The evolutionary history of Influenza A

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Influenza disease impacts annually up to 10% of the world's population, equating up to 500millions of people (Gerdil., 2003). Actual accounts of in?uenza in humans approximately date back to the 12th century. Possible pandemics are documented as far back as 1510, but the ?rst one to be clearly recognised was in 1580 ( Nguyen-Van-Tam & Hampson.,2003) .31 influenza pandemics have been documented with the five most recent in 1889,1900,1918,1957 and 1968 separated consecutively by evolutionary gaps of 11,18,39 and 11 years(Ansart et al.,2009).

Influenza A viruses can infect a large number of mammalian species from humans, pigs, horses, sea mammals and birds (Brown, 2000).

Pandemics are epidemics that spread rapidly on a global scale which are caused by pathogens in which humans usually have no immunity, infect a large quantity of the population, this in turn leads to associated serious illnesses and are usually of animal origin (Khiabanian et al., 2009).Four pandemics have occurred during the last two centuries, the A/ H1N1 (Spanish flu)-avian origin in 1918, the A/H2N2 in 1957 (Asian flu), A/ H3N2 in 1968 (Hong Kong flu), and most recently documented was the A/H1N1 (swine flu) which broke out in 2009. (Bragstad et al., 2008); (Smith et al., 2009). Pandemics are particularly distinguished by a shift in the virus subtype, a much higher mortality rate to younger populations, successive pandemic waves, increased transmissibility percentile than any other seasonal influenza, and varying mortality impacts in different geographic regions (Miller et al., 2009).

Structure of Influenza Virus

The Influenza A virus is a member of the Orthomyxoviridae family (Earn et al., 2002). Influenza A viruses are enveloped, spherical or filamentous structures, ranging from 80 to 120 nm in diameter (Noda et al.,2006).Its genome consists of eight single negative stranded RNA segments that encode ten viral proteins (Steinhauer & Skehel, 2002) with each of these varying from 890 to 2,341 nucleotides each (Noda et al.,2006). An influenza virion contains two main surface antigens, or subtypes: hemagglutinin (HA) and neuraminidase (NA) (Cox et al., 2004).

The HA antigen enables the virus to enter into cells, while the NA antigen facilitates cell-to-cell transmission. There are 16 known hemaglutinis and nine types of neuraminidases known but only three types of HA(H1,H2,H3) and two types of NA (N1,N2) have been widely prevalent in humans (Hsieh et al.,2006).

The subtypes of influenza A viruses are determined based on their antigenic surface glycoproteins- hemagglutinin and neuraminidase (Michael et al., 2009). Hemagglutinin binds to a2, 3-galactose- and a2, 6-galactose-linked sialic acids, with a2, 3-galactose sialic linkages present in avian species and a2, 6-galactose-linked sialic acids in humans. Both of these sites are present on the tracheal epithelium surface in pigs, making them vulnerable to both avian and human viruses (Brown et al., 2000).

The influenza virus contains 8 pieces of segmented RNA as can be seen in Figure 1 above. Segments 1, 3, 4, 5, and 6 individually encode a single protein corresponding to the polymerase basic 2 (PB2), polymerase acidic (PA), hemaglutinin (HA), nucleoprotein (NP), and neuraminidase (NA), respectively (Rogers and Paulson, 1983). Segments 2, 7, and 8, however, code for two proteins each. Segment 2 are coded for by PB1 and PB1-F2 and matrix (M1) and M2 by segment 7; and non-structural 1 (NS1) and NS2 by segment 8 (Zhou et al., 2006).

PB1-F2, takes on the role of apoptosis i.e cell death (Chen et al., 2001) and M1 and M2 are prominent targets for infection-induced antibodies. The M2 protein functions as an ion channel functioning in the initial and final stages of infection. The matrix protein (M1) is the protein layer underneath the lipid envelope. The nucleoprotein (NP) coats the RNA particles and the polymerase proteins (PB1, PB2, and PA) are used during replication of the virus (Portela & Digard, 2002).


