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What Is Swine Flu?
Swine flu (also called swine influenza, or simply, flu) is an acute respiratory disease of pigs (also called hogs or swine) caused by a tiny spheroid virus that belongs to the Influenza A virus group. Symptoms of swine flu in swine herds include fever, inactivity, nasal discharge, labored breathing, mouth breathing, and paroxysmal coughing when the pigs are moved. All ages are susceptible. Mortality rates are generally low and pigs recover within 5 to 7 days after initial symptoms.
Swine influenza A viruses are divided into categories on the basis of approximately 500 distinct surface protein spikes that project from the surface of the virus. The protein spikes are of two kinds: 1. Neuraminidase (NA) and 2. Hemagglutinin (HA).
To determine the type of influenza virus causing a flu outbreak in a swine herd, secretions are obtained and processed. Current common varieties of swine flu include H1N1, H3N2 and H1N2 (more on this below). What is the function of HA and NA viral surface projections anyway? The function of the HA protein is to bind virus particles to susceptible cells in the host animal. The function of the NA protein is mainly at the end of the life cycle of the virus at which time it facilitates the release of the virus particles from the infected cell surfaces during the budding processes. The HA and NA proteins are the antigens against which neutralizing antibodies are directed by the host animal’s immune defense system. The hallmark of the Influenza A virus is the ability of its HA and NA proteins to undergo change—either by “drift” or “shift”, allowing the influenza virus to have tremendous variability and survivability. Virologists have identified fifteen (15) distinct HA and nine (9) distinct NA subtypes of the influenza A virus to date. That’s a lot of potential variation. The epidemiology of influenza is essentially a story of the dog-fight between host defense and the wily influenza virus that attempts to dodge the host defense through drift and shift. This fact has also been the most difficult problem in making of a vaccine against influenza. Drift (also called antigenic drift) means that point mutations in the HA and/or NA genes accumulate during viral replication. Antibody produced in response to an influenza virus infection is very specific for the influenza virus type that stimulated antibody development in the first place. If sufficient drift occurs, previously developed host antibody will be ineffective against the new “drifted” virus type. Shift (also called antigenic shift) occurs when an influenza A virus containing an immunologically new HA or NA (or both) is introduced into an immunologically naïve population of, say, pigs. Shift occurs via three routes: 1. A virus bearing a new HA/NA can arise through genetic reassortment between species, as when, for example, a pig farmer sick with human influenza becomes co-infected with the swine influenza while he tends an infected herd. The farmer is “double infected.” A reassortment of viral genetic material from the human and the pig within the human host cell can occur, giving rise to a novel HA/NA strain. 2. A wholly species-specific influenza virus from one species (e.g., birds or swine) can infect another species (e.g., humans) directly without undergoing genetic reassortment as described in #1 above. This is exactly what scientists think is happening during the current avian flu epidemic in Asia in which humans are becoming ill with wholly avian flu virus (see SEMP Biot #149: “What Is Avian Flu?” available at: http://www.semp.us/biots/biot_149.html.) 3. An influenza virus can be passed from one species (e.g., birds) through an intermediate animal host (e.g., pigs) to a third species (e.g., humans). Pigs have been proposed to the “mixing vessel” for the generation of reassortment influenza A viruses between humans and birds because—and this is very important—pigs can easily support replication of both avian and human influenza A viruses within their cells.
Notes on the 1918 Flu Pandemic Influenza A virus was first isolated by RE Shope* in 1931 from swine and by W. Smith, et al.**, in 1933 from humans, approximately 15 years after the 1918 “Spanish” flu world pandemic. Recently, RNA sequences of the 1918 virus have been studied by researchers at the Armed Forces Institute of Pathology (AFIP) in Maryland, which had stored specimens of 70 human autopsy cases of the 1918 flu pandemic.* In addition, influenza RNA was extracted from a preserved bird from the 1915-1918 era stored at the Smithsonian Institution. The work done confirms that the 1918 virus was an H1N1 virus and was closely related to swine and human H1N1 viruses that Swope isolated in the 1930s. However, both 1930 human and swine viruses were genetically distinct from the 1918-era archived wild bird virus from the Smithsonian. Hence, the researchers hypothesize that the virus causing the 1918 pandemic was unlikely transmitted directly from birds to humans or pigs. Rather, they think that the H1N1 pandemic virus likely circulated among swine and/or humans for some period, undergoing drift, before leading to widespread illness in 1918.
Editor’s Note : Influenza virus A causes yearly epidemics that result in illness for humans, pigs, and domestic poultry. We now know that intra-species transmission is the norm. Indeed, pandemics are global epidemics among humans caused by the transmission of novel influenza A viruses generated via inter-species transmission. Pandemics are no longer thought of as tornadoes that suddenly thrust themselves upon human populations. Rather, we now know that herald epidemics in non-human and human species occur for variable amounts of time before a pandemic takes root. Thus, surveillance among human, swine and bird populations has become essential for early detection of viruses with pandemic potential and for initiation of prevention efforts, particularly vaccine development. Sources and Notes: *According to AFIP’s Dr. Jeffrey Taubenberger, the tissue specimens were contained in paraffin wax blocks that had sat at room temperature on shelves for 80 years. Of the 70 cases, 35 lung specimens were examined. Most of the specimens revealed bacteria because the victims had succumbed to secondary bacterial pneumonia. Taubenberger wanted to find victims who died very quickly after the onset of symptoms in order to try to capture the virus while it was still present and replicating. Of those six cases found, only one was positive. **Shope RE. Swine influenza III. Filtration experiments and etiology. J Exp Med 1931; 54:373-385. *** Smith W, et al. A virus obtained form influenza patients. Lancet 1933; ii:66-68. Other excellent background sources:
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