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{{Influenza}}
{{Influenza}}
{{CMG}}
'''For more information about non-human (variant) influenza viruses that may be transmitted to humans, see [[Zoonotic influenza]]'''<br><br>
{{CMG}}; {{AE}} {{AL}}
==Overview==
Influenza-like symptoms have been reported for thousands of years, but the first pandemic outbreak recorded in Asia, Europe and Africa was in 1580.  Since then, several outbreaks have been reported, including the Spanish flu pandemic of 1918 that killed 50 to 100 million patients, the Asian flu pandemic of 1957, and the Hong Kong flu pandemic of 1968.  The first vaccine against influenza was developed in the 1940s to prevent outbreaks within the US military during World War II.


==Historical Perspective==
==Historical Perspective==
*The symptoms of human influenza were clearly described by [[Hippocrates]] roughly 2400 years ago.<ref>{{cite journal | last =Martin | first = P | coauthors = Martin-Granel E | title=2,500-year evolution of the term epidemic | url= http://www.cdc.gov/ncidod/EID/vol12no06/05-1263.htm#cit | journal=Emerg Infect Dis | year=2006 | month = Jun | volume=12 | issue=6 | id = PMID 16707055}}</ref><ref>{{cite web | author=Hippocrates | coauthors = [[Francis Adams (translator)|Adams, Francis]] (transl.) | title=Of the Epidemics | url= http://classics.mit.edu/Hippocrates/epidemics.html | date= 400 BCE | accessdate=2006-10-18}}</ref>
*Since then, the virus has caused numerous pandemics.
*Historical data on influenza are difficult to interpret, because the symptoms can be similar to those of other diseases, such as [[diphtheria]], [[pneumonic plague]], [[typhoid fever]], [[dengue]], or [[typhus]].
*The first convincing record of an influenza pandemic was of an outbreak in 1580, which began in Asia and spread to Europe via Africa.
*In Rome over 8,000 people were killed, and several Spanish cities were almost wiped out. 
*Pandemics continued sporadically throughout the 17th and 18th centuries, with the pandemic of 1830–1833 being particularly widespread; it infected approximately a quarter of the people exposed.<ref name=Potter>{{cite journal | last =Potter | first = CW| title=A History of Influenza | url= http://www.blackwell-synergy.com/doi/full/10.1046/j.1365-2672.2001.01492.x | journal= J Appl Microbiol. | year=2006 | month=Oct | volume=91 | issue= 4 | pages = 572–579 | id = PMID 11576290}}</ref>
{|style="float:right"
|[[Image:W curve2.png|thumb|300px|left|The difference between the influenza mortality age-distributions of the 1918 epidemic and normal epidemics. Deaths per 100,000 persons in each age group, United States, for the interpandemic years 1911–1917 (dashed line) and the pandemic year 1918 (solid line).<ref name = "Taubenberger">
{{cite journal | last = Taubenberger | first = J | coauthors = Morens D | title = 1918 Influenza: the mother of all pandemics. | url = http://www.cdc.gov/ncidod/EID/vol12no01/05-0979.htm | journal = Emerg Infect Dis | volume = 12 | issue = 1 | pages = 15–22 | year = 2006 | id = PMID 16494711}}</ref>]]
|}
===Spanish Flu Pandemic===
*The most famous and lethal outbreak was the so-called [[Spanish flu]] pandemic ([[Influenzavirus A|type A influenza]], [[H1N1]] subtype), which lasted from 1918 to 1919.
*Older estimates say it killed 40–50 million people<ref name=Patterson1>{{cite journal | last =Patterson | first = KD | coauthors = Pyle GF | title=The geography and mortality of the 1918 influenza pandemic. | journal= Bull Hist Med. | year=1991 | month=Spring | volume=65 | issue=1 | pages = 4–21 | id = PMID 2021692}}</ref> while current estimates say 50 million to 100 million people worldwide were killed.<ref name=Knobler>{{cite book | editor=Knobler S, Mack A, Mahmoud A, Lemon S | title = The Threat of Pandemic Influenza: Are We Ready? Workshop Summary (2005) | chapter=1: The Story of Influenza  | pages = 60–61 | chapterurl=http://darwin.nap.edu/books/0309095042/html/60.html | publisher=The National Academies Press | location=Washington, D.C.}}</ref>
*This pandemic has been described as "the greatest medical holocaust in history" and may have killed as many people as the [[Black Death]].<ref name=Potter/>
*This huge death toll was caused by an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by [[cytokine storm]]s.<ref name=Patterson1/>
*Indeed, symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, [[cholera]], or typhoid.
*The majority of deaths were from [[bacterial pneumonia]], a secondary infection caused by influenza, but the virus also killed people directly, causing massive [[bleeding|hemorrhages]] and [[edema]] in the lung.<ref name=Taubenberger>{{cite journal | last = Taubenberger | first = J | coauthors = Reid A, Janczewski T, Fanning T | title = Integrating historical, clinical and molecular genetic data in order to explain the origin and virulence of the 1918 Spanish influenza virus. | journal = Philos Trans R Soc Lond B Biol Sci | volume = 356 | issue = 1416 | pages = 1829–39 | year = 2001 | month=Dec 29 | id = PMID 11779381 | url= http://www.journals.royalsoc.ac.uk/(3sud2455cjw1ut55yowx1d45)/app/home/contribution.asp?referrer=parent&backto=issue,3,22;journal,61,225;linkingpublicationresults,1:102022,1}}</ref>
*The Spanish flu pandemic was truly global, spreading even to the Arctic and remote Pacific islands.
*The unusually severe disease killed between 2 and 20% of those infected, as opposed to the more usual flu epidemic [[mortality rate]] of 0.1%.<ref name=Taubenberger/><ref name=Knobler/>
*Another unusual feature of this pandemic was that it mostly killed young adults, with 99% of pandemic influenza deaths occurring in people under 65, and more than half in young adults 20 to 40 years old.<ref>{{cite journal | last = Simonsen | first = L | coauthors = Clarke M, Schonberger L, Arden N, Cox N, Fukuda K | title = Pandemic versus epidemic influenza mortality: a pattern of changing age distribution. | journal = J Infect Dis | volume = 178 | issue = 1 | pages = 53–60 | year = 1998 | month=Jul | id = PMID 9652423}}</ref>
*This is unusual since influenza is normally most deadly to the very young (under age 2) and the very old (over age 70).
*The total mortality of the 1918–1919 pandemic is not known, but it is estimated that 2.5% to 5% of the world's population was killed. As many as 25 million may have been killed in the first 25 weeks; in contrast, [[AIDS|HIV/AIDS]] has killed 25 million in its first 25 years.<ref name=Knobler/>


 
{{#widget:BlueTable}}
[[Image:Influenza1.png|thumb|300px|left|Negatively stained flu viruses; these were the causative agents of [[Hong Kong Flu]]. (magnified approximately 70,000 times)]]
{|class="BlueTable" style="float:right; font-size:90%"
 
|+ Known Flu Pandemics<ref name=Hilleman>{{cite journal |last=Hilleman |first=M |title=Realities and enigmas of human viral influenza: pathogenesis, epidemiology and control |journal=Vaccine |volume=20 |issue=25–26 |pages=3068–87 |date=19 August 2002 |pmid=12163258 |doi=10.1016/S0264-410X(02)00254-2}}</ref><ref name=Potter/><ref name="TenThings">{{cite web |url=http://www.who.int/csr/disease/influenza/pandemic10things/en/index.html |publisher=World Health Organization |date=14 October 2005 |title=Ten things you need to know about pandemic influenza|accessdate=26 September 2009 |archiveurl=http://web.archive.org/web/20090923231756/http://www.who.int/csr/disease/influenza/pandemic10things/en/index.html |archivedate=23 September 2009}}</ref>
[[Image:W curve2.png|thumb|300px|left|The difference between the influenza mortality age-distributions of the 1918 epidemic and normal epidemics. Deaths per 100,000 persons in each age group, United States, for the interpandemic years 1911–1917 (dashed line) and the pandemic year 1918 (solid line).<ref name = "Taubenberger">{{cite journal | last = Taubenberger | first = J | coauthors = Morens D | title = 1918 Influenza: the mother of all pandemics. | url = http://www.cdc.gov/ncidod/EID/vol12no01/05-0979.htm | journal = Emerg Infect Dis | volume = 12 | issue = 1 | pages = 15–22 | year = 2006 | id = PMID 16494711}}</ref>]]
! Name of pandemic !! Date !! Deaths !! Case fatality rate !! Subtype involved !!style="width:100px"| Pandemic Severity Index
 
