Where is swine flu most prevalent

Unrooted maximum likelihood tree of the gene sequences of the matrix proteins of S-OIV and the most closely related sequences in Genbank. Unrooted maximum likelihood tree of the haemagglutinin gene sequences of S-OIV and the most closely related sequences in Genbank. So, in summary, our analyses provide consistent evidence that the immediate parents were swine viruses.

The sampling dates of those isolates are congruent with the estimated lengths of 'unsampled ancestry' of the parents [ 8 ] and, together with differences in provenance support the conclusion that S-OIV had three parents; one from North America, one from Europe and the third from Asia.

The results of the phylogenetic analyses outlined above can be used to construct plausible scenarios of the ways in which S-OIV might have originated. This is a useful exercise as it may focus the search for new clues. Some of the crucial evidence provided by the phylogenetic analyses is that:. Two were sampled around 11 years ago, the third 17 years ago, whereas their sister and cousin lineages have been sampled frequently. S-OIV could have been generated by natural means.

The parental isolates could, for example, have been assembled in one place by migratory birds, however the consistent link of S-OIV's immediate ancestors with pigs suggests that human activity of some sort was involved in bringing together the parental viruses. At least two contrasting theories are congruent with this possibility and the available clues:.

The " unsampled pig herd" theory was suggested by Smith and his colleagues [ 8 ], who concluded that "the progenitor of the S-OIV epidemic originated in pigs", and the "long unsampled history observed for every segment" of the S-OIV genome "suggests that the reassortment of Eurasian and North American swine lineages may not have occurred recently, and it is possible that this single reassortant lineage has been cryptically circulating rather than two distinct lineages of swine flu", and that "Movement of live pigs between Eurasia and North America seems to have facilitated the mixing of diverse swine influenzas, leading to the multiple reassortment events associated with the genesis of the S-OIV strain.

This theory was implicitly supported by Trifonov and his colleagues in their report of a study of the numbers of gene sequences deposited in Genbank from human and pig influenzas sampled around the world in different years [ 25 ]. They had found that, although the number of influenza sequences deposited had increased greatly in the last decade, there were four times as many human as pig influenza sequences. Furthermore, whereas the sequenced human isolates came from all over the world, the pig isolates came only from North America, Asia, and Europe, and none from Africa, Oceania, or South America.

They concluded that, given "the lack of sampling" of pigs "in certain parts of the world, it is perhaps not surprising that the ancestors of the new human influenza A H1N1 virus have gone unnoticed for almost two decades. It is important to note that this theory depends on the intercontinental movement of live infected pigs, and requires at least two quarantine-breaching incursions involving three different countries.

It is likely that quarantine control of the spread of swine influenzas around the world varies greatly in its efficacy. However viruses of the Eurasian 'avian-like' lineage, and their genes, have never been found in North America before S-OIV appeared, even though they have been common in Europe for over three decades, and similarly 'triple reassortant' viruses and their genes have not been isolated in Europe, although they have been the dominant swine influenza virus in North America for more than a decade.

The "laboratory error" theory. We note that influenza viruses survive well in virus laboratories, that laboratories are not subject to routine surveillance, and that there are probably many laboratories in the world that share and propagate a range of swine influenza viruses from different sources and continents, and also share and use immortalized lines of cultured cells.

The viruses are used for research, diagnostic tests and for making vaccines, and the cells are used for propagating the viruses. Thus if S-OIV had been generated by laboratory activity, when one host was simultaneously infected with strains from the different parental lineages, this would explain most simply why S-OIV's genes had escaped surveillance for over a decade, and how viruses last sampled in North America, Europe and Asia became assembled in one place and generated a reassortant.

So what sort of laboratory event might produce mixed infections with different strains of influenza, and thereby generate S-OIV? The simplest is that S-OIV is a reassortant produced during research.

There is also the possibility that it was generated during the production of multivalent vaccines. Multivalent 'killed' vaccines are mixtures of virions that have been grown in hen's eggs and then chemically sterilized. Thus a reassortant might be produced if insufficient sterilant, usually formaldehyde or propiolactone, is added to the virion mixture. The live mixture could then infect pigs 'vaccinated' with it, and the growing viruses could reassort, infect piggery staff and hence spread to the broader human population.

Finally, it is possible that serially passaged cells, such as the Madin-Darby canine kidney MDCK cells now widely used in influenza laboratories, became latently and serially infected with different strains of influenza as a result of lax laboratory practices. This process could generate reassortants, and infect staff. There are clear historical precedents for most of the events described in the above scenarios.

Viruses do 'escape' from laboratories, even high security facilities. The H1N1 influenza lineage that circulated in the human population for four decades after the Spanish influenza epidemic, disappeared during the Asian influenza pandemic, was absent for two decades, but then reappeared in Gene sequences of the isolate and others collected in the s were almost identical, indicating that the virus had not replicated and evolved in the interim, and had probably been held in a laboratory freezer between and and 'escaped' during passaging.

