Pandemic swine influenza virus (H1N1): A threatening evolution

The Canadian veterinary journal. La revue vétérinaire canadienne, 2010

In the spring of 2009, a new human influenza A H1N1 virus emerged in Mexico and the United States. The strain was referred to as "swine flu" as it has strong similarities with current circulating swine influenza viruses, although the first outbreak on a swine farm was recorded more than 2 mo following the first human reports. This new strain, designated as pandemic (H1N1) 2009, has shown the ability to spread amongst the human population and can be found on all continents. The way influenza viruses and specifically this influenza A pandemic (H1N1) 2009 virus evolve is described in this manuscript.

Journal of Public Health and Epidemiology, 2011

Evolutionary process of swine-origin H1N1 influenza A viruses that infected humans from sporadic to pandemic is of high epidemiological significance but still remains obscure. To understand this process, we performed phylogenetic, bootscan, and adaptive evolution analyses using the sequences of the 8 gene segments from swine-origin H1N1 influenza A viruses that infected humans and the reference viruses. Classic swine H1N1 viruses occasionally infected humans before 1998. Sporadic human infection with the triple-reassortant swine-origin H1N1 viruses was firstly identified in 1998 and has become increasingly frequent since 2005. Except genes encoding the neuraminidase and matrix protein of swine influenza viruses of Eurasian lineage, other 6 genes of A/H1N1/2009 pandemic strain were most closely linked to those of A/Iowa/CEID23/2005(H1N1), a representative swine-origin triplereassortant virus that infected humans sporadically. Potential positive selections acting on the haemagglutinin gene evolved from classic swine H1N1 viruses to the triple-reassortant H1N1 viruses and on the neuraminidase gene evolved from Eurasian swine viruses to A/H1N1/2009 pandemic viruses might play a role in cross-species transmission and human infection. Surveillance of genetic evolution of influenza A viruses in swine workers might provide useful clues of influenza pandemic.

2010

Pandemic influenza has posed an increasing threat to public health worldwide in the last decade. In the 20th century, three human pandemic influenza outbreaks occurred in 1918, 1957 and 1968, causing significant mortality. A number of hypotheses have been proposed for the emergence and development of pandemic viruses, including direct introduction into humans from an avian origin and reassortment between avian and previously circulating human viruses, either directly in humans or via an intermediate mammalian host. However, the evolutionary history of the pandemic viruses has been controversial, largely due to the lack of background genetic information and rigorous phylogenetic analyses. The pandemic that emerged in early April 2009 in North America provides a unique opportunity to investigate its emergence and development both in human and animal aspects. Recent genetic analyses of data accumulated through long-term influenza surveillance provided insights into the emergence of this novel pandemic virus. In this review, we summarise the recent literature that describes the evolutionary pathway of the pandemic viruses. We also discuss the implications of these findings on the early detection and control of future pandemics.

Cold Spring Harbor Perspectives in Medicine

Influenza A viruses (IAVs) are the causative agents of one of the most important viral respiratory diseases in pigs and humans. Human and swine IAV are prone to interspecies transmission, leading to regular incursions from human to pig and vice versa. This bidirectional transmission of IAV has heavily influenced the evolutionary history of IAV in both species. Transmission of distinct human seasonal lineages to pigs, followed by sustained within-host transmission and rapid adaptation and evolution, represent a considerable challenge for pig health and production. Consequently, although only subtypes of H1N1, H1N2, and H3N2 are endemic in swine around the world, extensive diversity can be found in the hemagglutinin (HA) and neuraminidase (NA) genes, as well as the remaining six genes. We review the complicated global epidemiology of IAV in swine and the inextricably entangled implications for public health and influenza pandemic planning.

Emerging Infectious Diseases, 2014

Cell, 2005

Journal of Biosciences, 2009

At this critical juncture when the world has not yet recovered from the threat of avian influenza, the virus has returned in the disguise of swine influenza, a lesser known illness common in pigs. It has reached pandemic proportions in a short time span with health personnel still devising ways to identify the novel H1N1 virus and develop vaccines against it. The H1N1 virus has caused a considerable number of deaths within the short duration since its emergence. Presently, there are no effective methods to contain this newly emerged virus. Therefore, a proper and clear insight is urgently required to prevent an outbreak in the future and make preparations that may be planned well in advance. This review is an attempt to discuss the historical perspective of the swine flu virus, its epidemiology and route of transmission to better understand the various control measures that may be taken to fight the danger of a global pandemic.

Annals of Thoracic Medicine, 2009

The causal agent, in fact, is a swine-origin influenza A (H1N1) virus (S-OIV) that is characterized by a unique combination of gene segments that has not been previously identifi ed among human or swine infl uenza A viruses. Actually, the new H1N1 virus appears to be a mixture of avian, porcine, and human infl uenza RNA. Genomic analysis indicates that it is closely related to common reassortant swine infl uenza A viruses that have been isolated in North America, Europe, and Asia in the last 20 years. [4-6] Historically, there have been four to five pandemics of infl uenza during the 20 th century, which have occurred at intervals of 9-39 years. The 1918 pandemic, caused by worldwide spread of a human influenza A (H1N1) virus, was responsible for 40-50 million deaths. An estimated 4.9 million excess deaths, representing 2% of the population, occurred in India alone. [7] After the pandemic subsided, sporadic cases of human infl uenza H1N1 continued to occur worldwide. H1N1 then mysteriously disappeared in 1957, likely due to both competition with the emerging pandemic H2N2 strain as well as the development of immunity to H1N1 among populations. On January 1976, an outbreak of a respiratory The infl uenza pandemic the world was waiting for may have arrived on April 2009, although to date its virulence appears to be no greater than that of seasonal infl uenza. Mexico was the fi rst country where there was a sharp increase in reports of patients requiring hospitalization for pneumonia and an unusual series of deaths, leading to the suspicion that a new infl uenza virus strain was in circulation. During the same period, offi cials at the Centres for Disease Control and Prevention (CDC), Atlanta, uncovered two cases of infl uenza, the so-called 'swine infl uenza,' that were clearly due to a novel strain; the two patients were children living in neighbouring

Nature, 2009

Indian Journal of Microbiology, 2009

Influenza A virus is a potent pathogen of annual respiratory illness with huge potential of causing occasional pandemics of catastrophic consequences. In April 2009, a novel, swine-origin influenza A H1N1/09 virus was identified in Mexico which continued to spread globally. This unique virus emerged from an avian, human, Eurasian swine viral strain and a North American swine strain belonging to the lineage of the 1930 swine virus. Till date H1N1/09 pandemic has been relatively mild and lacks the previously described molecular markers of influenza A pathogenicity and transmissibility. In this review, we will discuss the molecular and antigenic determinants of this virus and its designation as a low pathogenic strain, which carries the potential to develop into a devastating strain with subsequent mutations and reassortments.