|-
The symptoms of human influenza were clearly described by [[Hippocrates]] roughly 2400 years ago.<ref>{{cite journal | last =Martin | first = P | coauthors = Martin-Granel E | title=2,500-year evolution of the term epidemic | url= http://www.cdc.gov/ncidod/EID/vol12no06/05-1263.htm#cit | journal=Emerg Infect Dis | year=2006 | month = Jun | volume=12 | issue=6 | id = PMID 16707055}}</ref><ref>{{cite web | author=Hippocrates | coauthors = [[Francis Adams (translator)|Adams, Francis]] (transl.) | title=Of the Epidemics | url= http://classics.mit.edu/Hippocrates/epidemics.html | date= 400 BCE | accessdate=2006-10-18}}</ref> Since then, the virus has caused numerous pandemics. Historical data on influenza are difficult to interpret, because the symptoms can be similar to those of other diseases, such as [[diphtheria]], [[pneumonic plague]], [[typhoid fever]], [[dengue]], or [[typhus]]. The first convincing record of an influenza pandemic was of an outbreak in 1580, which began in Asia and spread to Europe via Africa. In Rome over 8,000 people were killed, and several Spanish cities were almost wiped out.  Pandemics continued sporadically throughout the 17th and 18th centuries, with the pandemic of 1830–1833 being particularly widespread; it infected approximately a quarter of the people exposed.<ref name=Potter>{{cite journal | last =Potter | first = CW| title=A History of Influenza | url= http://www.blackwell-synergy.com/doi/full/10.1046/j.1365-2672.2001.01492.x | journal= J Appl Microbiol. | year=2006 | month=Oct | volume=91 | issue= 4 | pages = 572–579 | id = PMID 11576290}}</ref>
| 1889–1890 Flu Pandemic<br />(Asiatic or Russian Flu)<ref>{{cite journal |author=Valleron AJ, Cori A, Valtat S, Meurisse S, Carrat F, Boëlle PY |title=Transmissibility and geographic spread of the 1889 influenza pandemic |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=107 |issue=19 |pages=8778–81 |date=May 2010 |pmid=20421481 |doi=10.1073/pnas.1000886107 |pmc=2889325|bibcode = 2010PNAS..107.8778V }}</ref>
 
|1889–1890 ||1 million ||0.15% ||possibly [[H3N8]] <br /> or [[H2N2]]||N/A
The most famous and lethal outbreak was the so-called [[Spanish flu]] pandemic ([[Influenzavirus A|type A influenza]], [[H1N1]] subtype), which lasted from 1918 to 1919. Older estimates say it killed 40–50 million people<ref name=Patterson1>{{cite journal | last =Patterson | first = KD | coauthors = Pyle GF | title=The geography and mortality of the 1918 influenza pandemic. | journal= Bull Hist Med. | year=1991 | month=Spring | volume=65 | issue=1 | pages = 4–21 | id = PMID 2021692}}</ref> while current estimates say 50 million to 100 million people worldwide were killed.<ref name=Knobler>{{cite book | editor=Knobler S, Mack A, Mahmoud A, Lemon S | title = The Threat of Pandemic Influenza: Are We Ready? Workshop Summary (2005) | chapter=1: The Story of Influenza  | pages = 60–61 | chapterurl=http://darwin.nap.edu/books/0309095042/html/60.html | publisher=The National Academies Press | location=Washington, D.C.}}</ref> This pandemic has been described as "the greatest medical holocaust in history" and may have killed as many people as the [[Black Death]].<ref name=Potter/> This huge death toll was caused by an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by [[cytokine storm]]s.<ref name=Patterson1/> Indeed, symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, [[cholera]], or typhoid. One observer wrote, "One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and [[petechia|petechial hemorrhages]] in the skin also occurred."<ref name=Knobler/> The majority of deaths were from [[bacterial pneumonia]], a secondary infection caused by influenza, but the virus also killed people directly, causing massive [[bleeding|hemorrhages]] and [[edema]] in the lung.<ref name=Taubenberger>{{cite journal | last = Taubenberger | first = J | coauthors = Reid A, Janczewski T, Fanning T | title = Integrating historical, clinical and molecular genetic data in order to explain the origin and virulence of the 1918 Spanish influenza virus. | journal = Philos Trans R Soc Lond B Biol Sci | volume = 356 | issue = 1416 | pages = 1829–39 | year = 2001 | month=Dec 29 | id = PMID 11779381 | url= http://www.journals.royalsoc.ac.uk/(3sud2455cjw1ut55yowx1d45)/app/home/contribution.asp?referrer=parent&backto=issue,3,22;journal,61,225;linkingpublicationresults,1:102022,1}}</ref>
The Spanish flu pandemic was truly global, spreading even to the Arctic and remote Pacific islands. The unusually severe disease killed between 2 and 20% of those infected, as opposed to the more usual flu epidemic [[mortality rate]] of 0.1%.<ref name=Taubenberger/><ref name=Knobler/> Another unusual feature of this pandemic was that it mostly killed young adults, with 99% of pandemic influenza deaths occurring in people under 65, and more than half in young adults 20 to 40 years old.<ref>{{cite journal | last = Simonsen | first = L | coauthors = Clarke M, Schonberger L, Arden N, Cox N, Fukuda K | title = Pandemic versus epidemic influenza mortality: a pattern of changing age distribution. | journal = J Infect Dis | volume = 178 | issue = 1 | pages = 53–60 | year = 1998 | month=Jul | id = PMID 9652423}}</ref>  This is unusual since influenza is normally most deadly to the very young (under age 2) and the very old (over age 70). The total mortality of the 1918–1919 pandemic is not known, but it is estimated that 2.5% to 5% of the world's population was killed. As many as 25 million may have been killed in the first 25 weeks; in contrast, [[AIDS|HIV/AIDS]] has killed 25 million in its first 25 years.<ref name=Knobler/>
Later flu pandemics were not so devastating. They included the 1957 [[Asian Flu]] (type A, [[H2N2]] strain) and the 1968 [[Hong Kong Flu]] (type A, [[H3N2]] strain), but even these smaller outbreaks killed millions of people. In later pandemics [[antibiotic]]s were available to control secondary infections and this may have helped reduce mortality compared to the Spanish Flu of 1918.<ref name= Taubenberger/>
 
