<ref name=Kuzmin/>
 == Prevention ==
-Control and prevention of zoonotic diseases depends on appropriate global surveillance at various levels, including identification of novel pathogens,  [[public health surveillance]] (including [[serological survey]]s), and [[risk analysis|analysis of the risks]] of transmission.<ref name=Rahman2020/> The complexity of zoonotic events around the world predicates a multidisciplinary approach to prevention.<ref name=Rahman2020/> The [[One Health Model]] has been proposed as a global strategy to help prevent the emergence of zoonotic diseases in humans, including novel viral diseases.<ref name=Rahman2020>{{cite journal |vauthors=Rahman MT, Sobur MA, Islam MS, et al. |title=Zoonotic diseases: etiology, impact, and control |journal=Microorganisms |volume=8 |issue=9 |date=September 2020 |page=1405 |pmid=32932606 |doi=10.3390/microorganisms8091405 |pmc=7563794 |doi-access=free }}</ref> The One Health concept aims to promote the health of animals, humans, and the environment, both locally and globally, by fostering understanding and collaboration between practitioners of different interrelated disciplines, including [[wildlife biology]], [[veterinary science]], [[medicine]], [[agriculture]], [[ecology]], [[microbiology]], [[epidemiology]], and [[biomedical engineering]].<ref name=Rahman2020/><ref>{{Citation |last=von Csefalvay |first=Chris |title=Host-vector and multihost systems |date=2023 |url=https://linkinghub.elsevier.com/retrieve/pii/B978032395389400013X |work=Computational Modeling of Infectious Disease |pages=121–149 |publisher=Elsevier |language=en |doi=10.1016/b978-0-32-395389-4.00013-x |isbn=978-0-323-95389-4 |access-date=2023-03-02}}</ref>
+Control and prevention of zoonotic diseases depends on appropriate global surveillance at various levels, including identification of novel pathogens, [[public health surveillance]] (including [[Serology#Serological surveys|serological surveys]]), and [[Risk management|analysis of the risks]] of transmission.<ref name=Rahman2020/> The complexity of zoonotic events around the world predicates a multidisciplinary approach to prevention.<ref name=Rahman2020/> The [[One Health Model]] has been proposed as a global strategy to help prevent the emergence of zoonotic diseases in humans, including novel viral diseases.<ref name=Rahman2020>{{cite journal |vauthors=Rahman MT, Sobur MA, Islam MS, et al. |title=Zoonotic diseases: etiology, impact, and control |journal=Microorganisms |volume=8 |issue=9 |date=September 2020 |page=1405 |pmid=32932606 |doi=10.3390/microorganisms8091405 |pmc=7563794 |doi-access=free }}</ref> The One Health concept aims to promote the health of animals, humans, and the environment, both locally and globally, by fostering understanding and collaboration between practitioners of different interrelated disciplines, including [[Wildlife biologist|wildlife biology]], [[Veterinary medicine|veterinary science]], [[medicine]], [[agriculture]], [[ecology]], [[microbiology]], [[epidemiology]], and [[biomedical engineering]].<ref name=Rahman2020/><ref>{{Citation |last=von Csefalvay |first=Chris |title=Host-vector and multihost systems |date=2023 |url=https://linkinghub.elsevier.com/retrieve/pii/B978032395389400013X |work=Computational Modeling of Infectious Disease |pages=121–149 |publisher=Elsevier |language=en |doi=10.1016/b978-0-32-395389-4.00013-x |isbn=978-0-323-95389-4 |access-date=2023-03-02}}</ref>
 ==Virulence of emergent viruses==
