Physiology-eight single-stranded RNA segments. Glycoproteins: Hemagglutinin (H) and Neuraminidase (N)
-at least 15 different H, 9 different N subtypes
PathogenesisDevelopment of disease-Circulates in pigs/horses/birds and changes genetically
-changes by trading genetic material with other strains of influenza
-eventually one strain is able infect humans from animal
-influenza may or may not be transmissible from human-to-human now
-virus transferred through coughing, breathing, sneezing
-influenza enters host through respiratory tract
-H allows binding of virus at binding site, to get into cell, N cleaves receptor sites of acid residue
-virus is endocytosed into cell, where it uncoats and releases H+ ions to increase acidity of cell interior
-Influenza RNA is released into nucleus, and is then reproduced through transcription and translation
-virus exits through exocytosis and goes on to infect more cells
-causes inflammation of alveoli, spreading virus throughout the lungs, which allows the virus to be breathed out to infect others
Symptoms and Diagnosis-cough, fever, muscle aches, sore throat, nausea, vomiting, pneumonia
Consequences or complications-Death! Yay! Usually in the elderly!
Treatment-Vaccines:
-One blocks formation of ion channel that uncoat viruses, which would expose their interior to cells
-One acts as inhibitor to N enzyme
Summary!H1N1 Influenza A remains in animal hosts, swapping genetic information with other influenza strains. One may then eventually be able to infect humans from animals, but that does not necessarily mean that humans can infect other humans. The virus enters through the respiratory tract, and infects a cell by entering through the use of hemagglutinin. It then releases its RNA into the cell, where it will be reproduced. Eventually this causes inflammation of the alveoli, spreading the virus throughout the lungs. It can then be breathed out to infect others. Symptoms depend on the immune system of the infected person, but can range from simple coughing and sneezing, to fever and muscle aches, and pneumonia. In the elderly, or those with a weak immune system, this could lead to death if not treated. There are two forms of vaccines to treat influenza: one which inhibits the formation of an ion channel which uncoats the virus, which allows it to release its RNA. The other inhibits neuraminidase, meaning the virus cannot cleave required receptor sites to attach itself to.
Figure 1 Life expectancy from 1900 to 2001, showing impact of 1918 influenza pandemic.
Figure 2 Replication cycle of influenza A virus.
References:Behrens Georg, Stoll Matthias. [date unknown]. Pathogenesis and Immunology [Internet]. Influenza Report; [retrieved 2009 Oct 12]. Available from:
http://www.influenzareport.com/ir/pathogen.htmGarcía-Sastre Adolfo, Whitley Richard J. 2006. Lessons Learned from Reconstructing the 1918 Influenza Pandemic [online database]. Journal of Infectious Diseases 194, S127-S132. [retrieved 2009 Oct 11]. Available from: Academic Search Premier, EBSCOhost.
Palese, Peter. 2004. Influenza: old and new threats [online database]. Nature Medicine 10, S82-S87. [retrieved 2009 Oct 11]. Available from: Academic Search Premier, EBSCOhost.