{| class="wikitable" style="text-align:center"
|+ Known [[flu pandemic]]s<ref name=Hilleman>{{cite journal | last = Hilleman | first = M | title = Realities and enigmas of human viral influenza: pathogenesis, epidemiology and control. | journal = Vaccine | volume = 20 | issue = 25–26 | pages = 3068–87 | year = 2002 | month=Aug 19 | id = PMID 12163258}}</ref><ref name=Potter/>
! Name of pandemic !! Date !! Deaths !! Subtype involved !! [[Pandemic Severity Index]]
|-
|-
! Asiatic (Russian) Flu
| 1918 Flu Pandemic<br />(Spanish flu)<ref>{{cite journal |author=Mills CE, [[James Robins|Robins JM]], Lipsitch M |title=Transmissibility of 1918 pandemic influenza |journal=Nature |volume=432 |issue=7019 |pages=904–6 |date=December 2004 |pmid=15602562 |doi=10.1038/nature03063 |bibcode = 2004Natur.432..904M }}</ref>
| 1889–1890 || 1 million || possibly [[H2N2]] || ?
|1918–1920 ||20 to 100 million ||2%||[[H1N1]] ||5
|-
|-
! [[Spanish flu|Spanish Flu]]  
| [[H2N2#Asian flu|Asian Flu]]
| 1918–1920 || 40 million || [[H1N1]] || 5
|1957–1958 ||1 to 1.5 million ||0.13%||[[H2N2]] ||2
|-
|-
! [[H2N2#Asian Flu|Asian Flu]]
| [[H3N2#Hong Kong Flu|Hong Kong Flu]]
| 1957–1958 || 1 to 1.5 million || [[H2N2]] || 2
|1968–1969 ||0.75 to 1 million ||<0.1%||[[H3N2]] ||2
|-
|-
! [[H3N2#Hong Kong Flu|Hong Kong Flu]]  
| [[Influenza A virus subtype H1N1#Russian flu|Russian flu]]
| 1968–1969 || 0.75 to 1 million || [[H3N2]] || 2
| 1977–1978 || no accurate count || N/A || [[H1N1]] || N/A
|-
|-
| 2009 Flu Pandemic<ref>{{cite journal |author=Donaldson LJ |title=Mortality from pandemic A/H1N1 2009 influenza in England: public health surveillance study |journal=BMJ |volume=339 |issue= |pages=b5213 |year=2009 |pmid=20007665 |pmc=2791802 |doi=10.1136/bmj.b5213 |author-separator=, |author2=Rutter PD |author3=Ellis BM |display-authors=3 |last4=Greaves |first4=F. E C |last5=Mytton |first5=O. T |last6=Pebody |first6=R. G |last7=Yardley |first7=I. E}}</ref>
|2009–2010 ||105,700-395,600<ref>{{cite journal|last=Dawood|first=Fatimah S|coauthors=A Danielle Iuliano, Carrie Reed, Martin I Meltzer, David K Shay, Po-Yung Cheng, Don Bandaranayake, Robert F Breiman, W Abdullah Brooks, Philippe Buchy, Daniel R Feikin, Karen B Fowler, Aubree Gordon, Nguyen Tran Hien, Peter Horby, Q Sue Huang, Mark A Katz, Anand Krishnan, Renu Lal, Joel M Montgomery, Kåre Mølbak, Richard Pebody, Anne M Presanis, Hugo Razuri, Anneke Steens, Yeny O Tinoco, Jacco Wallinga, Hongjie, Sirenda Vong, Joseph Bresee, Marc-Alain Widdowson|journal=The Lancet Infectious Diseases|volume=12|issue=9|title= Estimated global mortality associated with the first 12 months of 2009 pandemic influenza A H1N1 virus circulation: a modelling study |url=http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(12)70121-4/abstract|date=26 June 2012|doi=10.1016/S1473-3099(12)70121-4|accessdate=19 March 2014|pmid=22738893|pages=687–95}}</ref>||0.03%||[[H1N1]] ||N/A
|}
|}


The [[etiology|etiological]] cause of influenza, the Orthomyxoviridae family of viruses, was first discovered in pigs by [[Richard Schope]] in 1931.<ref>{{cite journal | last =Shimizu | first = K | title= History of influenza epidemics and discovery of influenza virus | journal=Nippon Rinsho | year= 1997 | month=Oct | volume=55 | issue=10| pages=2505–201 | id = PMID 9360364}}</ref> This discovery was shortly followed by the isolation of the virus from humans by a group headed by [[Patrick Laidlaw]] at the [[Medical Research Council (UK)|Medical Research Council]] of the [[United Kingdom]] in 1933.<ref>{{cite journal | last =Smith | first = W | coauthors = Andrewes CH, Laidlaw PP | title=A virus obtained from influenza patients | journal=Lancet | year=1933 | volume=2 | pages = 66–68}}</ref> However, it was not until [[Wendell Stanley]] first crystallized [[tobacco mosaic virus]] in 1935 that the [[cell (biology)|non-cellular]] nature of viruses was appreciated.
===Other Flu Pandemics===
 
*Later flu pandemics were not so devastating.
The first significant step towards preventing influenza was the development in 1944 of a killed-virus vaccine for influenza by [[Thomas Francis, Jr.]]. This built on work by [[Frank Macfarlane Burnet]], who showed that the virus lost virulence when it was cultured in fertilized hen's eggs.<ref name = "Nobel">[http://nobelprize.org/nobel_prizes/medicine/laureates/1960/burnet-bio.html Sir Frank Macfarlane Burnet: Biography] The Nobel Foundation. Accessed 22 Oct 06</ref> Application of this observation by Francis allowed his group of researchers at the [[University of Michigan]] to develop the first [[flu vaccine]], with support from the U.S. Army.<ref>{{cite journal | last = Kendall | first = H | title = Vaccine Innovation: Lessons from World War II | url= http://docstore.ingenta.com/cgi-bin/ds_deliver/1/u/d/ISIS/32620254.1/pal/jphp/2006/00000027/00000001/art00005/FB2494BF0313967611615398189A7A906334373166.pdf?link=http://www.ingentaconnect.com/error/delivery&format=pdf | journal = Journal of Public Health Policy | volume = 27 | issue = 1 | pages = 38–57 | year = 2006}}</ref> The Army was deeply involved in this research due to its experience of influenza in World War I, when thousands of troops were killed by the virus in a matter of months.<ref name= Knobler/>
*They included the following:
 
:*The 1957 [[Asian Flu]] (type A, [[H2N2]] strain)
Although there were scares in New Jersey in 1976 (with the [[Swine Flu]]), world wide in 1977 (with the [[Russian Flu]]), and in Hong Kong and other Asian countries in 1997 (with [[H5N1]] avian influenza), there have been no major pandemics since the 1968 Hong Kong Flu. Immunity to previous pandemic influenza strains and vaccination may have limited the spread of the virus and may have helped prevent further pandemics.<ref name=Hilleman/>
:*The 1968 [[Hong Kong Flu]] (type A, [[H3N2]] strain)
 
*Even these smaller outbreaks killed millions of people.  
==Etymology==
*In later pandemics [[antibiotic]]s were available to control secondary infections and this may have helped reduce mortality compared to the Spanish Flu of 1918.<ref name= Taubenberger/>
The term influenza has its origins in 15th-century Italy, where the cause of the disease was ascribed to unfavourable astrological ''influences''.  Evolution in medical thought led to its modification to ''influenza del freddo'', meaning "influence of the cold." The word "influenza" was first attested in English in 1743 when it was borrowed during an outbreak of the disease in Europe.<ref name=Harper>{{cite web | last = Harper | first = D | title=Influenza | url=http://www.etymonline.com/index.php?search=influenza&searchmode=none  | publisher= Etymonlin}}</ref> Archaic terms for influenza include epidemic catarrh, grippe (from the French grippe, meaning flu; sometimes spelled "grip" or "gripe"), sweating sickness, and Spanish fever (particularly for the [[Spanish flu|1918 pandemic]] strain).<ref>{{cite web | last = Smith | first = P | title=Archaic Medical Terms | url= http://www.paul_smith.doctors.org.uk/ArchaicMedicalTerms.htm | accessdate = 2006-10-23}}</ref>
*Although there were scares in New Jersey in 1976 (with the [[Swine Flu]]), world wide in 1977 (with the [[Russian Flu]]), and in Hong Kong and other Asian countries in 1997 (with [[H5N1]] avian influenza), there have been no major pandemics since the 1968 Hong Kong Flu.  
 