-As hosts are immunologically naïve to pathogens they have not encountered before, emergent viruses are often extremely [[virulence|virulent]] in terms of their capacity to cause disease. Their high virulence is also due to a lack of adaptation to the new host; viruses normally exert strong [[evolutionary pressure|selection pressure]] on the immune systems of their natural hosts, which in turn exerts a strong selection pressure on viruses.<ref name="Dominguez">{{cite journal | vauthors = Domínguez-Andrés J, Netea MG | title = Impact of Historic Migrations and Evolutionary Processes on Human Immunity | journal = Trends in Immunology | volume = 40 | issue = 12 | pages = 1105–1119 | date = December 2019 | pmid = 31786023 | pmc = 7106516 | doi = 10.1016/j.it.2019.10.001 }}</ref> This [[coevolution]] means that the natural host is able to manage infection. However, when the virus jumps to a new host (e.g. humans), the new host is unable to deal with infection due to a lack of coevolution, which results in mismatch between host [[wikt:immunoeffector|immunoeffector]]s and virus [[Biological response modifier|immunomodulator]]s.{{cn|date=January 2023}}
+As hosts are immunologically naïve to pathogens they have not encountered before, emergent viruses are often extremely [[virulence|virulent]] in terms of their capacity to cause disease. Their high virulence is also due to a lack of adaptation to the new host; viruses normally exert strong [[evolutionary pressure|selection pressure]] on the immune systems of their natural hosts, which in turn exerts a strong selection pressure on viruses.<ref name="Dominguez">{{cite journal | vauthors = Domínguez-Andrés J, Netea MG | title = Impact of Historic Migrations and Evolutionary Processes on Human Immunity | journal = Trends in Immunology | volume = 40 | issue = 12 | pages = 1105–1119 | date = December 2019 | pmid = 31786023 | pmc = 7106516 | doi = 10.1016/j.it.2019.10.001 }}</ref> This [[coevolution]] means that the natural host is able to manage infection. However, when the virus jumps to a new host (e.g., humans), the new host is unable to deal with infection due to a lack of coevolution, which results in mismatch between host [[wikt:immunoeffector|immunoeffector]]s and virus [[Biological response modifier|immunomodulator]]s.{{cn|date=January 2023}}
-Additionally, in order to maximise transmission, viruses often naturally undergo attenuation (i.e. [[virulence]] is reduced) so that infected animals can survive long enough to infect other animals more efficiently.<ref name="Longdon">{{cite journal | vauthors = Longdon B, Hadfield JD, Day JP, Smith SC, McGonigle JE, Cogni R, Cao C, Jiggins FM | display-authors = 6 | title = The causes and consequences of changes in virulence following pathogen host shifts | journal = PLOS Pathogens | volume = 11 | issue = 3 | pages = e1004728 | date = March 2015 | pmid = 25774803 | pmc = 4361674 | doi = 10.1371/journal.ppat.1004728 | doi-access = free }}</ref> However, as attenuation takes time to achieve, new host populations will not initially benefit from this phenomenon. Moreover, as zoonotic viruses also naturally exist in [[natural reservoir|animal reservoirs]],<ref name=Eidson/> their survival is not dependent on transmission between new hosts; this means that emergent viruses are even more unlikely to attenuate for the purpose of maximal transmission, and they remain virulent.{{cn|date=January 2023}}
+Additionally, in order to maximize transmission, viruses often naturally undergo attenuation (i.e., [[virulence]] is reduced) so that infected animals can survive long enough to infect other animals more efficiently.<ref name="Longdon">{{cite journal | vauthors = Longdon B, Hadfield JD, Day JP, Smith SC, McGonigle JE, Cogni R, Cao C, Jiggins FM | display-authors = 6 | title = The causes and consequences of changes in virulence following pathogen host shifts | journal = PLOS Pathogens | volume = 11 | issue = 3 | pages = e1004728 | date = March 2015 | pmid = 25774803 | pmc = 4361674 | doi = 10.1371/journal.ppat.1004728 | doi-access = free }}</ref> However, as attenuation takes time to achieve, new host populations will not initially benefit from this phenomenon. Moreover, as zoonotic viruses also naturally exist in [[natural reservoir|animal reservoirs]],<ref name=Eidson/> their survival is not dependent on transmission between new hosts; this means that emergent viruses are even more unlikely to attenuate for the purpose of maximal transmission, and they remain virulent.{{cn|date=January 2023}}
