When was avian flu

Since its widespread re-emergence in , rare, sporadic human infections with this virus have been reported in Asia, and later in Africa, Europe, and the Middle East. Human infections with Asian H5N1 viruses have been associated with severe disease and death.

Most human infections with avian influenza viruses, including HPAI Asian H5N1 viruses, have occurred after prolonged and close contact with infected birds.

Rare human-to-human spread with this virus has occurred, but it has not been sustained and no community spread of this virus has ever been identified. The H5N1 virus recently detected in U. Flu viruses are constantly changing and animal flu viruses can change such that they may gain the ability to infect people easily and spread among people, causing a pandemic.

Human infections with novel avian influenza virus like Asian H5N1 are concerning because of this pandemic potential. CDC takes routine public health preparedness measures whenever a virus with pandemic potential is identified.

Because Asian H5N1 continues to circulate and has been responsible for a number of human infections, Asian H5 preparedness efforts have been extensive. Asian H5N1 vaccine is being stockpiled for pandemic preparedness by the United States government. Anthrax is a rare but potentially fatal bacterial disease that occasionally infects humans. The Western obsession with cleanliness may be partly responsible for the increase in allergic asthma and conditions such as rhinitis.

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Actions for this page Listen Print. Summary Read the full fact sheet. On this page. How avian influenza virus is spread Symptoms of bird flu Complications of bird flu Tell your doctor if you have been to a country where there is bird flu Influenza viruses can mutate Australia is ready to respond to an outbreak Treatment and vaccines for bird flu Advice for travellers and Australians living overseas Where to get help Things to remember.

How avian influenza virus is spread Water birds such as wild ducks are believed to be the carriers of all avian influenza type A viruses. Symptoms of bird flu Although there have been too few human cases to determine the exact incubation period of bird flu, it would be expected to be from three to 10 days. The symptoms of bird flu in humans are similar to those of regular influenza and include: fever sore throat cough headache aching muscles. Complications of bird flu Bird flu in humans can cause a range of serious and potentially fatal complications, including: eye infections pneumonia, including viral pneumonia acute respiratory distress inflammation of the brain and heart.

Tell your doctor if you have been to a country where there is bird flu If you have recently returned from a country that had an outbreak of bird flu and you get flu symptoms, see your doctor immediately. Influenza viruses can mutate Influenza viruses that infect animal species can mutate and infect humans.

Australia is ready to respond to an outbreak Federal and state governments have been working together to plan their response to an outbreak of bird flu. Treatment and vaccines for bird flu Several antiviral medications used to treat human influenza are also effective for bird flu.

Advice for travellers and Australians living overseas People making short visits to affected countries do not need to have antiviral medications.

Suggestions include: Avoid contact with wild or domesticated birds. Stop young children from putting contaminated objects or their own fingers into their mouths.

Eggshells may be contaminated with bird faeces. Wash eggs thoroughly before breaking and wash your hands thoroughly after handling eggs. Avoid foods that contain uncooked egg, such as mayonnaise. Typically, these infections are severe in humans, often causing death, and potential zoonotic epidemics are of ongoing concern.

Specific episodes with H5 and H7 viruses are considered in more detail later. Water fowl, especially Anseriformes ducks, geese and swans and Charadriiformes gulls, terns and sandpipers , are thought to be the natural reservoir of IAV [ 2 , 53 ], and infection in these host species is not only typically low pathogenic but can be asymptomatic [ 2 , 54 — 57 ].

It has also been shown that migratory birds may carry HPAI as well as LPAI viruses asymptomatically over long distances [ 53 , 58 — 60 ], and that avian IAV lineages can spread along migratory flyways [ 61 — 66 ]. For example, remote sensing and phylogenetic analyses showed that the distribution of H5N1 viruses in Eastern Asia followed wild bird migratory flyways in the time period — [ 63 ].

Transmission between places and host species can be inferred by phylodynamic and phylogeographical analyses [ 67 , 68 ], and these techniques are particularly suitable for understanding avian influenza systems since they make use of the fast-evolving viral sequence data to reveal dispersion patterns see box 2 for details. Phylogeographic analyses have revealed the role of migratory wild birds in the intra-continental circulation of LPAI in North America [ 61 , 62 , 89 ], and have implicated wild birds following North American flyways in the introduction of H7N3 strains into Mexico in — [ 64 ].