*Immunity to previous pandemic influenza strains and vaccination may have limited the spread of the virus and may have helped prevent further pandemics.<ref name=Hilleman/>
:''See [[H5N1]] for the current [[epizootic]] (an [[epidemic]] in nonhumans) and panzootic (a disease affecting animals of many species especially over a wide area) of H5N1 influenza''
 
Wild [[fowl]] act as natural [[asymptomatic carrier]]s of Influenza A viruses. Prior to the current [[H5N1]] epizootic, strains of Influenza A virus had been demonstrated to be transmitted from wild fowl to only [[bird]]s, [[pig]]s, [[horse]]s, [[Pinniped|seal]]s, [[whale]]s and [[human]]s; and only between humans and pigs and between humans and domestic fowl; and not other pathways such as domestic fowl to horse. <ref>[http://www.nap.edu/books/0309095042/html/30.html NAP Books] National Academies Press Books - ''The Threat of Pandemic Influenza: Are We Ready? Workshop Summary (2005)'' - page 30</ref>
 
Wild aquatic birds are the natural hosts for a large variety of [[influenza]] A viruses. Occasionally viruses are transmitted from these birds to other species and may then cause devastating outbreaks in domestic poultry or give rise to human influenza [[pandemic]]s.<ref name=sobrino6>{{cite book |chapterurl=http://www.horizonpress.com/avir|author=Klenk et al|year=2008|chapter=Avian Influenza: Molecular Mechanisms of Pathogenesis and Host Range|title=Animal Viruses: Molecular Biology|publisher=Caister Academic Press|id=[http://www.horizonpress.com/avir ISBN 978-1-904455-22-6]}}</ref> <ref name=Kawaoka>{{cite book | author = Kawaoka Y (editor). | title = Influenza Virology: Current Topics | publisher = Caister Academic Press | year = 2006 | url=http://www.horizonpress.com/flu | id = [http://www.horizonpress.com/flu ISBN 978-1-904455-06-6 ]}}</ref>
 
[[H5N1]] has been shown to be transmitted to tigers, leopards, and domestic cats that were fed uncooked domestic fowl (chickens) with the virus. [[H3N8]] viruses from [[horse]]s have crossed over and caused outbreaks in [[dog]]s. Laboratory mice have been infected successfully with a variety of avian flu genotypes. <ref>[http://www.nap.edu/books/0309095042/html/82.html NAP Books] National Academies Press Books - ''The Threat of Pandemic Influenza: Are We Ready? Workshop Summary (2005)'' - page 82 - "Interestingly, recombinant influenza viruses containing the 1918 HA and NA and up to three additional genes derived from the 1918 virus (the other genes being derived from the A/WSN/33 virus) were all highly virulent in mice (Tumpey et al., 2004). Furthermore, expression microarray analysis performed on whole lung tissue of mice infected with the 1918 HA/ NA recombinant showed increased upregulation of genes involved in apoptosis, tissue injury, and oxidative damage (Kash et al., 2004). These findings were unusual because the viruses with the 1918 genes had not been adapted to mice. The completion of the sequence of the entire genome of the 1918 virus and the reconstruction and characterization of viruses with 1918 genes under appropriate biosafety conditions will shed more light on these findings and should allow a definitive examination of this explanation. Antigenic analysis of recombinant viruses possessing the 1918 HA and NA by hemagglutination inhibition tests using ferret and chicken antisera suggested a close relationship with the A/swine/Iowa/30 virus and H1N1 viruses isolated in the 1930s (Tumpey et al., 2004), further supporting data of Shope from the 1930s (Shope, 1936). Interestingly, when mice were immunized with different [[H1N1]] virus strains, challenge studies using the 1918-like viruses revealed partial protection by this treatment, suggesting that current vaccination strategies are adequate against a 1918-like virus (Tumpey et al., 2004)."</ref>
 
Influenza A viruses spread in the air and in [[manure]] and survives longer in cold weather.  It can also be transmitted by contaminated feed, water, equipment and clothing; however, there is no evidence that the virus can survive in well-cooked meat. Symptoms in animals vary, but virulent [[strain (biology)|strain]]s can cause death within a few days.


"Highly pathogenic avian influenza virus is on every top ten list available for potential agricultural bioweapon agents". <ref>[http://www.nap.edu/books/0309095042/html/285.html NAP Books] National Academies Press Books - ''The Threat of Pandemic Influenza: Are We Ready? Workshop Summary (2005)'' - page 285 - "As of October 2001, the potential for use of infectious agents, such as anthrax, as weapons has been firmly established. It has been suggested that attacks on a nation’s agriculture might be a preferred form of terrorism or economic disruption that would not have the attendant stigma of infecting and causing disease in humans. Highly pathogenic avian influenza virus is on every top ten list available for potential agricultural bioweapon agents, generally following foot and mouth disease virus and Newcastle disease virus at or near the top of the list. Rapid detection techniques for bioweapon agents are a critical need for the first-responder community, on a par with vaccine and antiviral development in preventing spread of disease."</ref>
===Influenza Virus===
*The etiology of influenza, the Orthomyxoviridae family of viruses, was first discovered in pigs by [[Richard Schope]] in 1931.<ref>{{cite journal | last =Shimizu | first = K | title= History of influenza epidemics and discovery of influenza virus | journal=Nippon Rinsho | year= 1997 | month=Oct | volume=55 | issue=10| pages=2505–201 | id = PMID 9360364}}</ref>
*This discovery was shortly followed by the isolation of the virus from humans by a group headed by [[Patrick Laidlaw]] at the [[Medical Research Council (UK)|Medical Research Council]] of the United Kingdom in 1933.<ref>{{cite journal | last =Smith | first = W | coauthors = Andrewes CH, Laidlaw PP | title=A virus obtained from influenza patients | journal=Lancet | year=1933 | volume=2 | pages = 66–68}}</ref>
*However, it was not until [[Wendell Stanley]] first crystallized [[tobacco mosaic virus]] in 1935 that the [[cell (biology)|non-cellular]] nature of viruses was appreciated.


Avian influenza viruses that the [[OIE]] and others test for in order to control poultry disease include: [[H5N1]], [[H7N2]], [[H1N7]], [[H7N3]], [[H13N6]], [[H5N9]], [[H11N6]], [[H3N8]], [[H9N2]], [[H5N2]], [[H4N8]], [[H10N7]], [[H2N2]], [[H8N4]], [[H14N5]], [[H6N5]], [[H12N5]] and others.
===Flu Vaccine===
*The first significant step towards preventing influenza was the development in 1944 of a killed-virus vaccine for influenza by Thomas Francis, Jr.
*This built on work by Frank Macfarlane Burnet, who showed that the virus lost virulence when it was cultured in fertilized hen's eggs.<ref name = "Nobel">[http://nobelprize.org/nobel_prizes/medicine/laureates/1960/burnet-bio.html Sir Frank Macfarlane Burnet: Biography] The Nobel Foundation. Accessed 22 Oct 06</ref>
*Application of this observation by Francis allowed his group of researchers at the University of Michigan to develop the first [[flu vaccine]], with support from the U.S. Army.<ref>{{cite journal | last = Kendall | first = H | title = Vaccine Innovation: Lessons from World War II | url= http://docstore.ingenta.com/cgi-bin/ds_deliver/1/u/d/ISIS/32620254.1/pal/jphp/2006/00000027/00000001/art00005/FB2494BF0313967611615398189A7A906334373166.pdf?link=http://www.ingentaconnect.com/error/delivery&format=pdf | journal = Journal of Public Health Policy | volume = 27 | issue = 1 | pages = 38–57 | year = 2006}}</ref>
*The Army was deeply involved in this research due to its experience of influenza in World War I, when thousands of troops were killed by the virus in a matter of months.<ref name= Knobler/>


