Influenza A Virus
Influenza A Virus
|Disease(s) Caused||Mild to severe respiratory illness|
|Symptoms||Fever, headache, cough, stuffy/runny nose, sore throat, muscle aches, exhaustion|
|Potential Complications||Bronchitis, sinus/ear infections, pneumonia|
|Transmission Mode||Largely airborne via respiratory droplets produced by coughing and sneezing, potential for indirect transmission by fomites|
|Natural Reservoirs||Birds, humans, swine|
|Well-Known Outbreak Strains||Spanish Flu (H1N1), 1918|
Asian Flu (H2N2), 1957
Hong Kong Flu (H3N2), 1968
Bird Flu (H5N1), 2004
Swine Flu (H1N1), 2009
Importance of Influenza A Virus
Influenza A is a significant viral pathogen that has caused several recurrent epidemics marked by severe respiratory illness in the human population. Despite the advent of more stringent public health measures over the past century (examples: ongoing influenza vaccine development and educational hand-washing campaigns), infection from influenza A virus continues to result in substantial morbidity (sickness) and mortality (death), particularly among the most vulnerable populations (young children, the elderly, and immuno-comprimised individuals).
Structure and Function of Influenza A Virus
Influenza A virus is “enveloped”, meaning that a lipid-containing covering (envelope) surrounds the viral nucleocapsid. The lipids in the envelope of Influenza A are derived from the cellular (plasma) membrane of the host cell as new virions undergo the process of budding towards the end of replication and are subsequently released into the extracellular environment.
Influenza viruses are characterized by two surface glycoproteins - hemagglutinin (HA) and neuraminidase (NA). To date, sixteen subtypes of hemagglutinin are known (H1 to H16), while 9 unique NA subtypes have been identified (N1 to N9). HA is vital for the ability of influenza A to infect host cells. Following the “priming” of HA via conformational changes (induced by acidic pH) and proteolytic cleaving (proteases provided by the host), hemagglutinin promotes fusion of the viral membrane with the target host cell membrane by way of the sialic acid receptor for initiation of infection.
The importance of NA arises during and upon release of newly packaged virions from the host cell. NA cleaves the sialic acid residues present on the surfaces of the new virions as well as those present on the host cell. This prevents aggregation of the virions, as well as attachment of the newly packaged virions to the surface of the already infected host cell as they are released. Neuraminidase is the target of several widely-prescribed anti-influenza remedies including oseltamavir, also popularly known as Tamiflu.
The Epidemic Threat of Influenza
The subtype designations of these surface antigens have served as the calling cards for the epidemic outbreak strains of influenza over the past century. The most recognized of these designations is H1N1, most recently implicated in the “Swine Flu” epidemic of 2009. Another H1N1 variant caused the “Spanish Flu” pandemic of 1918 that saw exceedingly high death rates in young adults (ages 15 – 34) relative to previous outbreaks, and even resulted in a drastic drop in overall life expectancy for the U.S. population. Additional outbreak strains include H2N2 (Asian Flu, 1957) and H3N2 (Hong Kong Flu, 1968).
Of increasing importance are the avian strains (H5N1 and H7N1) that are primarily implicated in flu outbreaks in bird populations. These strains have managed to jump species due primarily to centuries-old animal husbandry which place humans in close, consistent proximity with a variety of domesticated fowl (ducks, for example) and swine, both of which are natural reservoirs of the virus with the latter being pinpointed as a “mixing vessel” for various strains of influenza virus to undergo genetic recombination to new strains. Humans infected with the avian strains are faced with high levels of mortality (50%). However, human-to-human transmission has yet to be reported.
The Importance of Disinfection: Survival of Influenza A on Surfaces and Transmission Potential via Fomites
Although Influenza A virus is spread primarily from person-to-person by way of contaminated aerosols, transmission potential via fomites (porous and non-porous surfaces and/or objects) has increasingly become of concern. This is largely due to the fact that viruses, which are obligate intracellular parasites, maintain infectivity when deposited onto inanimate surfaces over various periods of time. For influenza, this can occur when contaminated aerosols settle onto objects that may later come into contact with the hands (or perhaps mucous membranes of non-infected individuals). Alternately, contaminated bodily secretions (for example, expelled mucous) on the hands of an infected individual can allow influenza A to find its way to dozens of objects including (but not limited to) door knobs, remote controls, telephone receivers, and the hands/body parts of other individuals.
The factors influencing virus survival on surfaces are varied and many and include intrinsic virus properties, such as structure (enveloped vs. non-enveloped) and strain, characteristics of the surrounding environment (for example, humidity), and fomite traits, such as cleanliness. Studies have documented the ability of influenza viruses to remain infectious on objects from several hours to days in a variety of environments including day care centers and nursing homes.
Although data directly implicating fomites as the causative source of illness from viruses such as influenza is lean, their ability to maintain viability over the course of time (albeit waning) indicates the necessity of maintaining clean, hygienic conditions by use of disinfecting agents and/or pre-treated surfaces capable of inactivating pathogenic viruses, particularly in high-risk settings with the potential for amplified transmission rates (for example: schools, hospitals, and nursing homes).
Selected Pertinent Literature
Ansaldi, F. et al. 2004. SARS-CoV, influenza A and syncytial respiratory virus resistance against common disinfectants and ultraviolet radiation. Journal of Preventative Medicine and Hygiene. 45: 5-8.
Noyce, J.O., H. Michels, and C.W. Keevil. 2007. Inactivation of influenza A virus on copper versus stainless steel surfaces. Applied and Environmental Microbiology. 73(8): 2748-2750.
Rice, E.W. et al. 2007. Chlorine inactivation of highly pathogenic avian influenza virus (H5N1). Emerging Infectious Diseases. 13(10): 1568-1570.
Boone, S.A. and C.P. Gerba. 2007. Significanace of fomites in the spread of respiratory and enteric viral disease. Applied and Environmental Microbiology. 73(6): 1687-1696.
Sattar, S.A., and V.S. Springthorpe. “Chapter 8: Transmission of viral infections through animate and inanimate surfaces and infection control though chemical disinfection”, from Modeling Disease Transmission and Its Prevention by Disinfection, C.J. Hurst. Cambridge University Press, Cambridge, England. 1996.
Strauss, J.H. and E.G. Strauss. Viruses and Human Disease. Elsevier Academic Press, Burlington, MA. 2008.
Weber, T.P. and N.I. Stilianakis. 2008. Inactivation of influenza A viruses in the environment and modes of transmission: a critical review. Journal of Infection. 57: 361-373.