Hoornweg, T.E. (2009) Novel Influenza A (H1N1): the twenty-first century influenza pandemic. Bachelor's Thesis, Biology.
|
Text
LST_BMW_2009_T.E._Hoornweg.pdf - Published Version Download (632kB) | Preview |
Abstract
On June 11, 2009 the World Health Organization has for the first time in over 40 years raised its alert status to phase 6 of the worldwide pandemic alert scale and officially declared Novel Influenza A (H1N1) pandemic. To date (09-07-09) a total of 94512 cases leading to 429 deaths (CFR=0.45%) have been reported all around the world. Influenza A, a virus belonging to the family of Orthomyxoviridae, is best known for the annual influenza epidemics, usually causing a self-limiting disease characterized by the abrupt onset of fever and chills, accompanied by headache, diffuse myalgia, rhinorrhea, sore throat and cough. However, excess deaths may occur in people with decreased immunity, leading to 0.5 million estimated deaths per year. For an influenza to become pandemic a process called ‘antigenic shift’ should occur, introducing a new surface haemagglutinin (HA) to which there is no pre-existing herd immunity into the human population. Also a sustained human-to-human transmissibility is required. Transmissibility is reflected by the viral ability to efficiently replicate in the human host and to replicate in the upper respiratory tract to enable viral transmission via the airways. For this purpose, the HA of new influenza strains must be able to recognize α2,6-linked sialic acid, which is widely expressed in the upper human respiratory tract. Factors associated with a high virulence and pathogenicity were indentified in two very pathogenic human influenza strains, namely the 1918 ‘Spanish influenza’ pandemic and H5N1 avian influenza. In both 1918 H1N1 and avian H5N1, virulence appeared to be associated with HA, the viral polymerases and the NS1 gene, as well as with a deregulated host immune response. Furthermore, all 20th century pandemics acquired an avian PB1 segment encoding a working PB1-F2 gene. Compared to 1918 H1N1 and avian H5N1, Novel Influenza A (H1N1) does not seem to possess a lot of pathogenicity factors, as it has a truncated PB1-F2, no pathogenicity-related PB2-627 Lysine and low-pathogenicity amino acids at all known pathogenicity-related positions of the NS1 segment, arguing in favor of a mildly virulent influenza strain. However, the virus does possess completely new surface proteins, of which haemagglutinin and neuramidase differ 27.2% and 18.2%, respectively, from the 2008 human H1N1 and to which no pre-existing immunity is expected. The basic reproduction rate, a measure of transmissibility, of Novel Influenza A (H1N1) is estimated between 1.4-1.6, numbers comparable to the lower estimates of previous pandemics. Therefore, it can be concluded that Novel Influenza A (H1N1) can substantially transmit from human-to-human. How Novel Influenza A (H1N1) will evolve in the coming months, cannot be predicted. The virus has already spread to pandemic proportions and has a case fatality rate (CFR) of 0.45%, which is higher than the 1957 and 1968 pandemics. Given the great increase of the human population in the last 50 years, this pandemic may have the potential to take a lot of lives, especially if it further adapts to the new human host. Therefore, sane use of antivirals and the relatively scarce amount of vaccine as well as common sense preventive measures are crucial to confine this pandemic and may save many excess deaths.
| Item Type: | Thesis (Bachelor's Thesis) |
|---|---|
| Degree programme: | Biology |
| Thesis type: | Bachelor's Thesis |
| Language: | English |
| Date Deposited: | 15 Feb 2018 07:28 |
| Last Modified: | 15 Feb 2018 07:28 |
| URI: | https://fse.studenttheses.ub.rug.nl/id/eprint/8553 |
Actions (login required)
 |
View Item |