;Known outbreaks of highly pathogenic flu in poultry 1959-2003<ref>[http://www.who.int/csr/don/2004_03_02/en/ WHO] Avian influenza A(H5N1)- update 31: Situation (poultry) in Asia: need for a long-term response, comparison with previous outbreaks - Known outbreaks of highly pathogenic flu in poultry 1959-2003. </ref>
==Past Flu Seasons<small><small><small> Adapted from CDC <ref>{{cite web|url=http://www.cdc.gov/flu/pastseasons/index.htm | title= CDC Morbidity and Mortality Weekly Report (MMWR) - Influenza Activity}} </ref></small></small></small>==
{|class="wikitable" width=500
{|style="float:right"
|-
|[[File:Influenza Activity 2006-2007.png|thumb|300px|<small>'''Graph obtained from CDC MMWR on Influenza Activity</small>''']]
!Year
!Area
!Affected
!Subtype
|-
| 1959
| Scotland
| chicken
| [[H5N1]]
|-
| 1963
| England
| turkey
| [[H7N3]]
|-
| 1966
| Ontario (Canada)
| turkey
| [[H5N9]]
|-
| 1976
| Victoria (Australia)
| chicken
| [[H7N7]]
|-
| 1979
| Germany
| chicken
| [[H7N7]]
|-
| 1979
| England
| turkey
| [[H7N7]]
|-
| 1983
| Pennsylvania (USA)*
| chicken,turkey
| [[H5N2]]
|-
| 1983
| Ireland
| turkey
| [[H5N8]]
|-
| 1985
| Victoria (Australia)
| chicken
| [[H7N7]]
|-
| 1991
| England
| turkey
| [[H5N1]]
|-
| 1992
| Victoria (Australia)
| chicken
| [[H7N3]]
|-
| 1994
| Queensland (Australia)
| chicken
| [[H7N3]]
|-
| 1994
| Mexico*
| chicken
| [[H5N2]]
|-
| 1994
| Pakistan* 
| chicken
| [[H7N3]]
|-
| 1997
| New South Wales (Australia)
| chicken
| [[H7N4]]
|-
|-
| 1997
|[[File:Influenza Activity 2007-2008.gif|thumb|300px|<small>'''Graph obtained from CDC MMWR on Influenza Activity</small>''']]
| Hong Kong (China)*
| chicken
| [[H5N1]]
|-
|-
| 1997
|[[File:Influenza Activity 2008-2009.gif|thumb|300px|<small>'''Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2008-2009<br>Graph obtained from CDC MMWR on Influenza Activity</small>''']]
| Italy
| chicken
| [[H5N2]]
|-
|-
| 1999
|[[File:Influenza Activity 2009-2010.gif|thumb|300px|<small>'''Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2009-2010<br>Graph obtained from CDC MMWR on Influenza Activity</small>''']]
| Italy*
| turkey
| [[H7N1]]
|-
|-
| 2002
|[[File:Influenza Activity 2010-2011.gif|thumb|300px|<small>'''Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2010-2011<br>Graph obtained from CDC MMWR on Influenza Activity</small>''']]
| Hong Kong (China)
| chicken
| [[H5N1]]
|-
|-
| 2002
|[[File:Influenza Activity 2011-2012.gif|thumb|300px|<small>'''Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2011-2012<br>Graph obtained from CDC MMWR on Influenza Activity</small>''']]
| Chile
| chicken
| [[H7N3]]
|-
|-
| 2003
|[[File:Influenza Activity 2012-2013.gif|thumb|300px|<small>'''Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2012-2013<br>Graph obtained from CDC MMWR on Influenza Activity</small>''']]
| Netherlands*
| chicken
| [[H7N7]]
|-
| colspan=4 |
<small>'' *Outbreaks with significant spread to numerous farms, resulting in great economic losses. Most other outbreaks involved little or no spread from the initially infected farms.'' </small>
|}
|}
===2006-2007===
* During October 1, 2006--May 19, 2007, the WHO and the National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 179,268 respiratory specimens for influenza viruses; 23,753 (13.2%) were positive.
*Of these, 18,817 (79.2%) were influenza A viruses and 4,936 (20.8%) were influenza B viruses.
*Among the influenza A viruses, 6,280 (33.4%) were subtyped; 3,912 (62.3%) were influenza A (H1) viruses and 2,368 (37.7%) were influenza A (H3) viruses.
*The proportion of specimens testing positive for influenza first exceeded 10% during the week ending December 23, 2006 (week 51), peaked at 28.0% during the week ending February 10, 2007 (week 6), and declined to less than 10% during the week ending April 28, 2007 (week 17).
*The proportion was above 10% positive for 14 consecutive weeks.
*The peak percentage of specimens testing positive for influenza during the previous three seasons ranged from 22.6% to 34.7%, and the peak occurred during early December to early March.
*During the previous three influenza seasons, the number of consecutive weeks during which more than 10% of specimens tested positive for influenza ranged from 13 to 17 weeks.


[[1979]]: "More than 400 harbor seals, most of them immature, died along the New England coast between [[1979#December|December 1979]] and [[October 1980]] of acute pneumonia associated with influenza virus, A/Seal/Mass/1/180 ([[H7N7]])." <ref>[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=7063847&query_hl=49 NCBI - NLM - NIH] National Center for Biotechnology Information (part of) U.S. National Library of Medicine (part of) National Institutes of Health (part of) US Government - Science. 1982 Feb 26;215(4536):1129-31. - ''Mass mortality of harbor seals: pneumonia associated with influenza A virus.'' - "More than 400 harbor seals, most of them immature, died along the New England coast between December 1979 and October 1980 of acute pneumonia associated with influenza virus, A/Seal/Mass/1/180 (H7N7). The virus has avian characteristics, replicates principally in mammals, and causes mild respiratory disease in experimentally infected seals. Concurrent infection with a previously undescribed mycoplasma or adverse environmental conditions may have triggered the epizootic. The similarities between this epizootic and other seal mortalities in the past suggest that these events may be linked by common biological and environmental factors." </ref>
===2007-2008===
 
*During September 30, 2007--May 17, 2008, the WHO and the National Respiratory and Enteric Virus Surveillance System collaborating laboratories in the United States tested 225,329 specimens for influenza viruses; 39,827 (18%) were positive.  
[[1995]]: "[V]accinated birds can develop asymptomatic infections that allow virus to spread, mutate, and recombine (ProMED-mail, 2004j). Intensive surveillance is required to detect these “silent epidemics” in time to curtail them. In Mexico, for example, mass vaccination of chickens against epidemic H5N2 influenza in [[1995]] has had to continue in order to control a persistent and evolving virus (Lee et al., [[2004]])." <ref>[http://www.nap.edu/books/0309095042/html/15.html NAP Books] National Academies Press Books - ''The Threat of Pandemic Influenza: Are We Ready? Workshop Summary (2005)'' - page 15 - "Unlike most other affected countries, Indonesia also instituted mass vaccination of healthy domestic birds against H5N1, followed by routine vaccination (China has a similar policy; other Asian countries are considering it [ProMED-mail, 2004j]) (Soebandrio, 2004). This is a risky strategy, because vaccinated birds can develop asymptomatic infections that allow virus to spread, mutate, and recombine (ProMED-mail, 2004j). Intensive surveillance is required to detect these “silent epidemics” in time to curtail them. In Mexico, for example, mass vaccination of chickens against epidemic H5N2 influenza in 1995 has had to continue in order to control a persistent and evolving virus (Lee et al., 2004)."</ref>
*Of the positive specimens, 28,263 (71%) were influenza A viruses, and 11,564 (29%) were influenza B viruses.  
 
*Among the influenza A viruses, 8,290 (29%) were subtyped; 2,175 (26%) were influenza A (H1N1), and 6,115 (74%) were influenza A (H3N2) viruses.  
[[1997]]: "Influenza A viruses normally seen in one species sometimes can cross over and cause illness in another species. For example, until [[1997]], only [[H1N1]] viruses circulated widely in the U.S. [[pig]] population. However, in [[1997]], [[H3N2]] viruses from humans were introduced into the pig population and caused widespread disease among pigs. Most recently, [[H3N8]] viruses from [[horse]]s have crossed over and caused outbreaks in [[dog]]s." <ref>[http://www.cdc.gov/flu/avian/gen-info/transmission.htm CDC] Centers for Disease Control and Prevention - ''Transmission of Influenza A Viruses Between Animals and People''</ref>
*The proportion of specimens testing positive for influenza first exceeded 10% during the week ending January 12, 2008 (week 2), peaked at 32% during the week ending February 9, 2008 (week 6), and declined to <10% during the week ending April 19, 2008 (week 16).  
 
*The proportion positive was above 10% for 14 consecutive weeks.  
[[2000]]: "In [[California]], [[poultry]] producers kept their knowledge of a recent [[H6N2]] avian influenza outbreak to themselves due to their fear of public rejection of poultry products; meanwhile, the disease spread across the western United States and has since become endemic." <ref>[http://www.nap.edu/books/0309095042/html/27.html NAP Books] National Academies Press Books - ''The Threat of Pandemic Influenza: Are We Ready? Workshop Summary (2005)'' - page 27.</ref>
*The peak percentage of specimens testing positive for influenza during the previous three seasons ranged from 22% to 34% and the peak occurred during mid-February to early March.  
 
