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Historical Perspective — Emergence of Influenza A (H1N1) Viruses
Oleh:
Zimmer, Shanta M.
;
Burke, Donald S.
Jenis:
Article from Journal - ilmiah internasional
Dalam koleksi:
The New England Journal of Medicine (keterangan: ada di Proquest) vol. 361 no. 03 (Jul. 2009)
,
page 279-285.
Topik:
influenza A (H1N1) virus
Ketersediaan
Perpustakaan FK
Nomor Panggil:
N08.K.2009.04
Non-tandon:
1 (dapat dipinjam: 0)
Tandon:
tidak ada
Lihat Detail Induk
Isi artikel
The emergence of influenza A (H1N1) 91 years ago led to a disastrous global pandemic. That virus is thought to have emerged almost simultaneously from birds into humans and swine. In contrast, S-OIV probably emerged from swine into humans. Although the immediate genetic event that led to the emergence of the new pandemic threat was a reassortment between two influenza A (H1N1) swine viruses, these two viruses were actually the products of at least four independent avian-to-mammalian cross-species transmissions, with at least four previous reassortments of gene segments among avian, human, and swine-adapted viruses (Figure 2). One consequence of this intertwined history is that S-OIV shares three gene segments with current seasonal human influenza A (H1N1) virus and three segments with human seasonal influenza A (H3N2) virus. It is not known whether low levels of cross-immunity against historically remote shared epitopes might confer some clinical protection against the newly emerging virus. The history of influenza A (H1N1) virus is punctuated by frequent, sporadic cross-species transmissions from swine to humans. Although the sporadically transmitted swine viruses are sufficiently pathogenic in humans to cause clinically apparent disease, they are rarely transmitted among humans. Exposure and infection are necessary but not sufficient for a new epidemic virus to emerge; the virus must also adapt and transmit.12 The one prominent exception to the general rule that these swine viruses are not transmitted among humans was the outbreak at Fort Dix. This virus was never transmitted beyond the military installation, probably because the intrinsic transmissibility of the virus was simply too low. Yet the global response to this outbreak was forceful, especially given that the outbreak self-quenched. The decision to mass-vaccinate the U.S. population resulted in the unfortunately large cluster of Guillain–Barré cases. Perhaps an even more serious consequence was the accidental release of human-adapted influenza A (H1N1) virus from a research study, with subsequent resurrection and global spread of this previously extinct virus, leading to what could be regarded as a "self-fulfilling prophecy" epidemic. The 1998 triple reassortant influenza A (H1N1) swine virus has shown what appears to be a proclivity to jump the species barrier and cause swine-to-human infections. The emergence of yet another serious global health threat from an animal source highlights the critical need for deeper understanding of zoonotic viruses, including in vivo studies of pathogenesis in animals, field epidemiologic studies, and surveillance in animal populations, along with the development of computational models. The presumptive origins of the S-OIV influenza epidemic outside the United States show the critical importance of international collaboration in efforts to predict and control future pandemic threats.
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