-Although emergent viruses are frequently highly virulent, they are limited by several host factors including: [[innate immune system|innate immunity]], [[Antibody#Natural antibodies|natural antibodies]] and [[binding selectivity|receptor specificity]]. If the host has previously been infected by a pathogen that is similar to the emergent virus, the host may also benefit from [[cross-reactivity|cross-protective immunity]].{{cn|date=January 2023}}
+Although emergent viruses are frequently highly virulent, they are limited by several host factors including: [[innate immune system|innate immunity]], [[Antibody#Natural antibodies|natural antibodies]], and [[binding selectivity|receptor specificity]]. If the host has previously been infected by a pathogen that is similar to the emergent virus, the host may also benefit from [[cross-reactivity|cross-protective immunity]].{{cn|date=January 2023}}
 ==Examples of emergent viruses==
@@ Line 46: / Line 46: @@
 [[File: EM of influenza virus.jpg| 210px|thumb|upright=0.4|right|alt=Electron micrograph of influenza virus, magnification is approximately 100,000.|Electron micrograph of influenza virus, magnification is approximately 100,000]]
-[[Influenza]] is a highly contagious respiratory infection, which affects approximately 9% of the global population and causes 300,000 to 500,000 deaths annually.<ref name="Clayville">{{cite journal | vauthors = Clayville LR | title = Influenza update: a review of currently available vaccines | journal = P & T | volume = 36 | issue = 10 | pages = 659–84 | date = October 2011 | pmid = 22346299 | pmc = 3278149 }}</ref><ref name="UNICEF">{{cite web |last1=UNICEF |title=Influenza |url=https://www.unicef.org/flu/ |website=UNICEF |access-date=14 April 2020}}</ref> Based on their core proteins, influenza viruses are classified into types A, B, C and D.<ref name="WHO">{{cite web |vauthors=((World Health Organization)) |title=Influenza |url=https://www.who.int/biologicals/vaccines/influenza/en/ |archive-url=https://web.archive.org/web/20130617180153/http://www.who.int/biologicals/vaccines/influenza/en/ |url-status=dead |archive-date=June 17, 2013 |publisher=World Health Organization |access-date=13 April 2020}}</ref><ref name="WHO2">{{cite web |vauthors=((World Health Organization)) |title=Influenza (Avian and other zoonotic) |url=https://www.who.int/news-room/fact-sheets/detail/influenza-(avian-and-other-zoonotic) |publisher=WHO |access-date=13 April 2020}}</ref> While both influenza A and B can cause epidemics in humans, influenza A also has pandemic potential and a higher mutation rate, therefore is most significant to public health.<ref name=WHO2/><ref name="CDC">{{cite web |last1=Centers for Disease Control and Prevention |title=Influenza (Flu) |date=18 November 2019 |url=https://www.cdc.gov/flu/about/viruses/types.htm |publisher=CDC |access-date=13 April 2020}}</ref>