*During the previous three influenza seasons, the number of consecutive weeks during which more than 10% of specimens tested positive for influenza ranged from 13 to 17 weeks
[[2003]]: In [[Netherlands]] [[H7N7]] influenza virus infection broke out in poultry on several farms.  <ref>[http://news.bbc.co.uk/1/hi/programmes/panorama/4412932.stm BBC News] ''Early bird flu warning for Dutch'' -  6 November 2005 </ref>


[[2004]]: In [[North America]], the presence of avian influenza strain [[H7N3]] was confirmed at several [[poultry]] farms in [[British Columbia]] in [[February 2004]]. As of [[April 2004]], 18 farms had been quarantined to halt the spread of the virus. <ref>[http://www.cdc.gov/ncidod/EID/vol10no12/04-0961.htm CDC detailed analysis] ''Human Illness from Avian Influenza H7N3, British Columbia''</ref>
===2008-2009===
*From September 28, 2008, to April 4, 2009, the (WHO) and the National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 173,397 respiratory specimens for influenza viruses, 24,793 (14.3%) of which were positive.
*Of these, 16,686 (67.3%) were positive for influenza A viruses, and 8,107 (32.7%) were positive for influenza B viruses.
*Of the 16,686 specimens positive for influenza A viruses, 6,735 (40.4%) were subtyped by real-time reverse transcription-polymerase chain reaction or by virus culture; 6,049 (89.8%) of these were influenza A (H1N1) viruses, and 686 (10.2%) were influenza A (H3N2) viruses.
*The percentage of specimens testing positive for influenza first exceeded the seasonal threshold of 10% during the week ending January 17, 2009, and peaked at 25.0% during the week ending February 14, 2009.  
*For the week ending April 4, 2009, 12.3% of specimens tested for influenza were positive.  
*The relative proportion of influenza B viruses increased during February and March, and since the week ending March 14, 2009, >50% of the positive influenza specimens have been influenza B.


[[2005]]: Tens of millions of birds died of [[H5N1]] influenza and hundreds of millions of birds were culled to protect humans from [[H5N1]]. [[H5N1]] is endemic in birds in southeast Asia and represents a long term pandemic threat.  
===2009-2010===
*Since April 2009, the beginning of the 2009 H1N1 pandemic, through June 12, 2010, approximately 740,000 influenza specimens were tested for influenza, and the number of laboratory-confirmed positives was approximately four times the average of the previous four seasons.
*Two peaks in percentage of specimens testing positive for influenza occurred: 43.1% in June during the initial pandemic wave, and 38.2% in October during the second wave.
*During August 30, 2009--June 12, 2010, the 2009--10 influenza season, the WHO and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 468,218 specimens for influenza viruses; 91,152 (19.5%) were positive.
*The proportion of specimens testing positive for influenza during the 2009--10 season exceeded 20% during the week ending August 30, 2009, peaked at 38.2% during the week ending October 24, and declined to less than 10% during the week ending December 12.
*Of the 91,152 positive specimens from 2009-10 season, 90,758 (99.6%) were influenza A viruses and 394 (0.4%) were influenza B viruses.
*Among the influenza A viruses, 67,022 (73.8%) were subtyped; 66,916 (99.8%) were 2009 pandemic H1N1, 72 (0.1%) were influenza A (H3N2), and 34 (0.1%) were seasonal influenza A (H1N1) viruses.


[[2006]]: [[H5N1]] spreads across the globe killing hundreds of millions of birds and over 100 people causing a significant [[H5N1 impact]] from both actual deaths and predicted possible deaths.
===2010-2011===
*During October 3, 2010--May 21, 2011, the WHO and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 246,128 specimens for influenza viruses; 54,226 (22%) were positive.
*Of the positive specimens, 40,282 (74%) were influenza A viruses, and 13,944 (26%) were influenza B viruses.
*Among the influenza A viruses, 28,545 (71%) were subtyped; 17,599(62%) were influenza A (H3N2) viruses, and 10,946 (38%) were 2009 influenza A (H1N1) viruses.
*The proportion of specimens testing positive for influenza during the 2010-11 season first exceeded 10%, indicating higher levels of virus circulation, during the week ending November 27, 2010.
*The proportion peaked at 36% during the week ending February 5, 2011, and declined to <10% during the week ending April 16, 2011.


===Evolution===
===2011-2012===
:{{See also|Punctuated equilibrium}}
*During October 2, 2011–May 19, 2012, the WHO) and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 169,453 specimens for influenza viruses; 22,417 (13%) were positive.
Taubenberger says:
*Of the positive specimens, 19,285 (86%) were influenza A viruses, and 3,132 (14%) were influenza B viruses.
:"All influenza A pandemics since [the [[Spanish flu]] pandemic], and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as [[H5N1]] and [[H7N7]]), have been caused by descendants of the 1918 virus, including "drifted" [[H1N1]] viruses and reassorted [[H2N2]] and [[H3N2]] viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated [[avian influenza]] genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all [[pandemic]]s.<ref> [http://www.cdc.gov/ncidod/EID/vol12no01/05-0979.htm CDC] ARTICLE ''1918 Influenza: the Mother of All Pandemics'' by Jeffery K. Taubenberger published January 2006</ref>
*Among the influenza A viruses, 14,968 (78%) were subtyped; 11,002 (74%) were influenza A (H3N2) viruses, and 3,966 (26%) were pH1N1 viruses.
*The proportion of specimens testing positive for influenza during the 2011–12 season first exceeded 10% (indicating higher levels of viral circulation) during the week ending February 4, 2012, and peaked at 32% during the week ending March 17, 2012.


Researchers from the [[National Institutes of Health]] used data from the [[Influenza Genome Sequencing Project]] and concluded that during the ten-year period examined most of the time the [[hemagglutinin]] gene in [[H3N2]] showed no significant excess of mutations in the antigenic regions while an increasing variety of strains accumulated. This resulted in one of the variants eventually achieving higher fitness, becoming dominant, and in a brief interval of rapid Darwinian [[evolution]] rapidly sweeping through the human population and eliminating most other variants.<ref> [http://www.sciencedaily.com/releases/2006/10/061026185115.htm Science Daily] article ''New Study Has Important Implications For Flu Surveillance'' published  October 27, 2006</ref>
===2012-2013===
*During September 30, 2012–May 18, 2013, the WHO and National Respiratory and Enteric Virus Surveillance System collaborating laboratories in the United States tested 311,333 specimens for influenza viruses; 73,130 (23%) were positive.
*Of the positive specimens, 51,675 (71%) were influenza A viruses, and 21,455 (29%) were influenza B viruses.
*Among the seasonal influenza A viruses, 34,922 (68%) were subtyped; 33,423 (96%) were influenza A (H3N2) viruses, and 1,497 (4%) were pH1N1 viruses.
*In addition, two variant influenza A (H3N2v) viruses were identified.
*Typically the influenza season is said to begin when certain key indicators remain elevated for a number of consecutive weeks.
*One of these indicators is the percent of respiratory specimens testing positive for influenza.  
*The proportion of specimens testing positive for influenza during the 2012–13 season first exceeded 10% during the week ending November 10, 2012 (week 45), and peaked at 38% during the week ending December 29, 2012 (week 52).


==References==
==References==
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{{Reflist|2}}
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Latest revision as of 22:24, 29 July 2020

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Alejandro Lemor, M.D. [2]

Overview

Influenza-like symptoms have been reported for thousands of years, but the first pandemic outbreak recorded in Asia, Europe and Africa was in 1580. Since then, several outbreaks have been reported, including the Spanish flu pandemic of 1918 that killed 50 to 100 million patients, the Asian flu pandemic of 1957, and the Hong Kong flu pandemic of 1968. The first vaccine against influenza was developed in the 1940s to prevent outbreaks within the US military during World War II.