Influenza A virus generates most new antigenic variants in two possible ways .The first and most common is by 'single nucleotide changes' in the genes encoding the antigenic sites of the Haemaglutinin (HA) and Neuraminidase (NA).Changes of this type are called antigenic drift (Downie., 2004). According to Khiabanian et al., 2009 'The evolution of the influenza virus is primarily shaped by the reassortment process.'

It is paramount for mutations to occur for RNA viruses to maintain diversity, this is usually made possible by its error prone nature when synthesising RNA (Racaniello, 2009). The genomic drift of influenza A virus proves to be a frequent event because of its high error rate and the antigenic pressure on the HA and NA segments. The influenza virus behaves differently to other viruses most likely due to its segmented genome and as a consequence of its interior structure it has effectively employed the reassortment mechanism which occurs between co-infecting viral strains, potentially causing an unpredictable evolutionary jump i.e. causing a genetic shift (Chen et al., 2006).

This process is illustrated in the figure 2 below, which shows a cell that has been co-infected with two influenza viruses named A1 and B2. 'The infected cell produces both parental viruses as well as a reassortant strain', R3. From this diagram we can see that the R3 virus has inherited one segment for parental virus uses A1 and seven segments from B2 strain.

Evolution of Influenza A viruses1918 H1N1

Taubenberger et al, 2006 recalls the 1918 virus in which approximately 500 million of the world's population were infected as the 'Mother of all Pandemics'. On a historical scale the influenza pandemic of 1918-1919 killed more people than in World War I (Billings, 2005).The legacy of the 1918 H1N1 virus has had a major impact on the 20th century history of viruses and as we will see, continued on to survive itself into the 21th century, it vindictively did this by shifting its internal genes into daughter strains expanding, I suppose you could call its primary life expectancy. This 'mother of all viruses' has been resurrecting herself for the past 90 years reassorting and causing 3 pandemics in recent global history.

Taubenberger & Morens, 2006 states that the impact of the pandemic of 1918 to 1919 did not effectively eradicate itself in these globally disastrous years.

He maintains all Influenza A pandemics since that time (excepting human infecting avian viruses such as H5N1 and H7N7) are derived from the evolutionary ancestors of the 1918 virus these would include the drifted H1N1 viruses and reassorted H2N2 and H3N2 viruses. Seroepidemiologic studies have linked that even in 1936- remnants of the 1918 virus were still in circulation (Shorpe, 1936).

The 1950s were a pivotal decade mainly due to the appearance of a new pandemic strain, H2N2 strain in 1957. Suddenly then twenty years later in 1977 human H1N1 viruses emerged ,it was effectively contained but have since continuously circulated epidemically (Kendel et al., 1978).

The Frequent Occurrence of Reassortment:

In a paper by Khiabanian et al,2009- reassortment of Influenza A viruses were crucially analysed by employing temporarily and geographically diverse information available from the 'Influenza Virus Resource of the National Centre for Biotechnology Information'. Reassortment pattern events were investigated by sequences available publicly.

Several tactical techniques were applied aiding to identify the differential variability of the segments in the genome and to count the number of independent reassortment events.

The following three experiments were taken from (Khiabanian et al., 2009)

Experiment 1

  • 150 strains were sequenced containing 99 H1N1, 25 H1N2, 23 H3N2 and 3 H3N1 strains.
  • For each segment the sequences of their coding regions were aligned using the Smith -Waterman algorithm and the Hamming distances at the third codon positions were calculated.
  • The segments have 'proportional substitution rates at the third codon positions; the 'differences between two segments of two strains should be proportional if the two segments have a common origin', this is seen from the experimental results. 'A violation of this rule indicates that the histories of the two segments are different i.e. there has been a reassortment event'. The distances between the two segments of different strains is plotted against each other ,the points corresponding to possible reassortment events lie off the diagonal(this has been indicated secondarily). 'It assumes that the lower the cumulative probability, the more likely it is that the two segments do not have a common ancestor, therefore, indicating reassortment'.

It was observed from this data that the cumulative probabilities were at least 10 -7 and a cumulative probability of at the most 10 -7 for two given segments of two strains indicates that a reassortment event occured.

