Because the 2009 H1N1 influenza virus was a novel (not previously identified) virus, and because the virus and associated flu became subjects of intense research, information about the virus accumulated rapidly. As of July 2009, the World Health Organization (WHO) offices reported over 94,000 laboratory-confirmed cases of 2009 H1N1 influenza in 135 countries. At least 700 deaths had been attributed to the novel virus, and WHO officials characterized the 2009 H1N1 flu as the fastest spreading pandemic on record.
Despite high initial estimates, by June 24, 2009, Mexico had reported 7,847 confirmed cases and 115 laboratory-confirmed deaths. The United States reported 21,449 confirmed cases and 87 deaths, and Canada reported 6,457 cases and 15 deaths. Deaths were also reported in Columbia, Costa Rica, Dominican Republic, Guatemala, the Philippines, and the United Kingdom. The spread of the virus into the Southern Hemisphere was evidenced by Australia's reporting of 2,857 cases, including two deaths; Argentina's reporting of 1,213 cases, including seven deaths; and Chile's reporting 4,315 cases, including four deaths. As with all reports related to a developing outbreak, daily reports of cases and deaths were simply considered by experts to be a snapshot of data; both the number of countries reporting and cases confirmed were expected to increase until the pandemic subsided. In July 2009, with the pandemic well established in both the Northern and Southern Hemispheres, WHO officials stopped accumulating individual case counts in favor of concentrating on pandemic flu mitigation strategies such as vaccine and antiviral medication development and delivery. In developing countries with established outbreaks, data were difficult to collect and prone to error. Counting individual cases was also difficult because many were mild and went unreported.
Newswires were often filled with unverified reports and even the time difference between offices reporting laboratory-confirmed results could seemingly swing figures rapidly. In addition, there was often a delay or backlog in such reporting. Uncertainties in the number of cases and confirmed deaths created a degree of uncertainty in assessments of the lethality of the virus and course of the outbreak. As of August 2009, there was no evidence that the H1N1 pandemic would be more lethal on a case-by-case basis than a typical seasonal flu. However, pandemic flu viruses often cause significant global deaths because so many more people are infected than in normal influenza seasons.
In April 2009, scientists at the U.S. Centers for Disease Control and Prevention (CDC) and at a research laboratory in Winnipeg, Canada, confirmed that a new strain of influenza was causing illness in humans. Genetic analysis showed that although the H1N1 virus is a novel genetic reassortment of genes of swine, human, and avian origin, the majority of the H1N1 genome is traceable and comparable to other viruses that cause seasonal influenza.
It remained a subject of intense research as to when and where the 2009 H1N1 flu virus may have entered the human population. Although the first cases erupted in Mexico and the United States in March and April 2009, this did not mean that that the genetic reassortment of the virus took place in Mexico or the United States or that the virus entered the human population in either country.
The 2009 H1N1 influenza virus was initially classified as a swine flu because it contains swine flu genes. This means only that the virus passed through swine at some point in its evolution. When and where the virus passed through swine was a subject of continued investigation. Although probable, it was not a certainty that the virus was most recently transmitted from swine to humans. Based on preliminary genetic analysis, experts conjectured such a transfer might have taken place in late 2008. As of June 12, 2009, however, none of the cases encountered in the 2009 H1N1 flu outbreak could be definitively traced to contact with pigs. In fact, the first confirmed outbreak of H1N1 recorded in swine was on a Canadian farm. Experts strongly suspected that a human farm worker who had traveled from Mexico infected the swine.
H1N1 strains of influenza are common in pigs, and swine flu viruses can be transmitted from pigs to humans who are in close contact with infected animals. However, before the 2009 H1N1 outbreak, documented transmission of recent swine flu viruses from person to person was extremely limited and had not resulted in documented outbreaks of human disease.
What made health experts in 2009 so concerned about the new H1N1 virus was its being a novel virus of unknown lethality that had gained the ability to efficiently pass from person to person (human transmission). Because 2009 H1N1 flu was new, humans had no immunity to it. As a result, the resources of the WHO, the CDC, state public health departments, and various international organizations charged with protecting public health were mobilized to attempt to mitigate a worldwide influenza pandemic.
Viruses are simple organisms consisting of a protein matrix containing genetic information. They are so small that they can be seen only with an electron microscope. Because they are metabolically inert outside a host cell, viruses cannot reproduce on their own. They are parasites and must enter a host cell and take over the host cell's resources in order to make millions of new virus particles.