+[[Influenza]] is a highly contagious respiratory infection, which affects approximately 9% of the global population and causes 300,000 to 500,000 deaths annually.<ref name="Clayville">{{cite journal | vauthors = Clayville LR | title = Influenza update: a review of currently available vaccines | journal = P & T | volume = 36 | issue = 10 | pages = 659–84 | date = October 2011 | pmid = 22346299 | pmc = 3278149 }}</ref><ref name="UNICEF">{{cite web |last1=UNICEF |title=Influenza |url=https://www.unicef.org/flu/ |website=UNICEF |access-date=14 April 2020}}</ref> Based on their core proteins, influenza viruses are classified into types A, B, C, and D.<ref name="WHO">{{cite web |vauthors=((World Health Organization)) |title=Influenza |url=https://www.who.int/biologicals/vaccines/influenza/en/ |archive-url=https://web.archive.org/web/20130617180153/http://www.who.int/biologicals/vaccines/influenza/en/ |url-status=dead |archive-date=June 17, 2013 |publisher=World Health Organization |access-date=13 April 2020}}</ref><ref name="WHO2">{{cite web |vauthors=((World Health Organization)) |title=Influenza (Avian and other zoonotic) |url=https://www.who.int/news-room/fact-sheets/detail/influenza-(avian-and-other-zoonotic) |publisher=WHO |access-date=13 April 2020}}</ref> While both influenza A and B can cause epidemics in humans, influenza A also has pandemic potential and a higher mutation rate and is therefore most significant to public health.<ref name=WHO2/><ref name="CDC">{{cite web |last1=Centers for Disease Control and Prevention |title=Influenza (Flu) |date=18 November 2019 |url=https://www.cdc.gov/flu/about/viruses/types.htm |publisher=CDC |access-date=13 April 2020}}</ref>
 Influenza A viruses are further classified into subtypes, based on the combinations of the surface [[glycoprotein]]s [[hemagglutinin]] (HA) and [[neuraminidase]] (NA). The primary natural reservoir for most influenza A subtypes are wild aquatic birds;<ref name=WHO2/> however, through a series of mutations, a small subset of these viruses have adapted for infection of humans (and other animals).<ref name="Byrd">{{cite journal | vauthors = Byrd-Leotis L, Cummings RD, Steinhauer DA | title = The Interplay between the Host Receptor and Influenza Virus Hemagglutinin and Neuraminidase | journal = International Journal of Molecular Sciences | volume = 18 | issue = 7 | pages = 1541 | date = July 2017 | pmid = 28714909 | pmc = 5536029 | doi = 10.3390/ijms18071541 | doi-access = free }}</ref> A key determinant of whether a particular influenza A subtype can infect humans is its binding specificity. Avian influenza A preferentially binds to cell surface receptors with a terminal α2,3‐linked [[sialic acid]], while human influenza A preferentially binds to cell surface receptors with a terminal α2,6‐linked sialic acid. Via mutation, some avian influenza A viruses have successfully altered their binding specificity from α2,3‐ to α2,6‐linked sialic acid.<ref name="Lewis">{{cite journal | vauthors = Lewis DB | title = Avian flu to human influenza | journal = Annual Review of Medicine | volume = 57 | pages = 139–54 | date = 2006 | pmid = 16409141 | doi = 10.1146/annurev.med.57.121304.131333 }}</ref> However, in order to emerge in humans, avian influenza A viruses must also adapt their [[RNA polymerase]]s for function in mammalian cells,<ref name=Long>{{cite journal | vauthors = Long JS, Giotis ES, Moncorgé O, Frise R, Mistry B, James J, Morisson M, Iqbal M, Vignal A, Skinner MA, Barclay WS | display-authors = 6 | title = Species difference in ANP32A underlies influenza A virus polymerase host restriction | journal = Nature | volume = 529 | issue = 7584 | pages = 101–4 | date = January 2016 | pmid = 26738596 | pmc = 4710677 | doi = 10.1038/nature16474 | bibcode = 2016Natur.529..101L }}</ref> as well as mutating for stability in the acidic respiratory tract of humans.<ref name="Lella">{{cite journal | vauthors = Di Lella S, Herrmann A, Mair CM | title = Modulation of the pH Stability of Influenza Virus Hemagglutinin: A Host Cell Adaptation Strategy | journal = Biophysical Journal | volume = 110 | issue = 11 | pages = 2293–2301 | date = June 2016 | pmid = 27276248 | pmc = 4906160 | doi = 10.1016/j.bpj.2016.04.035 | bibcode = 2016BpJ...110.2293D }}</ref>