Experiment 2

This figure (left) represents Raos quadratic equation entropy measured at the third codon positions for 150 swine influenza A viruses that have all the 8 fully sequenced segments deposited in the NCBI. The figure shows significant difference between NA, HA, and PB1 (these genes are circled in the following experiment) compared to PB2, PA, NP, M and NS.

Figure 3(right) shows the diversity in the swine classical H1N1 strains that were isolated in the 70s, 80s, and 90s.

In summary the eight segments do not have a common history with PB1, HA and NA, this presents a 'higher level' of diversity and that reassortment has occurred over these decades.

This table lists the Reassortant events represented by different strains H1N1, H1N2, H3N2 and H2N3.-A=Avian, H=human S= swine, genes circled indicate reassortment occurrences within these species.

Strains are taken from a vast demographic location ie, America, Europe and Asia. On examination it can be seen that the frequent incidence of NA, HA, and PB1 plays a crucial role in the reassortment process.

In summary as indicated in the experimental Data shown, that not every segment of the swine influenza virus reassorts in an equal format. It also forecasts from previous results compiled that the surface glycoproteins coding segments (HA and NA) of swine influenza virus 'reassort at a higher rate'. With the polymerase gene PB1 playing a particular role in inter host species (Khiabanian et al., 2009)

SOIV H1N1 2009

Early in March and April 2009, a 'novel H1N1 swine-origin influenza virus A(S-OIV A) 'surfaced in Mexico and the United States. It has been reported up until June 12, 2009 that the virus has spread to over 74 countries around the world with approximately 29,000 positive cases (Smith et al., 2009) ; (Chang et al .,2009) .As of September 28th 2009 approximately 5,000 deaths were documented worldwide (Manicassamy et al.,2010). On June 11, 2009, the World Health Organization declared an influenza pandemic, caused by novel S-OIV A (H1N1) (WHO- 2009). Where did this virus come from and how does its structure compare prevail as the fundamental questions?

In the circa years of the 1990s triple-Reassortant swine influenza A (H1) viruses containing genes from avian, human, and swine influenza viruses emerged and became established among pig herds in North America. Sporadic infection with triple-reassortant swine influenza A (H1) viruses was first documented in humans that had exposure to pigs from December 2005, patients that were immunocompromised and also fully healthy patients ultimately recovered but they did however display extreme influenza type symptoms (Shinde et al., 2009). This elucidates not only was this particular 'triple reassortant virus' unique in comparison but also proves that it is as high pathogenic potential and that it was not only evident zoonotically.

Shinde et al.,2009 states that between the 1930s and 1990s, the most commonly circulating swine influenza virus among pigs was the classic swine influenza A (H1N1) and that it 'underwent little change' during this time. However by the late 1990s evidence of multiple strains of subtypes (H1N1, H3N2, and H1N2) of triple reassortant swine influenza A H1 viruses were emerging and becoming rampant in North American pig herds. This is also reinstated by (Khiabanian et al., 2009) and by (Smith et al., 2009) that in 1998 two new swine H3N2 strains were identified. The results represented a double reassortment of swine classical H1N1 with a human H3N2 strain in which it reassorted with the PB1, HA, and NA from a H3N2 strain and secondly a triple reassortment of swine classical H1N1 was witnessed in which, the PB1, HA, and NA segments of a human H3N2 strain and the PB2 and PA segments from an avian lineage reassorted.

Manicassamy et al., 2010 demonstrates that the 2009 pandemic H1N1 virus found through serological analysis that there is a high prevalence of 2009 H1N1 cross reactive antibodies only in the older population, indicating that prior infection to the 1918 like viruses or vaccination against the 1976 swine H1N1 virus in the USA is likely to provide protection against the 2009 pandemic H1N1 virus. This is why our younger generation has suffered the most from the recent triple reassorted virus, because we were absent from previous outbreaks of this ilk of virus that had occurred in the last two centuries.

