Photomicrograph of Haemophilus influenzae as seen using a Gram stain technique. During the flu outbreak of 1918 H. influenzae was termed Pfeiffer's Bacillus, where it was found in the sputum of many influenza patients, and thought to be the cause of influenza.
The influenza virus, a member of the family Orthomyxoviridae (Greek myxa, means "mucus"),1 is one of the world’s most important and dangerous respiratory pathogens. Each year, it causes illness and death in millions of people globally.
The genetic information of influenza virus is encoded as single stranded RNA. Like all viruses, influenza must invade a host cell and hijack its machinery to manufacture more viruses.
There are three types of influenza virus—A, B and C—which are distinguished by differences in two of their internal proteins (nucleoprotein and matrix protein), differences in their pathogenicity (degree to which they cause disease), and differences in their organization of genetic information (influenza virus types A and B have eight RNA segments; type C has seven). Type A influenza, the most common form, is found in a wide variety of birds and mammals. The other two types, B and C, are found primarily in humans. Type C infection produces only mild respiratory symptoms and has not caused significant disease. Influenza A and B viruses are the two types that lead to flu in humans.1,2
Influenza A viruses are further divided into subtypes, based on characteristics of their surface proteins, hemagglutinin (H) and neuraminidase (N). Both of these proteins are present as spikes on the outer surface of the virus. Hemagglutinin has a role in attachment of the virus to cells in the respiratory system. Neuraminidase is involved in the release of new virus particles from host cells. To date, 15 subtypes of H (H1 through H15) influenza A viruses, along with nine subtypes of N (N1 through N9) influenza A viruses, have been found. Most of these subtypes only have been detected in birds.1
Each of the H and N subtypes reacts differently with antibodies produced by the immune system. In addition, since the H and N subtypes exist on different RNA segments, a host infected with different viral genotypes can produce new viruses with reassorted, and potentially unique, genotypes. Currently, subtypes H1N1 and H3N2 are responsible for outbreaks of human flu.3
The host immune system identifies and remembers invading influenza viruses primarily based on characteristics of their surface proteins, hemagglutinin and neuraminidase. Foreign molecules, such as these proteins, that stimulate an immune response, are called antigens. Slight changes in these antigenic proteins allow the virus to escape detection by the immune system.
The influenza virus continuously changes to evade its host's acquired immunity. It does so via two main mechanisms: antigenic drift and antigenic shift.5 Antigenic drift is defined as the random accumulation of mutations in all the virus genes, including those that code for the surface proteins. Many of these of mutations occur as a random change in a single nucleotide. These changes, called point mutations, are common in RNA viruses, such as influenza. Point mutations that involve coding for the surface proteins H and N can change the proteins enough that they no longer are recognized by the immune system. Therefore, influenza vaccines must be reformulated continuously to keep pace with the constant mutations of the flu virus.
Unlike antigenic drift, antigenic shift occurs at unpredictable intervals, when an existing influenza virus disappears and is replaced by a new subtype with new surface proteins.1 Antigenic shift happens as a result of mixing of the genome pieces from several different viruses that infected the same host cell. Antibodies made by the host immune system in response to the previous subtypes will not recognize the new subtype. Antigenic shift was responsible for the emergence of the "Hong Kong" flu in 1968, which was caused by subtype H3N2. This subtype arose from reassortment of the human H2N2 subtype with genes from viruses with the H3 subtype that primarily infected birds.3
In 2009, a new flu virus began infecting people around the world. Originally called "swine flu," because it is similar to a strain that infects pigs, the virus now is referred to as "novel H1N1." Scientists have discovered that novel H1N1 is a descendent not only of swine viruses, but also of the virus that caused the 1918 flu pandemic.
Influenza epidemics typically occur from November through April. Most annual epidemics are relatively mild. However, occasionally deadly worldwide epidemics arise.4 These outbreaks are called pandemics, because they occur over very wide geographic areas and affect an exceptionally high proportion of the population. Flu causes 36,000 approximately deaths annually in the United States and leads to the hospitalization of almost 200,000 persons each year.
According to the U.S. Department of Health and Human Services, "The single best way to prevent the flu is to get vaccinated each fall, but good health habits and antiviral medications are other measures that can help protect against the flu." Ongoing genetic changes in influenza viruses must be reflected in the composition of the influenza vaccine for each year. The World Health Organization's (WHO) Global Influenza Surveillance Network, a partnership of 112 National Influenza Centers in 83 countries, continually monitors viral strains found circulating in humans. Each year, WHO recommends a vaccine recipe that targets the three most active virulent strains worldwide.6 In 2009, two vaccines will be available: one for seasonal flu and a separate vaccine for novel H1N1.
Health officials in the U.S. and elsewhere are trying to address the limited availability of flu shots this year. There are not as many inoculations available as usual because one of major worldwide suppliers has been shut down. Since vaccination is the most effective way to prevent influenza outbreaks and the severe complications associated with the disease, health care providers are naturally concerned by this shortage. However there are many other healthy habits that can be used as preventative measures.
The first defense is an understanding of how the flu virus is transmitted. Most often, flu spreads through the respiratory droplets of coughs and sneezes of infected people. A person can become infected by direct contact with the infected person (getting sneezed or coughed on), or by touching surfaces on which the droplets have come to rest. It is thought that some viruses and bacteria can live two hours or longer on desks, doorknobs, and even cafeteria tables, so most surfaces are potential danger zones. This is why people are urged to wash their hands frequently. To protect themselves from infection, students should be encouraged to practice the following healthy habits.
- Avoid close contact with infected individuals.
- Stay home when you are sick to prevent the spread of disease.
- Cover your mouth and nose with a tissue when sneezing and coughing to prevent the spread of infectious droplets.
- Wash your hands often.
- Avoid touching your mouth, nose and eyes as much as possible.7
- New Insights into Novel H1N1, National Institutes of Health
- Interactive Tutorial on H1N1, Medline Plus
- Cox, RJ, Brokstad, KA, Ogra P. (2004). Influenza Virus: Immunity and Vaccination Strategies. Comparison of the Immune Response to Inactivated and Live, Attenuated Influenza Vaccines. Scandinavian Journal of Immunology, 59,1-15.
- Centers for Disease Control and Prevention. (2004). Morbidity and Mortality Report, 53(RR06). Accessed 10/07/04 from http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5306a1.htm
- Frank SA. (2002). Immunology and Evolution of Infectious Disease. Princeton, NJ: Princeton University Press.
- Thompson WW, Shay DK, Weintruab E, et al. (2003). Mortality Associated with Influenza and Respiratory Syncytial Virus in the United States . JAMA, 289, 179-186.
- Centers for Disease Control and Prevention. (2005). Preventing the flu. Retrieved 10-27-2005 from http://www.cdc.gov/flu/protect/preventing.htm
- World Health Organization. 2003. Influenza. Retrieved 10-27-2005 from http://www.who.int/mediacentre/factsheets/fs211/en/