-Following [[adaptation]] and [[host switch]], influenza A viruses have the potential to cause epidemics and pandemics in humans. Minor changes in HA and NA structure ([[antigenic drift]]) occur frequently, which enables the virus to cause repetitive outbreaks (i.e. [[flu season|seasonal influenza]]) by evading immune recognition.<ref name=WHO/> Major changes in HA and NA structure ([[antigenic shift]]), which are caused by genetic reassortment between different influenza A subtypes (e.g. between human and animal subtypes), can instead cause large regional/global [[pandemic]]s.<ref name=WHO/> Due to the emergence of antigenically different influenza A strains in humans, four pandemics occurred in the 20th century alone.<ref name="Alexander">{{cite journal | vauthors = Alexander DJ | title = Avian influenza viruses and human health | journal = Developments in Biologicals | volume = 124 | pages = 77–84 | date = 2006 | pmid = 16447497 }}</ref>
+Following [[adaptation]] and [[host switch]], influenza A viruses have the potential to cause epidemics and pandemics in humans. Minor changes in HA and NA structure ([[antigenic drift]]) occur frequently, which enables the virus to cause repetitive outbreaks (i.e., [[flu season|seasonal influenza]]) by evading immune recognition.<ref name=WHO/> Major changes in HA and NA structure ([[antigenic shift]]), which are caused by genetic reassortment between different influenza A subtypes (e.g., between human and animal subtypes), can instead cause large regional/global [[pandemic]]s.<ref name=WHO/> Due to the emergence of antigenically different influenza A strains in humans, four [[Influenza pandemic|influenza pandemics]] occurred in the 20th century alone.<ref name="Alexander">{{cite journal | vauthors = Alexander DJ | title = Avian influenza viruses and human health | journal = Developments in Biologicals | volume = 124 | pages = 77–84 | date = 2006 | pmid = 16447497 }}</ref>
-Additionally, although animal influenza A viruses (e.g. [[swine influenza]]) are distinct from human influenza viruses, they can still cause zoonotic infection in humans. These infections are largely acquired following direct contact with infected animals or contaminated environments, but do not result in efficient human-human transmission; examples of this include [[Influenza A virus subtype H5N1|H5N1 influenza]] and [[Influenza A virus subtype H7N9|H7N9 influenza]].<ref name=WHO2/>
+Additionally, although animal influenza A viruses (e.g., [[swine influenza]]) are distinct from human influenza viruses, they can still cause zoonotic infection in humans. These infections are largely acquired following direct contact with infected animals or contaminated environments, but do not result in efficient human-to-human transmission; examples of this include [[Influenza A virus subtype H5N1|H5N1 influenza]] and [[Influenza A virus subtype H7N9|H7N9 influenza]].<ref name=WHO2/>
-===SARS-CoV===
+===SARS-CoV-1===
 [[File: SARS virion.gif| 210px|thumb|upright=0.4|left|alt=Electron micrograph of SARS-CoV.|Electron micrograph of SARS-CoV]]