We can gather from this figure that the SOIV virus has made several leaps from birds to humans to pigs and back into humans again. This reconstruction concludes that the HA, NP, and NS plus the polymerase genes emerged from a triple reassortant virus circulating in North America swine (Smith et al., 2009) ; (Shiende et al,2009).We can see the polymerase genes, plus HA, NP and NS, emerged from a triple-reassortant virus circulating in North American swine. This triple-reassortant itself comprised of genes (PB2 and PA) derived from an avian origin, a human (PB1) H3N2 and classical swine (HA, NP and NS) lineages. In contrast, M and NA gene segments have their origin in the Eurasian avian-like swine H1N1 lineage.

It was also noted that seven out of the eight genetic segments found in a single isolate in 2004 (Sw/HK/915/04)H1N2 (location isolated HONGKONG) were also located in a sister lineage previous to the outbreak in 2009 reiterating that the 2009 H1N1 influenza virus was geographically widely distributed.

The evolutionary rate coming up to the S-OIV epidemic was 'entirely typical of swine influenza' .This data was further quantified by performing a' Bayesian molecular clock analysis' for each the genes PB2, PB1, PA, HA, NP, NA, M and NS. His results showed that the common ancestor of SOIV outbreak and the 'closest related swine viruses existed between 9.2 and 17.2 years ago', dependant on the genomic segments in question .Hence in average the ancestry lineages of the H1N1 virus have been circulating for the past decade. A contrary point was also made in that the currently circulating S-OIV shared a common ancestor as recently as January 2009 (no earlier than August 2008).

Another question raised is as to how is it being made possible that Reassortant viruses , are crossing over to humans from animals and consequently humans can inter infect in its own species then? In a study done by Yuki Furuse et al., 2009, 673 strains of Influenza were assessed based on their eight internal genes. Results indicated a very crucial discovery for efficient human to human transmission that retained segments introduced to new segments caused crucial and adaptive mutations leading to the H1N1/09 pandemic.


Pandemic influenza H2N2 viruses emerged in humans 'in 1957' causing a high rate of infection and mortality rates until 1968 .They were then displaced by emerging H3N2 viruses (Lindstrom et al., 2004).

In a paper by Scholtissek et al., 1978 he indicates that that the H2N2 subtype was derived from the H1N1 subtype by a recombination event retaining four H1N1 segments, while the other four segments were gained from another yet unknown strain. Lindstrom et al., 2004 compiled a genetic analysis of all the eight gene segments of human H3N2 viruses collected from 1957 until 1968 from widespread sample areas across different continents. Late H2N2 isolates were recognised in two distinct clades (1 & 2) and proved that H2N2 viruses emerged following reassortment between human H1N1 and avian H2N2 viruses.

The results were as follows the HA, NA, and PB1 genes originated from an Avian H2N2 virus and the remaining gene segments originated from a human H1N1 virus. For the next ten years H2N2 viruses circulated until they reassorted again with an avian H3 strain resulting in the emergence of H3N2 virus more widely known as the 'Hong-Kong Flu'. (Lindstrom et al., 2004)


Reassortant human influenza A (H1N2) virus was first reported in Japan in 1983, approximately six years later it was then detected in China. However this specific strain has since been undiscovered beyond China. In 2002; an H1N2 reassortant virus assigned A/Wisconsin /12/2001 was uncovered and isolated in December 2001.A surveillance study carried out between August 2001 and July 2002 reiterated that H1N2 was in wide circulation and from a sample of 890 A (H1) virus isolates a total of 51 H1N2 viruses were exuberant in 41 countries across four continents. It was found that these recent H1N2 viruses were reassortants containing H1 gene fragments similar to A/New Caledonia/20/99 -like H1N1 virus and the remainder seven gene fragments were found to be similar to A/Moscow/10/99-like H3N2 virus.

To provide a comprehensive view of the evolution and circulation of H1N2 reassortants, Chen et al .,2006 carried out one of the largest characterisations of A/H1N2 reassortant viruses ever to be compiled in a single study. The data period was beginning of 2001 to mid 2003 after its emergence in 2000.It was conducted in 20 countries including China/Hong Kong, India, Malaysia ,Japan, Philippines, Thailand, Singapore, Taiwan, Israel, Italy, Germany, Netherlands ,Scotland, Ireland, England, Poland, Brazil, Argentina, South Africa and Spain. Phylogenetic analysis of the 65 H1N2 viruses identified in conjunction with 56 already available in the Influenza Sequence Database was performed.