Similarly phylogeographic techniques have also been used to show the effects of HPAI H5N1 transportation by different bird species across Asia [ 90 ] and that the spread of LPAI H9N2 strains in Asia was a combination of long-range distribution by wild birds coupled with more localized spread via the domestic bird trade [ 91 ]. Viral sequence data sampled over a period of time, spatial locations and different host species can be used to infer transmission patterns e.

Typically for IAV, time-scaled phylogeny reconstruction is often performed using the programme BEAST Bayesian Evolutionary Analysis Sampling Trees [ 72 , 73 ] in which trees and relaxed molecular clock models used to represent the relationship between genetic distance and time, and other parameters, are jointly inferred.

Example of a time-scaled phylogenetic tree with tips coloured by host-type and the discrete trait host model a ; and the same tree mapped into space with continuous spatial coordinates with tips coloured by subtype b. To infer transmission rates between discrete locations or hosts, or to model subtype changes for example, the change of NA subtype with respect to a tree made from HA sequences , phylogenetic analysis with discrete traits can be used [ 74 ], where transitions from one state to another are inferred along the phylogeny as a continuous time Markov chain model [ 75 ] e.

Discrete trait analyses can be extended by parameterizing the transition rate matrix as a log—linear function of various potential covariates in a generalized linear modelling framework, to identify the host species or environmental factors associated with the observed spatial spread [ 7 , 76 — 78 ]. When the additional feature of interest is continuously distributed, e. In addition to trait-based approaches, BASTA [ 82 ] and MASCOT [ 83 ] make use of structural coalescent approximations [ 84 , 85 ] to reconstruct evolutionary trees while considering the size of the different sub-populations involved in the meta-population, improving inference of the migration rates between sub-populations.

Finally, by combining epidemiological data and recent phylogenetic inference techniques, several methods such as SCOTTI [ 86 ], Outbreaker [ 87 ] and Beastlier [ 88 ] are now able to reconstruct, with some success, the transmission tree of only partially observed epidemics. The effect that bird migratory flyways figure 4 have on the global circulation of IAV can be seen in the phylogeny of all segments, where two very distinct major clades corresponding either to the Americas or to Asia, Europe, Africa and Australasia can be observed [ 65 ].

Estimates of the time to most recent common ancestor TMRCA of these clades varies by segment and method, but appears to be in the region of years, a value close to the root of the major contemporary human, swine and avian lineages [ 40 ], and as such represents a deep divide also evident in figure 5. Although viral dissemination via wild birds can be thought of as occurring along flyways, different species have different migration patterns, and these general flyways overlap, as indicated in figure 4.

Consequently, cross-flyway e. In a study of northern pintails, Koehler et al. Flyways of migratory water fowl. Flyways run approximately north—south, and also overlap in northern regions, including in Siberia, Greenland, Alaska and across the Bering straits, which allows occasional transmission of influenza viruses between North America and Eurasia.

Time-scaled tree of a stratified subsample of H5 segment 4 HA. Tips are represented as circles and coloured by neuraminidase subtype from H5N1 red to H5N9 magenta.

However, even if migratory birds might be good vectors, transmission patterns indicate that circulation is partially maintained through trade of infected domestic birds [ 91 , 95 , 96 ].

Therefore, it is clear that the worldwide spread of avian IAV results from synergy between trade of infected domestic birds and wild bird movement through migratory flyways [ 91 , 97 ]. Since domestic ducks can share the same habitat, water and food as wild waterfowl [ , ], their presence and concentration are thought to make them key intermediate hosts between wild birds and poultry, and consequently they play an important role in the emergence and circulation of HPAI strains, especially in Asia [ — ].

