Swine influenza

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Swine flu (also swine influenza) refers to influenza caused by any virus of the family Orthomyxoviridae, that is endemic to pig (swine) populations. Strains endemic in swine are called swine influenza virus (SIV), and all known strains of SIV are classified as Influenzavirus A (common) or Influenzavirus C (rare).^[1] Influenzavirus B has not been reported in swine. All three clades, Influenzavirus A, B, and C, are endemic in humans.

People who work with poultry and swine, especially people with intense exposures, are at risk of infection from these animals if the animals carry a strain that is also able to infect humans. SIV can mutate into a form that allows it to pass from human to human. The strain responsible for the 2009 swine flu outbreak is believed to have undergone this mutation.^[2]

In humans, the symptoms of swine flu are similar to those of influenza and of influenza-like illness in general.

Influenza virus was first discovered in humans during the 1918 H1N1 influenza pandemic. Due to concomitant infection in pigs during the outbreak, it is thought that the first influenza virus infection among humans is caused by swine influenza. In the USA, the first swine influenza (H1N1) outbreak was reported in 1930.^[1] A new strain of H1N1, A/Veracruz/2009, emerged in 2009 and was responsible for the 2009 swine influenza pandemic among humans. Characteristically, the 2009 pandemic was not caused by a zoonotic influenza strain (i.e. no involvement of carrier pigs), and the transmission of the new H1N1 strain was human-to-human.

• Influenza virus was first discovered in humans during the 1918 H1N1 influenza pandemic. Due to concomitant infection in pigs during the outbreak, it is thought that the first influenza virus infection among humans is caused by swine influenza.^[2][3][4]
• In the USA, the first swine influenza (H1N1) outbreak was reported in 1930.^[1]
• It was not until 1970 in Taiwan that H3N2 was also discovered to be responsible for swine flu in humans.^[5]
• In 1999 and 2005, outbreaks caused by the second-generation H1N2 swine influenza were reported in the USA.^[6][7]
• A new strain of H1N1, A/Veracruz/2009, emerged in 2009 and was responsible for the 2009 swine influenza pandemic among humans. Characteristically, the 2009 pandemic was not caused by a zoonotic influenza strain (i.e. no involvement of carrier pigs), and the transmission of the new H1N1 strain was human-to-human.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Swine influenza may be classified according to the genera of the infective agent into either influenza A (common) or influenza C (rare). Influenza B has not been associated with development of swine influenza.

Swine influenza may be classified according to the genera of the infective agent into either influenza A (common) or influenza C (rare). Influenza B has not been associated with development of swine influenza.

• Influenza A subtypes include the following:

• H1N1
• H1N2
• H2N3
• H3N1
• H3N2

A new strain of H1N1, A/Veracruz/2009, emerged in 2009 and was responsible for the 2009 swine influenza outbreak in humans.

• Influenza C has been described in a few case reports in the USA and Japan.
• Influenza C is not thought to be genetically diverse, and accordingly it has not been associated with outbreaks among humans.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]

Swine influenza virus is usually transmitted from asymptomatic carrier pigs to humans. Novel H1N1 viruses are thought to have evolved from older influenza viruses by reassortment of formerly triple-reassortant swine flu viruses. Influenza virus contains hemagglutinin, neuraminidase, non-structural proteins, matrix proteins, polymerase proteins, and nucleoprotein that are responsible for viral pathogenesis in humans . The HA protein on the viral surface functions as a receptor binding site and binds to host receptors that contain sialic acid to allow viral fusion to the host cell in the respiratory tract. Following fusion, viral replication typically takes place within 1 day, and polymerase proteins and nucleoproteins are involved in viral replication, whereas the matrix protein is responsible for viral assembly prior to viral release via cytolytic or apoptotic mechanisms. Viral proteins are, at least in part, responsible for down-regulation of cytotoxic T-cell activity, evasion of immune responses, and activation of cytokines and pro-inflammatory mechanisms that contribute to host tissue injury. Swine influenza undergoes antigenic drifts and shifts that ultimately result in genetic reassortment and capacity to reinfect the same host.

• Data regarding the exact pathogenesis of swine influenza infection in hosts is limited, but is thought to be similar to other influenza viruses (human avian influenza viruses).
• Novel H1N1 viruses are thought to have evolved from older influenza viruses by reassortment of formerly triple-reassortant swine flu viruses.

• Swine influenza virus is usually transmitted from asymptomatic carrier pigs to humans.
• Human-to-human transmission of swine influenza is thought to occur by either aerosols of respiratory secretions or by the fecal-oral route.