The results showed a temporal sequence of a phenotypic range of small number of closely related of H1N2 viruses in 2001-2003 and support the theory that they originated from a single reassortment event which occurred in Asia and spread to Europe, Middle East, Africa and America.


H3N2 subtypes influenza appeared in humans 'in 1968' and caused n immense pandemic and is one of the main subtypes of influenza which circulates in humans and swine populations throughout the world today. H3N2 viruses contained the HA and PB1 genes of the H3 avian virus and the other six gene segments of previously circulating human H2N2 viruses. In 1968, the H3N2 viruses replaced H2N2 viruses, in the human population and caused the 'Hong Kong'' Pandemic. In a phylogenic study of the genetic characterization of the entire genome of H2N2 & H3N2 it was found that analysis of late H2N2 and early H3N2 viruses proved that H2N2 was an ancestral virus of the H3N2 virus and this was indicative to the H3N2 virus evolved nature due to reassortment occurrences(Lindstrom et al.,2004).

According to Scholtissek et al.,1978 The H3N2 subtype is derived from a H2N2 subtype and contains seven segments of the H2N2 subtype while the gene coding for the HA is obtained from a Ukrainian duck.

Since 1998 the H3N2 disease has had substantial implications in pigs throughout swine production regions in the U.S. In 2008 a study was carried out by Lei Sun and his associates to find 1 the genetic correlations and 2. The stature of influenza virus during tantamount seasons .Samples were collected in 2005; 450 nasal swabs and lung tissue samples were collected from off larger pig farms, and 90 nasopharyngeal swab specimens were collected from patients who displayed influenza like symptoms where the patients had no clear contact to pigs. Over all, 'reassortment is identified phlogenetically, when segments of a viral genome have inconsistent associations with distinct clades of virusus in segment -specific phlogenies'.

It was seen through a phylogenetic construction of the gene segments that the five H3N2 human influenza viruses that were isolated in conjunction with the 2000s human isolates formed a cluster, and that the majority of the H3N2 swine isolates along with the 1990s human isolated formed another cluster except the M and NS gene of A/swine /Guangdong /01/2005 and PA gene of A/Swine /Guangdong/02/2005 fell into the cluster of classic swine influenza virus which were circulating in the 1990s this gives a clear indication that reassortment between H3N2 human and H1N1 swine influenza viruses were in existence and proved that reassortment was ' common in recent years'. It also proved a contrariety in that H3N2 swine influenza viruses in 2005 did not originate in the 2000's but in the 1990s decade (Sun et al., 2008).

Up until the 1990s it was thought that swine influenza in North America was exclusively caused by H1N1 viruses. A study that was implemented between March 1998 and March 1999 to contradict this theory .Four H2N2 virus were isolated from pigs in Midwestern USA along with one from Canada in 1997 and from a pig in Colorado in 1977. The full length protein coding regions of all eight RNA segments were sequenced. The results were unprecedented. Phylogenetic analysis revealed that 1977 Colorado isolates and 1997 isolates were wholly human influenza viruses. However since 1998 triple reassortment occurrence was confirmed in pigs .The isolates taken from Mid western pigs in 1998 revealed that it contained the hemaglutinin, neuraminidase and PB1 polymerase genes from human influenza viruses ,the matrix, non-structural and nucleoprotein genes from classical swine viruses and the PA and PB2 polymerase genes from avian viruses (Karasin et al.,2000).

This figure shows a comparison between antigenic and genetic evolution of Influenza H3N2 virus .In (A) a phylogenetic ML (maximum likely hood)tree displays the H1 nucleotide sequences and are colour coded to correlate between the antigenic clusters B and C.(B)Genetic map of the H1 amino acid sequences colour coded according to the clusters in figure ( ) The spacing between grid lines corresponds to 2.5 amino acid substitutions.(C)-The same antigenic map as figure 1 except a rigid body rotation and the virus strains are colour circles and anti sera represent open squares with the arrows indicating the two cluster transitions for which the amino acid substitution N145 K is the only cluster difference substitution.