The bridging role of domestic ducks between wild birds and domestic Galliformes has been particularly emphasized in the H7N9 IAV outbreaks in China [ ], most notably in areas where high concentrations of free-grazing ducks live in close contact with potentially infected wild birds, such as the Poyang and Dongting Lakes [ ]. Agricultural practices, such as the release of high quantities of juvenile ducks in paddy fields prior to the arrival of the wild birds, might further exacerbate transmission and circulation of the virus between wild and domestic animals.

As noted above box 1 , H5 and H7 avian strains of IAV are further classified as highly pathogenic on the basis of their ability to cause disease and mortality in chickens [ 25 ]. This has since been confirmed by many detailed sequencing analyses of outbreaks where direct LPAI precursors have been identified, even down to individual poultry sheds e.

Dhingra et al. As HPAI in poultry has a rapid onset and high mortality rate, farm outbreaks can be short lived, partly because a large percentage of the birds die in a few days, but also because HPAI is a notifiable disease with mandatory control measures, including culling remaining birds and movement bans to limit the spread to neighbouring areas [ 25 ].

However, on some notable occasions HPAI outbreaks have caused major losses in domestic birds see [ 13 ] for a review up to Apart from the widespread HPAI H5s originating in Asia from onwards, and the associated H7s which are described in detail next, other outbreaks resulting in huge impacts i. Phylogenetic studies of whole virus genomes revealed that around — several different genotypes of H5N1 arose from reassortment events between the original HPAI H5N1 virus with other LPAI strains circulating in both domestic and wild bird populations [ 95 , — ].

By , one genotype Z had become dominant [ ], and in addition to further human cases in Hong Kong in , there were poultry outbreaks in mainland China and other countries in Southeast and East Asia [ ]. Associated with these poultry outbreaks, there were also fatal human cases in Vietnam, Thailand and China [ ]. In the spring of , a mass die-off of wild birds occurred at Qinghai Lake in west China [ ]. The outbreak virus was thought most likely to have originated from poultry in southern China and had been transported by migratory birds to Qinghai Lake [ 95 , , ].

Furthermore, the virus contained a mutation in a polymerase gene PB2 K that had been shown to increase H5N1 virulence in mice, a model for mammalian infection capability [ ]. A single H5N1-infected migratory flamingo was found in Kuwait in November [ ], and by February Iraq and Iran were reporting virus in backyard poultry and wild birds, as well as human and domestic cat cases [ ].

In January and February , there were several first detections reported in southern and western European countries [ ]. H5N1 was first reported in Africa in Nigerian poultry in February [ ], closely followed by reports of poultry outbreaks in Egypt [ , — ]. The virus continued to spread in Africa, west and northwards in Europe and through the Middle East and South Asian subcontinent in and Questions had already been raised about H5N1 as the source of the next influenza pandemic [ , ], so its spread out of Asia was of continued concern.

Reinforcing these fears, by early H5N1 was endemic through southeastern Asia, had spread through Eurasia and Africa, and was established in domestic bird populations. There was also evidence for limited person to person spread [ , ].

Fortunately, there was no human transmissible H5N1 pandemic in , something that might have caused the deaths of millions assuming that a human transmissible form retained high pathogenicity. Despite mostly mild symptoms in humans, the lack of immunity to this quite different strain from the previously circulating H1N1 seasonal virus meant that a significant fraction of the population had probably been infected. The internal gene segments were from a combination of H9N2 virus lineages circulating in poultry [ — ], one of which probably also donated internal segments to the HPAI H5N1 viruses [ , , ].

The H7N9 viruses proved to be zoonotic as the first human cases were found in February in Shanghai and Anhui, China [ , ]. From February to July , there have been confirmed human cases and deaths, mostly in China [ , ]. Between February and July , there were five seasonal waves of human H7N9 infections [ ], with waves 2—5 starting around October and lasting until around June.

However, there were mutations in the HA, including QL using H3 HA numbering , that were associated with increased binding to human sialic-acid receptors and airborne transmission between mammals [ , , ].

However, although these viruses were shown to be transmissible in ferret studies [ ], human to human transmission actually remained limited [ ] and most cases were associated with contact with infected poultry or live bird markets [ ]. To control the disease, live poultry markets in affected central urban areas were closed [ ], and the total number of human cases per wave decreased from wave 2 to wave 4 [ ].