-In 2002, a highly pathogenic [[Severe acute respiratory syndrome coronavirus|SARS-CoV]] (Severe Acute Respiratory Syndrome Coronavirus) strain emerged from a zoonotic reservoir; approximately 8000 people were infected worldwide, and mortality rates approached 50% or more in the elderly.<ref name="Bolles">{{cite journal | vauthors = Bolles M, Donaldson E, Baric R | title = SARS-CoV and emergent coronaviruses: viral determinants of interspecies transmission | journal = Current Opinion in Virology | volume = 1 | issue = 6 | pages = 624–34 | date = December 2011 | pmid = 22180768 | pmc = 3237677 | doi = 10.1016/j.coviro.2011.10.012 }}</ref> As SARS-CoV is most contagious post-symptoms, the introduction of strict public health measures effectively halted the pandemic.<ref name=Bolles/> The natural reservoir host for SARS-CoV is thought to be [[horseshoe bat]]s, although the virus has also been identified in several small carnivores (e.g. palm [[civet]]s and [[racoon dog]]s). The emergence of SARS-CoV is believed to have been facilitated by Chinese wet markets, in which civets positive for the virus acted as intermediate hosts and passed SARS-CoV onto humans (and other species).<ref name=Bolles/><ref name="Wang">{{cite book | vauthors = Wang LF, Eaton BT | title = Wildlife and Emerging Zoonotic Diseases: The Biology, Circumstances and Consequences of Cross-Species Transmission | chapter = Bats, Civets and the Emergence of SARS | series = Current Topics in Microbiology and Immunology | volume = 315 | pages = 325–44 | year = 2007 | pmid = 17848070 | pmc = 7120088 | doi = 10.1007/978-3-540-70962-6_13 | isbn = 978-3-540-70961-9 }}</ref> However, more recent analysis suggests that SARS-CoV may have directly jumped from bats to humans, with subsequent cross-transmission between humans and civets.<ref name=Bolles/>
+In 2002, a highly pathogenic [[SARS-CoV-1|SARS-CoV]] (severe acute respiratory syndrome coronavirus) strain emerged from a zoonotic reservoir; approximately 8,000 people were infected worldwide, and mortality rates approached 50% or more in the elderly.<ref name="Bolles">{{cite journal | vauthors = Bolles M, Donaldson E, Baric R | title = SARS-CoV and emergent coronaviruses: viral determinants of interspecies transmission | journal = Current Opinion in Virology | volume = 1 | issue = 6 | pages = 624–34 | date = December 2011 | pmid = 22180768 | pmc = 3237677 | doi = 10.1016/j.coviro.2011.10.012 }}</ref> As SARS-CoV-1 is most contagious post-symptoms, the introduction of strict public health measures effectively halted the epidemic.<ref name=Bolles/> The natural reservoir host for SARS-CoV-1 is thought to be [[horseshoe bat]]s, although the virus has also been identified in several small carnivores (e.g., palm [[civet]]s and [[Nyctereutes|racoon dogs]]). The emergence of SARS-CoV-1 is believed to have been facilitated by Chinese wet markets, in which civets positive for the virus acted as intermediate hosts and passed SARS-CoV-1 onto humans (and other species).<ref name=Bolles/><ref name="Wang">{{cite book | vauthors = Wang LF, Eaton BT | title = Wildlife and Emerging Zoonotic Diseases: The Biology, Circumstances and Consequences of Cross-Species Transmission | chapter = Bats, Civets and the Emergence of SARS | series = Current Topics in Microbiology and Immunology | volume = 315 | pages = 325–44 | year = 2007 | pmid = 17848070 | pmc = 7120088 | doi = 10.1007/978-3-540-70962-6_13 | isbn = 978-3-540-70961-9 }}</ref> However, more recent analysis suggests that SARS-CoV-1 may have directly jumped from bats to humans, with subsequent cross-transmission between humans and civets.<ref name=Bolles/>
-In order to [[infection|infect]] cells, SARS-CoV uses the spike surface [[glycoprotein]] to recognise and bind to host [[Angiotensin-converting enzyme 2|ACE-2]], which it uses as a cellular entry receptor;<ref name=Bolles/> the development of this characteristic was crucial in enabling SARS-CoV to ‘jump’ from bats to other species.
+In order to [[infection|infect]] cells, SARS-CoV-1 uses the spike surface [[glycoprotein]] to recognize and bind to host [[Angiotensin-converting enzyme 2|ACE-2]], which it uses as a cellular entry receptor;<ref name=Bolles/> the development of this characteristic was crucial in enabling SARS-CoV-1 to 'jump' from bats to other species.