Historical Perspective

  • The symptoms of human influenza were clearly described by Hippocrates roughly 2400 years ago.[1][2]
  • Since then, the virus has caused numerous pandemics.
  • Historical data on influenza are difficult to interpret, because the symptoms can be similar to those of other diseases, such as diphtheria, pneumonic plague, typhoid fever, dengue, or typhus.
  • The first convincing record of an influenza pandemic was of an outbreak in 1580, which began in Asia and spread to Europe via Africa.
  • In Rome over 8,000 people were killed, and several Spanish cities were almost wiped out.
  • Pandemics continued sporadically throughout the 17th and 18th centuries, with the pandemic of 1830–1833 being particularly widespread; it infected approximately a quarter of the people exposed.[3]
The difference between the influenza mortality age-distributions of the 1918 epidemic and normal epidemics. Deaths per 100,000 persons in each age group, United States, for the interpandemic years 1911–1917 (dashed line) and the pandemic year 1918 (solid line).[4]

Spanish Flu Pandemic

  • The most famous and lethal outbreak was the so-called Spanish flu pandemic (type A influenza, H1N1 subtype), which lasted from 1918 to 1919.
  • Older estimates say it killed 40–50 million people[5] while current estimates say 50 million to 100 million people worldwide were killed.[6]
  • This pandemic has been described as "the greatest medical holocaust in history" and may have killed as many people as the Black Death.[3]
  • This huge death toll was caused by an extremely high infection rate of up to 50% and the extreme severity of the symptoms, suspected to be caused by cytokine storms.[5]
  • Indeed, symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, cholera, or typhoid.
  • The majority of deaths were from bacterial pneumonia, a secondary infection caused by influenza, but the virus also killed people directly, causing massive hemorrhages and edema in the lung.[4]
  • The Spanish flu pandemic was truly global, spreading even to the Arctic and remote Pacific islands.
  • The unusually severe disease killed between 2 and 20% of those infected, as opposed to the more usual flu epidemic mortality rate of 0.1%.[4][6]
  • Another unusual feature of this pandemic was that it mostly killed young adults, with 99% of pandemic influenza deaths occurring in people under 65, and more than half in young adults 20 to 40 years old.[7]
  • This is unusual since influenza is normally most deadly to the very young (under age 2) and the very old (over age 70).
  • The total mortality of the 1918–1919 pandemic is not known, but it is estimated that 2.5% to 5% of the world's population was killed. As many as 25 million may have been killed in the first 25 weeks; in contrast, HIV/AIDS has killed 25 million in its first 25 years.[6]

Known Flu Pandemics[8][3][9]
Name of pandemic Date Deaths Case fatality rate Subtype involved Pandemic Severity Index
1889–1890 Flu Pandemic
(Asiatic or Russian Flu)[10] 		1889–1890 1 million 0.15% possibly H3N8
or H2N2		 N/A
1918 Flu Pandemic
(Spanish flu)[11] 		1918–1920 20 to 100 million 2% H1N1 5
Asian Flu 1957–1958 1 to 1.5 million 0.13% H2N2 2
Hong Kong Flu 1968–1969 0.75 to 1 million <0.1% H3N2 2
Russian flu 1977–1978 no accurate count N/A H1N1 N/A
2009 Flu Pandemic[12] 2009–2010 105,700-395,600[13] 0.03% H1N1 N/A

Other Flu Pandemics

  • Later flu pandemics were not so devastating.
  • They included the following:
  • Even these smaller outbreaks killed millions of people.
  • In later pandemics antibiotics were available to control secondary infections and this may have helped reduce mortality compared to the Spanish Flu of 1918.[4]
  • Although there were scares in New Jersey in 1976 (with the Swine Flu), world wide in 1977 (with the Russian Flu), and in Hong Kong and other Asian countries in 1997 (with H5N1 avian influenza), there have been no major pandemics since the 1968 Hong Kong Flu.
  • Immunity to previous pandemic influenza strains and vaccination may have limited the spread of the virus and may have helped prevent further pandemics.[8]

Influenza Virus

Flu Vaccine

  • The first significant step towards preventing influenza was the development in 1944 of a killed-virus vaccine for influenza by Thomas Francis, Jr.
  • This built on work by Frank Macfarlane Burnet, who showed that the virus lost virulence when it was cultured in fertilized hen's eggs.[16]
  • Application of this observation by Francis allowed his group of researchers at the University of Michigan to develop the first flu vaccine, with support from the U.S. Army.[17]
  • The Army was deeply involved in this research due to its experience of influenza in World War I, when thousands of troops were killed by the virus in a matter of months.[6]

Past Flu Seasons Adapted from CDC [18]

Graph obtained from CDC MMWR on Influenza Activity
Graph obtained from CDC MMWR on Influenza Activity
Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2008-2009
Graph obtained from CDC MMWR on Influenza Activity
Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2009-2010
Graph obtained from CDC MMWR on Influenza Activity
Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2010-2011
Graph obtained from CDC MMWR on Influenza Activity
Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2011-2012
Graph obtained from CDC MMWR on Influenza Activity
Number and percentage of respiratory specimens testing positive for influenza, by type, surveillance week, and year. WHO and NREVSS laboratories, United States, 2012-2013
Graph obtained from CDC MMWR on Influenza Activity

2006-2007

  • During October 1, 2006--May 19, 2007, the WHO and the National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 179,268 respiratory specimens for influenza viruses; 23,753 (13.2%) were positive.
  • Of these, 18,817 (79.2%) were influenza A viruses and 4,936 (20.8%) were influenza B viruses.
  • Among the influenza A viruses, 6,280 (33.4%) were subtyped; 3,912 (62.3%) were influenza A (H1) viruses and 2,368 (37.7%) were influenza A (H3) viruses.
  • The proportion of specimens testing positive for influenza first exceeded 10% during the week ending December 23, 2006 (week 51), peaked at 28.0% during the week ending February 10, 2007 (week 6), and declined to less than 10% during the week ending April 28, 2007 (week 17).
  • The proportion was above 10% positive for 14 consecutive weeks.
  • The peak percentage of specimens testing positive for influenza during the previous three seasons ranged from 22.6% to 34.7%, and the peak occurred during early December to early March.
  • During the previous three influenza seasons, the number of consecutive weeks during which more than 10% of specimens tested positive for influenza ranged from 13 to 17 weeks.

2007-2008

  • During September 30, 2007--May 17, 2008, the WHO and the National Respiratory and Enteric Virus Surveillance System collaborating laboratories in the United States tested 225,329 specimens for influenza viruses; 39,827 (18%) were positive.
  • Of the positive specimens, 28,263 (71%) were influenza A viruses, and 11,564 (29%) were influenza B viruses.
  • Among the influenza A viruses, 8,290 (29%) were subtyped; 2,175 (26%) were influenza A (H1N1), and 6,115 (74%) were influenza A (H3N2) viruses.
  • The proportion of specimens testing positive for influenza first exceeded 10% during the week ending January 12, 2008 (week 2), peaked at 32% during the week ending February 9, 2008 (week 6), and declined to <10% during the week ending April 19, 2008 (week 16).
  • The proportion positive was above 10% for 14 consecutive weeks.
  • The peak percentage of specimens testing positive for influenza during the previous three seasons ranged from 22% to 34% and the peak occurred during mid-February to early March.
  • During the previous three influenza seasons, the number of consecutive weeks during which more than 10% of specimens tested positive for influenza ranged from 13 to 17 weeks

2008-2009

  • From September 28, 2008, to April 4, 2009, the (WHO) and the National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 173,397 respiratory specimens for influenza viruses, 24,793 (14.3%) of which were positive.
  • Of these, 16,686 (67.3%) were positive for influenza A viruses, and 8,107 (32.7%) were positive for influenza B viruses.
  • Of the 16,686 specimens positive for influenza A viruses, 6,735 (40.4%) were subtyped by real-time reverse transcription-polymerase chain reaction or by virus culture; 6,049 (89.8%) of these were influenza A (H1N1) viruses, and 686 (10.2%) were influenza A (H3N2) viruses.
  • The percentage of specimens testing positive for influenza first exceeded the seasonal threshold of 10% during the week ending January 17, 2009, and peaked at 25.0% during the week ending February 14, 2009.
  • For the week ending April 4, 2009, 12.3% of specimens tested for influenza were positive.
  • The relative proportion of influenza B viruses increased during February and March, and since the week ending March 14, 2009, >50% of the positive influenza specimens have been influenza B.