Nevertheless, the virus, asymptomatic or with mild clinical signs for birds, continued to circulate in poultry populations via trade in China, and diversified into several clades [ ]. The fifth wave starting September saw a rapid increase in the number of human cases and geographic expansion out of southern and eastern China despite the surveillance and control measures [ ].

Also of concern was the presence and ease of acquisition of E K or DN mutations in PB2 in the human isolates, since, similarly to HPAI H5N1 cases, these are associated with increased virulence and adaptation in mammals [ , ]. A nationwide vaccination programme for poultry in China was begun in September by the Chinese Ministry of Agriculture [ ]. Recombinant H5 and H7 bivalent inactivated vaccines were used [ ] with subsequent testing of post-vaccination immunization, and also continued surveillance.

Only a few 11 out of over 80 in December samples from birds or their environment tested positive for H7N9, and there were only three human cases of H7N9 in the time period September —June expected to show a sixth wave of human infection, compared with over the previous year.

The risk of spread of H7N9 to surrounding countries in Southeast Asia is still considered to be moderate via live bird trade, but low for poultry products and negligible for onward spread via wild birds [ ]. The risk of human occupational exposure in live bird markets is also considered to be moderate to low [ ].

In clade 2, there are several sub-lineages that are notable for the number of birds they have infected, their geographical spread, and spill-over to humans, including 2. In the process, sub-clade 2. H5NX viruses were detected in poultry farms and live bird markets, particularly in ducks, as part of the ongoing surveillance effort in China from onwards [ — ].

In , H5N8 viruses re-appeared in eastern China in with some internal segment reassortments from H5N1 strains [ ], were detected in wild mallards e.

From detailed time-scaled phylogeographic analysis, it was inferred that H5N8 had entered South Korea via overwintering wild waterfowl which subsequently infected domestic ducks [ 70 , ]. Both phylogeographic analysis of sampled sequences and knowledge of bird migration patterns indicated that the virus was transported by migrating wild Anseriformes from the eastern Asia region, up to the summer breeding grounds in the north by the East Asian flyway, and then down into Europe via the East Atlantic flyway or to North America via Beringia Pacific and Central flyways [ 69 , 93 , ].

The control measures were successful, however, and by the autumn of , H5N2 was not reported either from industry [ ], nor from North American wild bird surveillance studies [ ]. Clade 2. In Asia from onwards H5NX lineages continued to circulate in wild and domestic bird populations, and as well as H5N8, two different H5N6 reassortant lineages were detected in Sichuan and Jiangxi provinces of China, respectively in [ — ].

Both of these lineages spread within poultry in China [ , , ], and to wild bird populations [ ]. It is also likely that H5N6 has been transmitted on the East Asian—Australian flyway by wild migratory birds [ ], since Japan has been bombarded with H5N6 reassortants [ , ], and it is also possible that H5N6 was introduced into The Philippines via wild birds for the first time in the summer of [ ].

Multiple incursions of these HPAI H5NX strains into European countries occurred [ ], causing the worst epidemic so far in Germany, affecting both domestic and wild birds [ ]. Most recently September , The Netherlands and Germany have reported their first H5N6 detection of the autumn season [ , ].

In this brief history of bird flu, we have seen that current avian influenza virus strains have been circulating and diversifying in wild bird populations for at least the last years. Wild migratory birds can transport IAV along their migration routes, and contact between wild and domestic avian populations sometimes results in transmission between the two. Direct transmission of the virus from wild birds to humans appears to be very rare or non-existent , presumably due to the low frequency of contact between the two populations; however, transmission from domestic avian species to humans does occur, especially in live bird markets in Asia.

It is clear that H5 and H7 viruses have the capacity to evolve on multiple occasions an HPAI phenotype, probably as result of transmission in high bird density settings and the susceptibility of chicken and other domestic Galliformes species. In recent years, one such H5 lineage has become widely established in Asian domestic bird populations.

Both H5 and H7 HPAI viruses have been sporadically transmitted to humans from domestic poultry, and for H5 at least been transmitted back into wild populations. However, because HPAI does not necessarily kill its anseriform hosts, reassortment with co-circulating LPAI viruses can occur, furthering evolution of the virus, while the low severity symptoms allow the long-range and intercontinental transport of the disease.