Influenza is caused by a hardy group of viruses belonging to the Orthomyxoviridae family. There are three types of influenza viruses: types A, B, and C. Type A influenza virus is the most threatening to humans. The type B virus is stable, changing little from year to year, and can be effectively controlled through vaccination. Type C influenza viruses cause only mild illness in humans. The type A virus, however, easily changes, or mutates, into new strains or subtypes. Each strain contains slightly different genetic information. Because of this difference, no single vaccine is completely effective against all type A viruses, and whenever a new strain arises, as in the case of the 2009 H1N1, the body's immune system treats the virus as a completely new antigen.
Humans are not the only animals vulnerable to influenza A infections. Different strains of influenza A cause disease in other animals, including wild birds, chickens, ducks, and turkeys (collectively called avian or bird flu), in addition to pigs, horses, ferrets, whales, seals, and dogs. Pigs and birds are the critical species in the development of new flu strains that can infect humans. Wild birds serve as a reservoir for the influenza A viruses; some strain of avian flu is always present in the wild bird population. Birds shed live virus in their droppings (feces), and because many species of bird migrate long distances, they can infect large areas. Pigs carry their own strains of influenza A, but they also can become infected with avian influenza if they are exposed to infected bird droppings or contaminated water. If a pig simultaneously becomes infected with a strain of swine influenza and a strain of avian influenza, when the virus reproduces, genetic information can be exchanged so that new strains of influenza A develop that incorporate some genetic material from the avian virus and some genetic material from the swine virus.
Most new strains of influenza that result from a recombination or reassortment of avian and swine flu viruses do not survive, cannot infect humans, or die out quickly. Occasionally, however, a strain develops that can infect humans and that has the ability to pass from pig to human and from person to person. Because the virus is new to humans, the body has few defenses against it, and the vaccines included in seasonal flu shots are ineffective against it. When a new strain of flu arises that can pass easily from person to person, it has the potential to cause a pandemic, rapidly infecting and sometimes killing millions of people across the world.
Influenza pandemics have occurred during thousands of years of recorded history. The worst influenza pandemic in modern history occurred in 1918–1919 and killed an estimated 20 to 40 million people. In 1957, another pandemic known as the Asian flu killed about 70,000 Americans. This was followed by the pandemic Hong Kong flu in 1968. Then in 1976, Americans experienced a swine flu scare. During February 1976, several recruits at the Army Fort Dix in New Jersey developed unusually severe flu symptoms. When samples from some of the sick men were sent to the CDC for analysis, four samples showed a previously unknown flu virus that appeared to be similar to the virus that caused the 1918–1919 pandemic. After one soldier died of flu, the United States began a $135 million emergency immunization program. However, the 1976 virus proved to be much less dangerous than the 1918 virus. In the end, the 1976 swine flu never spread beyond Fort Dix. About 500 people became sick and only one person died.
People who were most likely to become infected with the 2009 H1N1 influenza were those who had close contact with someone who is infected. The incubation period was uncertain, although it was most likely less than seven days. The disease was passed to others through infected droplets that were spread by coughing, sneezing, kissing, and close physical contact. The virus could also spread indirectly. Tests of other viral strains typically show that Type A viruses can live up to two hours on hard surfaces such as door knobs, telephones, or children's toys. This means that an infected person can leave the flu virus on objects where it can be picked up by another person who then touches his or her own mouth, nose, or eyes and becomes infected. People are contagious for about one day before symptoms appear. Adults remain contagious for about seven days after they begin to show symptoms; children can remain contagious for up to ten days.
The 2009 H1N1 flu was caused by a newly identified strain of influenza virus. Genetic tests established that H1N1 strains encountered before that were consistent (nearing 99% genetic matches among viruses examined from patient samples taken from six countries). Of particular interest to infectious disease research were the genes that control hemagglutinin (H), neuraminidase (N), two surface proteins with subtypes that are numbered, hence H1N1 flu or H5N1 avian flu virus, genes that control the nucleoprotein, the surrounding matrix, and three key polymerase enzymes (designated PA, PB1, and PB2) that the virus must have to reproduce. Genetically, the 2009 H1N1 presented a mixed background, with these key genes derived from human, swine, and avian sources (a triple reassortment). The hemagglutinin [H] produced was equidistant to the swine flu sequences found in the North America, Europe, and Asia. The neuraminidase and matrix genes sequences were close to genes found in swine flu strains found in Asia. Early evidence indicated similarities to influenza strains where the PB1 gene is of human origin and the PA and PB2 genes are from avian sources.