Between the different types of data seen here there is a consistent similarity between the specific positions of clusters in both the genetic A and antigenic maps B and C. The correlation between the ML phylogenetic tree distance and the antigenic distance between strains is averagely 0.78, and an ML distance of 0.0085 corresponds to a 1-unit chance in antigenic distance.

This in essence concludes that though the clusters are adjacent to each other and consequently the rate of antigenic evolution is at a continuous rate however it is vital not to rely wholly on this genetic data alone because from the tree alone it is difficult to distinguish the branch and lineages to a similar or contrasting antigenic cluster and in the genetic map it is enigmatic on where the cluster ends or begins. This is elucidated by looking at the distance between Sichuan1987 (SI87) and Beijing 1989(BE89) which are genetically closely related based on the tree but antigenic ally different. However Smith et al., 2004 also notes that a single substitution between SI87 and BE89 and between BE92 and WU95 this is suprising because on average a 'single amino acid substituion causes only 0.37 units of antigenic change' hence this N145 K caused a remarkable antigenic affect in cluster transition. The severity of the 1968 pandemic was dampened by widespread immunity to its neuraminidase protein ,which it shared with H2N2 (Reid et al.,2001).


In 1997 H5N1 'bird-flu' emerged in Hong Kong killing six people out of the eighteen in total infected (Guan et al.,2001).That is a 50% fatality rate which is extremely high. This virus is a result of an avian virus that could transmit directly to humans (Steinhauer & Skehel, 2002); because of its pathogenicity avian virus was classified as a rudimentary pandemic and was executed with the mass slaughter of all poultry across Hong Kong Sar. The virus is thought to have arisen from a reassortment from a number of inaugural avian viruses and a virus related to Goose/Guangdong/1/96(H5N1)(Gs/Gd/96)was the likely donor of the H5 hemaglutinin isolated a year before. Prior to the human outbreak, the H5N1 virus was found to cause extensive death in chickens in three farms in 'Hong Kong'. The signi?cance of this outbreak raised worldwide concern on the possibilities that such an in?uenza virus may become the next in?uenza pandemic strain. (Tam, 2002).

The 1918 pandemic H1N1 influenza virus and the H5N1 avian influenza virus are different among influenza A virus isolates in their high virulence for humans and their lethal impact for a variety of animal species without prior adaptation. Reverse genetic studies have implicated several viral genes as virulence determinants these being PB-1 and NS1. For both the 1918 and H5N1 viruses, the hemagglutinin and the polymerase complex contribute to high virulence. (Baslar & Aguilar, 2008). In an interview with Yi -Guan a leading virologist in Hong Kong university

He claims that if H1N1 and H5N1 reassorted we could witness an 'Armageddon virus' but also reiterates that the chance is 'very low that these two viruses will mix together' but the possibility of this happening could not be ruled out. H5N1 exists in more than 60 countries and is panzootic in animals this is the equivalent of pandemic in humans. (Guan, 2009).H5N1 was predicted to be the next pandemic threat (Vana & Westover., 2008) .What happens if a similar outbreak to 1997 occurs again and the containment procedure doesn't render as successfully? According to Tumpey et al., 2007 an MX1 gene existing in wild type mice gives an advantageous immunity over standard laboratory mice and shows that it is highly resistant to the 1918 virus and a H5N1 viral strain from Vietnam. In essence this could be a lifeline and an area to be focused on if these panzootics as Yi- Guan speak of persists. It is that genes are playing key roles in how infectious a disease can be and even with a slight mutation or reassortment the whole dogma of one virus can turn into a whole new pathogenic virus. It has always been known that mice can be altered to mimic the human immune system a term formally known as knockout mice in which c certain genes can be turned on or off etc. In summary according to Fornek et al., 2009 ;A ''substitution of glutamic acid for lysine at position 627 of the PB2 protein of H5N1 has been determined as a factor leading to increased virulence within its host.'' Mice infected with H5N1 viruses containing lysine at amino acid 627 in the PB2 protein exhibited an increased severity of lesions in the lung parenchyma and the spleen, increased apoptosis in the lungs, and a decrease in oxygen saturation'.