In some senses, the dynamics of human influenza in humans and avian influenza in birds are similar—both can be thought of as stratified into layers with different connectivity: age for humans—with locally moving children and long-range moving adults; and domestic and wild species for birds—with domestic birds moving via trade and Anseriformes by long-range migration.

However, unlike human IAV, where reassortment between the few dominant subtypes is rare, reassortment is a common feature for avian IAVs, especially in wild bird populations. Consequently, avian IAVs are far more diverse and more easily generate novel strains than the more specialized human viruses.

Looking to the future, we should expect the emergence of more HPAI strains. Experience teaches that this has previously occurred somewhere in the world approximately once or twice per decade; and the fundamental driver of leaving H5 and H7 LPAI viruses uncontrolled in a host-dense environment until de novo mutation into HPAI forms occurs has not been removed.

Also, it seems quite possible that HPAI H5 will continue to circulate and diversify, especially for clade 2. Hence increasing biosecurity and vaccination in domestic poultry are likely to be important strategies to keep outbreaks in these populations to a minimum. Ongoing avian influenza virus spill-overs into human cases suggest that zoonotic bird flu is a continued threat to human health; however, the apparent success of the H7N9 vaccination programme in China suggests that it is possible to control virus circulation in domestic birds and thus vastly reduce the number of human infections and the risk of ongoing human to human spread.

Therefore, if we continue the disease surveillance programmes in avian, human and other domestic animal populations, and control avian influenza in domestic avian populations, then we can surely reduce the risks of a new human avian influenza pandemic. All authors revised the manuscript and approved the final version. National Center for Biotechnology Information , U. Published online May 6.

Samantha J. Lycett , Florian Duchatel , and Paul Digard. Author information Article notes Copyright and License information Disclaimer. Accepted Jan This article has been cited by other articles in PMC. Data from: A brief history of bird flu Dryad Digital Repository. Data for segments 1,2,3,5,7,8 - taxa.

Data for segments 1,2,3,5,7,8 - taxa for display. Data for segment 4 subtype H5 - taxa. Abstract In , a strain of influenza A virus caused a human pandemic resulting in the deaths of 50 million people.

Keywords: avian influenza virus, epidemiology, phylogenetics, pandemic, zoonotic. Introduction a Influenza viruses Influenza viruses are part of the Orthomyxoviridae family [ 1 ] and are negative sense single-stranded RNA viruses with segmented genomes. Open in a separate window. Figure 1. Box 1.

Figure 2. Global patterns of avian influenza circulation Water fowl, especially Anseriformes ducks, geese and swans and Charadriiformes gulls, terns and sandpipers , are thought to be the natural reservoir of IAV [ 2 , 53 ], and infection in these host species is not only typically low pathogenic but can be asymptomatic [ 2 , 54 — 57 ]. Box 2. Inference of transmission routes using phylodynamics and phylogeography.

Figure 3. Figure 4. Figure 5. Rise of highly pathogenic avian influenza As noted above box 1 , H5 and H7 avian strains of IAV are further classified as highly pathogenic on the basis of their ability to cause disease and mortality in chickens [ 25 ].

Concluding remarks In this brief history of bird flu, we have seen that current avian influenza virus strains have been circulating and diversifying in wild bird populations for at least the last years.

Supplementary Material Supplementary Text: Click here to view. Supplementary Material Data for segments 1,2,3,5,7,8 - taxa: Click here to view. Supplementary Material Data for segments 1,2,3,5,7,8 - taxa for display: Click here to view. Supplementary Material Data for segment 4 subtype H5 - taxa: Click here to view. Authors' contributions S.

Competing interests We have no competing interests. References 1. Amsterdam, The Netherlands: Elsevier; Evolution and ecology of influenza A viruses. Chen R, Holmes EC. Avian influenza virus exhibits rapid evolutionary dynamics. Molecular mechanisms enhancing the proteome of influenza A viruses: an overview of recently discovered proteins.

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