2009-2010

  • Since April 2009, the beginning of the 2009 H1N1 pandemic, through June 12, 2010, approximately 740,000 influenza specimens were tested for influenza, and the number of laboratory-confirmed positives was approximately four times the average of the previous four seasons.
  • Two peaks in percentage of specimens testing positive for influenza occurred: 43.1% in June during the initial pandemic wave, and 38.2% in October during the second wave.
  • During August 30, 2009--June 12, 2010, the 2009--10 influenza season, the WHO and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 468,218 specimens for influenza viruses; 91,152 (19.5%) were positive.
  • The proportion of specimens testing positive for influenza during the 2009--10 season exceeded 20% during the week ending August 30, 2009, peaked at 38.2% during the week ending October 24, and declined to less than 10% during the week ending December 12.
  • Of the 91,152 positive specimens from 2009-10 season, 90,758 (99.6%) were influenza A viruses and 394 (0.4%) were influenza B viruses.
  • Among the influenza A viruses, 67,022 (73.8%) were subtyped; 66,916 (99.8%) were 2009 pandemic H1N1, 72 (0.1%) were influenza A (H3N2), and 34 (0.1%) were seasonal influenza A (H1N1) viruses.

2010-2011

  • During October 3, 2010--May 21, 2011, the WHO and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 246,128 specimens for influenza viruses; 54,226 (22%) were positive.
  • Of the positive specimens, 40,282 (74%) were influenza A viruses, and 13,944 (26%) were influenza B viruses.
  • Among the influenza A viruses, 28,545 (71%) were subtyped; 17,599(62%) were influenza A (H3N2) viruses, and 10,946 (38%) were 2009 influenza A (H1N1) viruses.
  • The proportion of specimens testing positive for influenza during the 2010-11 season first exceeded 10%, indicating higher levels of virus circulation, during the week ending November 27, 2010.
  • The proportion peaked at 36% during the week ending February 5, 2011, and declined to <10% during the week ending April 16, 2011.

2011-2012

  • During October 2, 2011–May 19, 2012, the WHO) and National Respiratory and Enteric Virus Surveillance System (NREVSS) collaborating laboratories in the United States tested 169,453 specimens for influenza viruses; 22,417 (13%) were positive.
  • Of the positive specimens, 19,285 (86%) were influenza A viruses, and 3,132 (14%) were influenza B viruses.
  • Among the influenza A viruses, 14,968 (78%) were subtyped; 11,002 (74%) were influenza A (H3N2) viruses, and 3,966 (26%) were pH1N1 viruses.
  • The proportion of specimens testing positive for influenza during the 2011–12 season first exceeded 10% (indicating higher levels of viral circulation) during the week ending February 4, 2012, and peaked at 32% during the week ending March 17, 2012.

2012-2013

  • During September 30, 2012–May 18, 2013, the WHO and National Respiratory and Enteric Virus Surveillance System collaborating laboratories in the United States tested 311,333 specimens for influenza viruses; 73,130 (23%) were positive.
  • Of the positive specimens, 51,675 (71%) were influenza A viruses, and 21,455 (29%) were influenza B viruses.
  • Among the seasonal influenza A viruses, 34,922 (68%) were subtyped; 33,423 (96%) were influenza A (H3N2) viruses, and 1,497 (4%) were pH1N1 viruses.
  • In addition, two variant influenza A (H3N2v) viruses were identified.
  • Typically the influenza season is said to begin when certain key indicators remain elevated for a number of consecutive weeks.
  • One of these indicators is the percent of respiratory specimens testing positive for influenza.
  • The proportion of specimens testing positive for influenza during the 2012–13 season first exceeded 10% during the week ending November 10, 2012 (week 45), and peaked at 38% during the week ending December 29, 2012 (week 52).

References

  1. ↑ Martin, P (2006). "2,500-year evolution of the term epidemic". Emerg Infect Dis. 12 (6). PMID 16707055. Unknown parameter |coauthors= ignored (help); Unknown parameter |month= ignored (help)
  2. ↑ Hippocrates (400 BCE). "Of the Epidemics". Retrieved 2006-10-18. Unknown parameter |coauthors= ignored (help); Check date values in: |date= (help)
  3. ↑ 3.0 3.1 3.2 Potter, CW (2006). "A History of Influenza". J Appl Microbiol. 91 (4): 572–579. PMID 11576290. Unknown parameter |month= ignored (help)
  4. ↑ 4.0 4.1 4.2 4.3 Taubenberger, J (2006). "1918 Influenza: the mother of all pandemics". Emerg Infect Dis. 12 (1): 15–22. PMID 16494711. Unknown parameter |coauthors= ignored (help)
  5. ↑ 5.0 5.1 Patterson, KD (1991). "The geography and mortality of the 1918 influenza pandemic". Bull Hist Med. 65 (1): 4–21. PMID 2021692. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help)
  6. ↑ 6.0 6.1 6.2 6.3 Knobler S, Mack A, Mahmoud A, Lemon S (ed.). "1: The Story of Influenza". The Threat of Pandemic Influenza: Are We Ready? Workshop Summary (2005). Washington, D.C.: The National Academies Press. pp. 60–61.
  7. ↑ Simonsen, L (1998). "Pandemic versus epidemic influenza mortality: a pattern of changing age distribution". J Infect Dis. 178 (1): 53–60. PMID 9652423. Unknown parameter |month= ignored (help); Unknown parameter |coauthors= ignored (help)
  8. ↑ 8.0 8.1 Hilleman, M (19 August 2002). "Realities and enigmas of human viral influenza: pathogenesis, epidemiology and control". Vaccine. 20 (25–26): 3068–87. doi:10.1016/S0264-410X(02)00254-2. PMID 12163258.
  9. ↑ "Ten things you need to know about pandemic influenza". World Health Organization. 14 October 2005. Archived from the original on 23 September 2009. Retrieved 26 September 2009.
  10. ↑ Valleron AJ, Cori A, Valtat S, Meurisse S, Carrat F, Boëlle PY (May 2010). "Transmissibility and geographic spread of the 1889 influenza pandemic". Proc. Natl. Acad. Sci. U.S.A. 107 (19): 8778–81. Bibcode:2010PNAS..107.8778V. doi:10.1073/pnas.1000886107. PMC 2889325. PMID 20421481.
  11. ↑ Mills CE, Robins JM, Lipsitch M (December 2004). "Transmissibility of 1918 pandemic influenza". Nature. 432 (7019): 904–6. Bibcode:2004Natur.432..904M. doi:10.1038/nature03063. PMID 15602562.
  12. ↑ Donaldson LJ; Rutter PD; Ellis BM; et al. (2009). "Mortality from pandemic A/H1N1 2009 influenza in England: public health surveillance study". BMJ. 339: b5213. doi:10.1136/bmj.b5213. PMC 2791802. PMID 20007665. Unknown parameter |author-separator= ignored (help)
  13. ↑ Dawood, Fatimah S (26 June 2012). "Estimated global mortality associated with the first 12 months of 2009 pandemic influenza A H1N1 virus circulation: a modelling study". The Lancet Infectious Diseases. 12 (9): 687–95. doi:10.1016/S1473-3099(12)70121-4. PMID 22738893. Retrieved 19 March 2014. Unknown parameter |coauthors= ignored (help)
  14. ↑ Shimizu, K (1997). "History of influenza epidemics and discovery of influenza virus". Nippon Rinsho. 55 (10): 2505–201. PMID 9360364. Unknown parameter |month= ignored (help)
  15. ↑ Smith, W (1933). "A virus obtained from influenza patients". Lancet. 2: 66–68. Unknown parameter |coauthors= ignored (help)
  16. ↑ Sir Frank Macfarlane Burnet: Biography The Nobel Foundation. Accessed 22 Oct 06
  17. ↑ Kendall, H (2006). "Vaccine Innovation: Lessons from World War II" (PDF). Journal of Public Health Policy. 27 (1): 38–57.
  18. ↑ "CDC Morbidity and Mortality Weekly Report (MMWR) - Influenza Activity".

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