These are all severe symptoms which inevitably lead to fatality. So any pinpoint mutation whether it is a single change or accumulation change can wreak havoc on the development of Influenza viruses. As I see ,if there is increasing proliferation of certain influenza incidences in animals then this is where we need to up the surveillance system of these strains before giving them a chance to adapt on cross the species barrier into humans.

Reassortment Restrictions

It is already known that attachment of all influenza A virus strains to cells requires sialic acids.With avian influenza strains preferably binding to sialic acids attached to a galactose via an alpha (2,3) linkage ,whilst humans require a sialic acid bonded to galactose by an alpha (2,6) linkage and lastly the pig species which produces both alpha(2,3) and alpha (2,6) linked sialic acids on its epithelial tract(Racaniello,2009).It is normally conceived that the 'factors controlling reassortment are not exactly known'(Downie ,2004)however according to( Downie et al.,2003) evidence has suggested that the PB1 gene may be essential for gene reassortment in influenza viruses. In mixed infection experiments pertaining A/USSR/90/77, A/Shearwater/37/72 and a human H3N2 virus strain, an H6N1 reassortant was isolated. RNA-RNA hybridisation and gene sequence analysis showed that the only gene segment transferred from the H3N2 parent to the H6N A Reassortant was the H3 PB1 polymerase segment.


It is quite apparent that reassortment occurs often in nature ,this is evidentially noted through the vast amount of reassortant viruses isolated across the globe.What remains the more vital criterion is how often it happens and does this consequently precipitate a dangerous effect on human populations. Yes and No.Reassortment remains consistent in nature and fortunately it rarely causes a pandemic, with just three emerging in the last two centuries from a direct result of reassortment of genes.

Luckily there are improving ways of dealing with pandemics through anti sera studies and regular vaccination programs which helps eleviate the threats of Influenza viruses.

In the recent outbreak of Swine flu which caused a recent pandemic last year, we can see this was a result of unusual reassortant viruses, the severity of this virus really hung in the balance as to how severe it was going to redeem itself on human populations. It is not known why cases in Mexico and those in other regions are respectively milder in contrast these could be due to discrepancies' in varying human immunities. The main issue here is that this virus has picked up a few tricks along the way maybe not so much dangerous as forecasted but all it takes is for another unusual shift to take place between two what may seem exemplary influenza strains to become the Worlds next deadly killer.

It is necessary to note that reassortment occurs frequently yes in nature but also has constriction factors as discussed with one of the gene segments PB1 and with specific glycosidic linkaging between hosts therefore luckily it does have its boundaries unlike some more extreme viruses like SARS, Ebola, hepatitis etc.

In summary we can see that there has been an increasing amount of Reassortant viruses coming into circulation especially within the last few decades with the surface glycoprotein's reassorting most often .Also reassortment isn't limited to one area as seen through the vast reassortant virus strains isolated, though southern China is postulated as the epicentre of Influenza epidemics mainly due to its agricultural based community and high population density giving influenza viruses perfect opportunity to proliferate and reassort.

As we seen in Smith et al., 2009 and other profiles of reassortant strains there seems to be an implosion of Reassortant viruses in the last few decades. Why is this? We can make a pretty clear assumption that the human population today differs from previous generations.

For most of our history, we lived in geographically disparate populations. So viruses could enter from animals into humans, spread locally and go extinct'. Human populations vastly connected either' spatially and/or temporally' in a way that's 'unprecedented in the history of vertebrate biology' (Wolf, 2009). This in turn provides new ways for viruses and this case Influenza A have to spread amongst new and immunologically naive host populations leading to greater reassortment events and adaptability. In summary we can conclude that not only is reassortment widely observed it is also happening at a consistently higher rate than previously observed and the only way to control this is frequent genetic surveillance.

Article name: The evolutionary history of Influenza A essay, research paper, dissertation