Not an autumn comes without that unwelcome guest, influenza. Most years, the seasonal flu epidemic ramps up around Thanksgiving, lays waste to many New Year's Eve plans and dies down after Valentine's day, only to reemerge the following fall. More than an inconvenience, influenza epidemics typically kill thousands or tens of thousands of U.S. residents each year, according to estimates from the Centers for Disease Control and Prevention. Scientists have studied influenza for nearly 100 years and now have insight into the pathogens responsible for this complex, contagious disease.
1. A Risk for Everyone
Influenza is a viral illness characterized by the sudden onset of fever, aches and respiratory symptoms. Anyone can get influenza; according to the National Institutes of Health, 5 percent to 20 percent of Americans do so annually. Children 5 and younger, adults over 65 and those with chronic medical problems are most likely to develop complications, require hospitalization or die from influenza. The viruses that cause influenza change constantly, making it impossible for people to develop permanent immunity. Catching influenza or getting a flu vaccination one year doesn't offer protection for future years. Each fall, flu infections rise and by spring return to the baseline in a classic epidemic pattern.
2. Disease by Invasion
The influenza virus is a tiny package of genetic material. Unable to reproduce on its own, it invades human cells and turns them into reproductive machines that stay busy churning out more viruses. The newly created viruses spread by leapfrogging from person to person through uncovered coughs and sneezes.
3. A Shifter and a Drifter
As it circulates, an influenza virus is constantly altering its surface antigens, or proteins. These antigens are the exact characteristics used by our immune systems to recognize and fight infection. Minor alterations in surface antigens are known as “drifts.” They allow epidemics, as many people's immune systems can no longer recognize the changed virus. Rarely, major alterations, or “shifts,” arise. Shifts are changes so drastic that essentially the entire global population no longer recognizes the virus and is defenseless against it. Shifts lead to influenza pandemics such as the 2009 H1N1 pandemic. Influenza is usually caused by 1 of 3 strains of viruses: influenza A, B or C. Influenza A is the most changeable. Immunity to influenza A is rapidly outdated as surface antigens mutate to unrecognizable forms. As a result, influenza A is the most frequent cause of influenza illness. Influenza B, a more stable virus, is responsible for a minority of infections. Influenza C infections are uncommon.
4. Toward a Flu-less Fall and Winter
You can take many actions to stay free of the flu. Annual immunization offers the best protection. Influenza vaccines protect against both A and B strains of virus. It's updated annually to match the most recent versions of influenza and maintain effectiveness. Antibiotics cannot kill viruses, but antiviral medications such as oseltamivir (Tamiflu) and zanamivir (Relenza) can decrease the length of time a person is sick and prevent some flu spread. Covering coughs and sneezes, frequent hand washing and staying home when sick also decrease the spread of flu. Scientists continue to seek better ways to combat this daunting virus.
- Centers for Disease Control and Prevention: ACIP Recommendations for 2013-14
- Centers for Disease Control and Prevention: Antiviral Agents for the Treatment and Chemoprophylaxis of Influenza
- World Health Organization: Recommended Composition of Influenza Virus Vaccines
- National Institutes of Health: The Pathogenesis of Influenza Virus Infections -- The Contributions of Virus and Host Factors
- BMC Infectious Diseases: Impact of Viral Drift on Vaccination Dynamics and Patterns of Seasonal Influenza
- Centers for Disease Control and Prevention: Principles of Epidemiology in Public Health Practice
- Centers for Disease Control and Prevention: Estimates of Deaths Associated With Seasonal Influenza -- United States, 1976-2007
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