The suggestion that persistently infected cells might be involved is also not outlandish; influenza virus can persistently and latently infect MDCK cells [ 27 ], and viruses do travel between laboratories in cells [ 28 ]. Multivalent 'killed' vaccines are widely used to control swine influenzas, particularly in North American piggeries [ 29 ], indeed one of the viruses identified by us and others e.

We also note that isolates selected from the three clusters of viruses we find to be closest to S-OIV would probably make a useful trivalent vaccine for international use as they would provide a mixture of haemagglutinins of the swine H3, H1 'classical swine' and H1 'Eurasian avian-like' lineages. The patchy occurrence of S-OIV infections in piggeries over the past six months is interesting and may be significant. Pigs have been shown to be fully susceptible to S-OIV.

They shed the virus and readily transmit it between themselves, but whereas S-OIV has been reported in humans worldwide, it has not yet been reported from a pig farm in the USA October By contrast it has been found in two piggeries each in Australia, Canada and Ireland, and one each in Argentina, Indonesia and Japan. In the outbreaks in Argentina, Australia and Canada, at least, the pigs had not been vaccinated Jorge H.

Dillon, J. Keenliside and Alain Laperle, personal communication , and became infected from infected farm staff. Circumstantial evidence must always be treated with caution. One major uncertainty in trying to determine the origin of S-OIV is that one cannot predict which characters of the parental viruses have remained or changed during the reassortment process that produced S-OIV.

If, for example, the significant infectiousness of S-OIV is an 'emergent' property of S-OIV, and not shown by its parents, then one could conclude that the final reassortment probably occurred at about the time it emerged in early However it is not yet known whether S-OIV's infectiousness is novel; the reassortment may have occurred a decade ago, and a recent mutation may have enhanced its infectiousness.

Another widely reported feature of S-OIV is that it replicates poorly in embryonated eggs, but again this may be merely a specific feature of S-OIV and not its immediate parents.

Similarly the fact that the evolutionary rate of all of the genes of S-OIV seem to be 'normal' during their unsampled pre-emergent period [ 8 , 11 ]] does not prove that the virus or its parents have been maintained in "unsampled" pig herds and precluded the possibility of human involvement, as viruses grown for vaccines evolve, and indeed might be expected to show an increased evolutionary rate [ 32 , 33 ] while adapting to eggs, a new host, although such an increase may have been offset by the practice of storing 'seed stocks' for use in several 'production cycles' in vaccine production, so that the evolutionary age of a vaccine virus may be less than its sidereal age, and the average could then appear to be 'normal'.

Finally there is the report that the first human S-OIV infections were in Perote, a small Mexican town with a very large number of large piggeries, although it was also reported that none of the pigs showed signs of influenza. Among the earliest cases were some in Oaxaca, kms to the south [ 34 ]. Perote is an unlikely place for an infected migratory pig to arrive from an intercontinental trip, as the town is in a remote high valley surrounded by mountains, kms to the east of Mexico City where there is the nearest major airport, and kms from the nearest port at Vera Cruz.

Like influenza viruses in humans and other animals, swine flu viruses change constantly. Pigs can be infected by avian influenza and human influenza viruses as well as swine influenza viruses.

When influenza viruses from different species infect pigs, the viruses can reassort i. Over the years, different variations of swine flu viruses have emerged.

Swine flu viruses are thought to be spread among pigs mostly through close contact and possibly from contaminated objects moving between infected and uninfected pigs. Infected swine herds, including those vaccinated against swine flu, may have sporadic disease, or may show only mild or no symptoms of infection. Signs of swine flu in pigs can include fever, depression, coughing barking , discharge from the nose or eyes, sneezing, breathing difficulties, eye redness or inflammation, and going off feed.

Some pigs infected with influenza, however, may show no signs of illness at all. H1N1 and H3N2 swine flu viruses are endemic among pig populations in the United States and something that the industry deals with routinely. Outbreaks among pigs normally occur in colder weather months late fall and winter , but can occur year round. A vaccine programme for children has also been introduced, which aims to protect children and reduce their ability to infect others.

Page last reviewed: 02 September Next review due: 02 September Swine flu H1N1. It's often shortened to "H1N1". This content does not have an Arabic version. Overview The H1N1 flu, commonly known as swine flu, is primarily caused by the H1N1 strain of the flu influenza virus.

More Information Self-care for the flu. Request an Appointment at Mayo Clinic. More Information He's the bravest kid I've ever seen. More Information Flu masks Flu vaccine: Safe for people with egg allergy? Share on: Facebook Twitter. Show references Key facts about human infections with variant viruses.

Centers for Disease Control and Prevention. Accessed Jan. Dolin R. Epidemiology of influenza. Grohskopf LA, et al. Prevention and control of seasonal influenza with vaccines: Recommendations of the Advisory Committee on Immunization Practices — United States, influenza season. Cohen J, et al. Influenza viruses. In: Infectious Diseases. Philadelphia, Pa.

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