H1N1
Introduction
Starting in April, 2009, a wide-spread epidemic infected the world’s population and perhaps even more so, infected the media. H1N1 Influenza A virus, or better known as swine flu, made nearly 22,000 people ill and killed 125 of them by August, 2009. In all, by that time, the virus had spread through 69 countries and/or regions of the world (starting in Mexico). This specific strain of influenza is particularly concerning due to its uncommon ability to be passed from human to human (unlike most swine and avian A influenzas). While examining the mechanisms and characterization of the virus is important, incorporating these findings with the evolutionary capabilities and mutability of H1N1 novel influenza A represent an optimal way of examining the virus and potentially using this information to develop a cure for infected hosts.
Characterization of Influenza Viruses
General
Influenza A viruses, the type that are capable of human infection, are characterized by two proteins. More specifically, the glycoproteins hemagglutinin and neuraminidase are numbered based on their identified character and are the two methods of categorization. Hemagglutinin is labeled “H” and numbered 1-16 (H16 was discovered very recently) and can be differentiated by amino acid composition. Its viral function is to aid in host cell binding. Specifically, it links to sialic acid located on the surface of the targeted host cell. This greatly contributes to infection capability. The other element used for subtype categorization for influenza A is the neuraminidase glycoprotein. Its role in infection is similar to that of hemagglutinin, but neuraminidase cleaves the poly-sialic surface acids in order to allow for the exiting of viral “offspring.” Neuraminidase has nine different amino acid sequences and is thus labeled N1-N9. While there clearly are many combinations of the two glycoproteins that cooperate to infect a host cell, only three influenza A subtypes have been commonly found to successfully infect and transmit from human cell to human cell. This narrowing of possibilities has been crucial in fighting the biological war to control, vaccinate, and potentially someday cure the debillitating, and even sometimes fatal, virus in humans.
Hemagglutinin and Neuraminidase
A study by Al Farress et al. (2005) takes a look at the evolutionary aspect of these two glycoproteins. The study predicted that over time, based on the phylogeny of the hemagglutinin glycoprotein’s genetic origins that characterizes the type of influenza, there would be the possibility of so great a divergence between the antigenic characteristics of H1N1 and H1N2 influenza A subtypes that they could require significant changes to the vaccinations and treatments of the two strands of influenza. The implications of this conclusion and prediction by Al Faress et al.(2005) may already be felt in the form of novel H1N1 influenza A’s pandemic infection. This immediately brings to the forefront the necessity of the comprehension of the capabilities of such virus evolution and the possibilities of vaccination adaptation and thus resistance that they carry in order to prevent similar cases of influenza epidemic. Samples of genetic regions that code for the hemagglutinin (HA 1 sequences-obtained from AH-1 strains) from three different time periods were isolated from humans experiencing influenza-like symptoms in the winters of 2001-2002, 2002-2003, and 2003-2004 in southern France. The genetic sequences were amplified by PCR. A bootstrap analysis was replicated 1000 times to perform a phylogenetic analysis. Likelihood of genetic distances was then calculated to verify the results.
Section 2
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Section 3
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Conclusion
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References
[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.