Symptoms of 2009 H1N1 flu were similar to the symptoms of seasonal influenza. These included fever, cough, sore throat, runny nose, body aches, headaches, chills, loss of appetite, and exhaustion. Some people experienced nausea, vomiting, and diarrhea. Although most cases of 2009 H1N1 flu were mild to moderate, complications such as severe pneumonia could result in respiratory failure and death. Neurological complications, including seizures, were also linked to 2009 H1N1 flu in children. The case fatality rate was only 0.03% compared with more than 2.5% in the Spanish flu epidemic of 1918–1919. Worldwide there may have been between 14,000 and 18,000 deaths from the H1N1 flu during the 2009 pandemic.
The most accurate test for influenza is done by taking a mucus sample from the throat of an infected person. Because of the time delay involved in testing, knowing the strain of flu does not provide much help to the patient, but this information helps the CDC and WHO understand how and where flu is spreading. During an influenza pandemic, physicians often forgo laboratory confirmation of influenza, relying on signs and symptoms for diagnosis. In the United Kingdom, persons with flu symptoms are given access to antiviral drugs after answering questions that indicate an influenza diagnosis on a government-sponsored public health website. This saves physician resources for handling severe or emergent cases, provides quick access to treatment, and helps the person with symptoms to stay home, thereby reducing the pool of infected persons in public available to infect others.
Supportive treatment for H1N1 (2009) appears to be the same as for all influenza viruses and includes drinking plenty of fluids, extended bed rest, and use of acetaminophen to treat aches and fever. The 2009 H1N1 influenza A virus also responded to two antiviral drugs, oseltamivir (Tamiflu) and zanamivir (Relenza). These drugs do not prevent or cure flu, but if taken within 48 hours of the start of symptoms, they reduce the severity and duration of the disease. In late April 2009, the U.S. government released stockpiled supplies of these antiviral drugs to combat 2009 H1N1 flu. Initial tests showed that 2009 H1N1 was resistant to two other antiviral drugs, amantadine (Symmetrel, Symadine), and rimantadine (Flumandine), making these drugs ineffective. Antibiotics also were ineffective against all viruses, including H1N1, but could be used to treat bacterial complications of influenza, such as pneumonia.
In late June 2009, public health officials in Denmark reported the first case of 2009 A/H1N1 influenza that was resistant to oseltamivir. Although some cases of resistance normally occurred and developed with seasonal influenzas, any emergence of Tamiflu-resistant 2009 A/H1N1 influenza virus put public health officials on alert for appearance of the resistant virus elsewhere. Isolated cases of Tamiflu-resistant 2009 H1N1 were identified in Japan, Hong Kong (Special Administrative Region of China), and Canada. Thus far, the Tamiflu-resistant viral influenza remained treatable with zanamivir (Relenza), the other antiviral drug usually effective against the A/H1N1 virus.
No scientific testing exists to validate any claim of effectiveness of any alternative medical treatments specific to H1N1 flu. Although claims of effectiveness (and/or potential harm) for any alternative medical treatment should be carefully scrutinized for supporting scientific evidence, there are a number of alternative treatments commonly used to support relief of symptoms. Because there is no scientifically validated antiviral treatment, if flu is suspected, persons should consult a physician to determine if they are in need of antiviral medicines.
Alternative practitioners recommend herbal teas to soothe the throat and allegedly boost the immune system. Other herbal treatments recommended by alternative practitioners for seasonal flu routinely include the following:
The best ways to prevent H1N1 (2009) infection are the following:
Note that surgical masks are unlikely to protect against the influenza virus but are effective in reducing dissemination of droplets that can contain viral particles. Also, antiviral medications do not prevent influenza; they simply help shorten the intensity and duration of the illness.
The first H1N1-specific vaccine was anticipated by late September or early October 2009. World public health officials recommended prioritizing vaccine recipients according to individual risk, as well as to ensure the greatest benefit for overall public health. Pregnant women and people caring for infants, children, young people under 25 years of age, and persons with underlying health conditions such as asthma or diabetes were recommended to receive priority vaccination against pandemic 2009 H1N1 influenza. In addition, healthcare workers were suggested to be among the first immunized in order to keep hospitals, doctors' offices, and other critical healthcare infrastructure functional during the pandemic flu.
Public health officials acknowledged that even under the best scenarios, production of the H1N1 vaccine was expected tp fall far short of global demand. As of 2009 production rates, 900 million doses of the new H1N1 vaccine could be produced each year (as two doses are required per person, enough to vaccinate 450 million people). The vaccine is produced in only a handful of countries and there were concerns these countries, along with wealthier nations, would obtain the vast majority of vaccine produced. The shortages might also hinder WHO efforts to secure donations of vaccine or agreements that will enable poorer countries to purchase vaccine at a lower price.
See also Asthma ; Avian flu ; Pandemic ; Parasites ; Vaccination ; Viruses .
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Brenda Wilmoth Lerner
Revised by Tish Davidson, AM