 ===MERS-CoV===
 [[File: MERS-CoV electron micrograph1.jpg| 210px|thumb|upright=0.4|right|alt=Electron micrograph of MERS-CoV.|Electron micrograph of MERS-CoV]]
-First reported in 2012, [[Middle East respiratory syndrome-related coronavirus|MERS-CoV]] (Middle East Respiratory Syndrome Coronavirus) marks the second known introduction of a highly pathogenic coronavirus from a zoonotic reservoir into humans. The case mortality rate  of this emergent virus is approximately 35%, with 80% of all cases reported by Saudi Arabia.<ref name="WHO3">{{cite web |last1=WHO |title=Middle East respiratory syndrome coronavirus (MERS-CoV) |url=https://www.who.int/news-room/fact-sheets/detail/middle-east-respiratory-syndrome-coronavirus-(mers-cov) |website=WHO |access-date=15 April 2020}}</ref> Although MERS-CoV is likely to have originated in bats,<ref name="Sharif-Yakan">{{cite journal | vauthors = Sharif-Yakan A, Kanj SS | title = Emergence of MERS-CoV in the Middle East: origins, transmission, treatment, and perspectives | journal = PLOS Pathogens | volume = 10 | issue = 12 | pages = e1004457 | date = December 2014 | pmid = 25474536 | pmc = 4256428 | doi = 10.1371/journal.ppat.1004457 | doi-access = free }}</ref> [[dromedary|dromedary camels]] have been implicated as probable intermediate hosts. MERS-CoV is believed to have been circulating in these mammals for over 20 years,<ref name=Sharif-Yakan/> and it is thought that novel camel farming practices drove the spillover of MERS-CoV into humans.<ref name="Farag">{{cite journal | vauthors = Farag E, Sikkema RS, Vinks T, Islam MM, Nour M, Al-Romaihi H, Al Thani M, Atta M, Alhajri FH, Al-Marri S, AlHajri M, Reusken C, Koopmans M | display-authors = 6 | title = Drivers of MERS-CoV Emergence in Qatar | journal = Viruses | volume = 11 | issue = 1 | pages = 22 | date = December 2018 | pmid = 30602691 | pmc = 6356962 | doi = 10.3390/v11010022 | doi-access = free }}</ref> Studies have shown that humans can be infected with MERS-CoV via direct or indirect contact within infected dromedary camels, while human-human transmission is limited.<ref name=WHO3/>
+First reported in 2012, [[MERS-related coronavirus|MERS-CoV]] (Middle East respiratory syndrome coronavirus) marks the second known introduction of a highly pathogenic coronavirus from a zoonotic reservoir into humans. The case mortality rate of this emergent virus is approximately 35%, with 80% of all cases reported by Saudi Arabia.<ref name="WHO3">{{cite web |last1=WHO |title=Middle East respiratory syndrome coronavirus (MERS-CoV) |url=https://www.who.int/news-room/fact-sheets/detail/middle-east-respiratory-syndrome-coronavirus-(mers-cov) |website=WHO |access-date=15 April 2020}}</ref> Although MERS-CoV is likely to have originated in bats,<ref name="Sharif-Yakan">{{cite journal | vauthors = Sharif-Yakan A, Kanj SS | title = Emergence of MERS-CoV in the Middle East: origins, transmission, treatment, and perspectives | journal = PLOS Pathogens | volume = 10 | issue = 12 | pages = e1004457 | date = December 2014 | pmid = 25474536 | pmc = 4256428 | doi = 10.1371/journal.ppat.1004457 | doi-access = free }}</ref> [[dromedary|dromedary camels]] have been implicated as probable intermediate hosts. MERS-CoV is believed to have been circulating in these mammals for over 20 years,<ref name=Sharif-Yakan/> and it is thought that novel camel farming practices drove the spillover of MERS-CoV into humans.<ref name="Farag">{{cite journal | vauthors = Farag E, Sikkema RS, Vinks T, Islam MM, Nour M, Al-Romaihi H, Al Thani M, Atta M, Alhajri FH, Al-Marri S, AlHajri M, Reusken C, Koopmans M | display-authors = 6 | title = Drivers of MERS-CoV Emergence in Qatar | journal = Viruses | volume = 11 | issue = 1 | pages = 22 | date = December 2018 | pmid = 30602691 | pmc = 6356962 | doi = 10.3390/v11010022 | doi-access = free }}</ref> Studies have shown that humans can be infected with MERS-CoV via direct or indirect contact within infected dromedary camels, while human-to-human transmission is limited.<ref name=WHO3/>
 MERS-CoV gains cellular entry by using a spike surface protein to bind to the host [[Dipeptidyl peptidase-4|DPP4]] surface receptor; the core subdomain of this spike surface protein shares similarities with that of SARS-CoV, but its receptor binding subdomain (RBSD) significantly differs.<ref name=Sharif-Yakan/>
@@ Line 72: / Line 72: @@
 [[File:Bluetongue in Captive Yak.png| 275px|thumb|upright=0.4|left|alt=Domestic [[yak]] with Bluetongue disease - tongue is visibly swollen and cyanotic.| Domestic [[yak]] with Bluetongue disease - tongue is visibly swollen and cyanotic]]
-[[Bluetongue disease]] is a [[infectious disease#Contagiousness|non-contagious]] [[vector (epidemiology)|vector-borne]] disease caused by bluetongue virus, which affects species of [[ruminant]]s (particularly [[sheep]]).<ref name="CFSPH">{{cite web |last1=The Center for Food Security and Public Health |first1=Iowa State University |title=Bluetongue |url=http://www.cfsph.iastate.edu/FastFacts/pdfs/bluetongue_F.pdf |website=CFSPH |access-date=14 April 2020}}</ref> Climate change has been implicated in the emergence and global spread of this disease, due to its impact on vector distribution. The natural vector of the bluetongue virus is the African midge [[culicoides imicola|''C. imicola'']], which is normally limited to Africa and subtropical Asia. However, global warming has extended the geographic range of ''C. imicola'', so that it now overlaps with a different vector (''C. pulcaris'' or [[Culicoides obsoletus|''C. obsoletus'']]) with a much more northward geographic range. This change enabled the bluetongue virus to jump vector, thus causing the northward spread of bluetongue disease into Europe.<ref name="Purse">{{cite journal | vauthors = Purse BV, Mellor PS, Rogers DJ, Samuel AR, Mertens PP, Baylis M | s2cid = 62802662 | title = Climate change and the recent emergence of bluetongue in Europe | journal = Nature Reviews. Microbiology | volume = 3 | issue = 2 | pages = 171–81 | date = February 2005 | pmid = 15685226 | doi = 10.1038/nrmicro1090 }}</ref>
+[[Bluetongue disease]] is a [[Infection#Contagiousness|non-contagious]] [[Disease vector|vector-borne]] disease caused by bluetongue virus, which affects species of [[ruminant]]s (particularly [[sheep]]).<ref name="CFSPH">{{cite web |last1=The Center for Food Security and Public Health |first1=Iowa State University |title=Bluetongue |url=http://www.cfsph.iastate.edu/FastFacts/pdfs/bluetongue_F.pdf |website=CFSPH |access-date=14 April 2020}}</ref> Climate change has been implicated in the emergence and global spread of this disease, due to its impact on vector distribution. The natural vector of the bluetongue virus is the African midge [[culicoides imicola|''C. imicola'']], which is normally limited to Africa and subtropical Asia. However, global warming has extended the geographic range of ''C. imicola'', so that it now overlaps with a different vector (''C. pulcaris'' or [[Culicoides obsoletus|''C. obsoletus'']]) with a much more northward geographic range. This change enabled the bluetongue virus to jump vector, thus causing the northward spread of bluetongue disease into Europe.<ref name="Purse">{{cite journal | vauthors = Purse BV, Mellor PS, Rogers DJ, Samuel AR, Mertens PP, Baylis M | s2cid = 62802662 | title = Climate change and the recent emergence of bluetongue in Europe | journal = Nature Reviews. Microbiology | volume = 3 | issue = 2 | pages = 171–81 | date = February 2005 | pmid = 15685226 | doi = 10.1038/nrmicro1090 }}</ref>
 == See also ==
@@ Line 78: / Line 78: @@
 * [[Biosecurity]]
 * [[Emerging infectious disease]]
-* [[History of emerging infectious diseases]]
+* [[Discovery of disease-causing pathogens]]
-* [[Laboratory biosafety]]
+* [[Biocontainment]]
 * [[Viral quasispecies]]