Hemagglutinin, neuraminidase, polymerase proteins, nucleoproteins, and matrix proteins are involved in the pathogenesis of swine influenza:

• Hemagglutinin (HA): Surface protein that acts as a receptor binding site. HA is targeted by host antibodies to neutralize the virus.^[1][2][3]
• Neuraminidase (NA): Cleaves progeny virions from host cell receptors.^[1]
• Polymerase proteins: PB1, PB2, PA, and PB1-F2. These proteins form the polymerase complex. Together with the NP protein, form the ribonucleoprotein (RNP) complex to induce replication and transcription. Additionally, PB1-F2 has a role in inducing apoptosis.^[1][4]
• Nucleoprotein (NP): Together with the polymerase proteins, NP forms the RNP complex to induce replication and transcription.^[1]
• Non-structural proteins: NS1 and NS2. NS1 processes mRNA and helps the virus evade the host immune responses. NS2 controls the exporting process of RNP from the host nucleus.^[1]
• Matrix proteins: M1 and M2. M1 has a role in viral assembly. M2 controls pH in the Golgi body.^[1]

• The exact pathogenesis of swine influenza in humans is not fully understood.
• The HA protein (receptor binding site) on the viral surface binds to host receptors that contain sialic acid.^[3]
• The precursor HA molecule undergoes proteolytic activation and cleaves to produce 2 molecules: HA1 and HA2.
• Following proteolytic activation, the virus fuses with the host cell.
• The number of residues at the cleavage site is directly associated with the virulence of the virus (Highly cleavable HA with more residues at the cleavage site is thought to be activated by intracellular proteases and result in systemic infections).

• Following fusion, viral replication typically takes place within 1 day in the upper and lower respiratory tracts, including the nasopharynx, trachea, and lungs. Less commonly, replication occurs in extrapulmonary organs, including the intestines, brain, heart, or placenta.^[3]
• Similar to human and avian influenza, swine influenza is thought to replicate intracellularly via cytolytic or apoptotic mechanisms.
• The poylmerase proteins are the main constituents of the polymerase complex that is involved in viral replication. NP encapsulates the RNA gene segments, which allows these segments to be recognized by the polymerase complex.^[4]
• During replication, NS proteins play a major role in evading the host immune responses by deactivating immune responses mediated by pro-inflammatory cytokines.^[4]
• Following replication, the matrix proteins, which are present near the viral envelope, assemble the newly synthesized viruses.^[5]
• M2 provides the adequate pH in the Golgi apparatus for the viruses to replicate and assemble. Mutations in M2 protein have been associated with adaptive mechanisms of the virus to infect new hosts.^[5]

Following infection, the expression of cytokines and chemokines in the lungs significantly increases. The exaggerated up-regulation of these cytokines and chemokines may partly be responsible for the tissue injury associated with the influenza virus.^[1] The expression of the following proteins increases with influenza infection^[1]:

• Tumor necrosis factor-α

• Macrophage inflammatory protein 1-α

• Interferon-γ and interferon-β
• IL-6

It is thought that following infection, the TRAIL death receptor ligand is activated and is responsible for triggering apoptosis.

• These are small changes in the genes of influenza viruses that happen continually over time as the virus replicates.
• These small genetic changes usually produce viruses that are pretty closely related to one another, which can be illustrated by their location close together on a phylogenetic tree.
• Viruses that are closely related to each other usually share the same antigenic properties and an immune system exposed to an similar virus will usually recognize it and respond. (This is sometimes called cross-protection.)
• But these small genetic changes can accumulate over time and result in viruses that are antigenically different (further away on the phylogenetic tree).
• When this happens, the body’s immune system may not recognize those viruses.
• This process works as follows:

• A person infected with a particular flu virus develops antibody against that virus.
• As antigenic changes accumulate, the antibodies created against the older viruses no longer recognize the “newer” virus, and the person can get sick again.
• Genetic changes that result in a virus with different antigenic properties is the main reason why people can get the flu more than one time.

• This is also why the flu vaccine composition must be reviewed each year, and updated as needed to keep up with evolving viruses.

Adapted from CDC ^[6]

• Antigenic shift is an abrupt, major change in the influenza A viruses, resulting in new hemagglutinin and/or new hemagglutinin and neuraminidaseproteins in influenza viruses that infect humans.
• Shift results in a new influenza A subtype or a virus with a hemagglutinin or a hemagglutinin and neuraminidase combination that has emerged from an animal population that is so different from the same subtype in humans that most people do not have immunity to the new (e.g. novel) virus.
• Such a “shift” occurred in the spring of 2009, when an H1N1 virus with a new combination of genes emerged to infect people and quickly spread, causing a pandemic.
• When shift happens, most people have little or no protection against the new virus.
• While influenza viruses are changing by antigenic drift all the time, antigenic shift happens only occasionally.
• Influenza type A viruses undergo both kinds of changes
• Influenza type B viruses change only by the more gradual process of antigenic drift.

• 
  Antigenic Drift
  Click on the image to expand.
  Image courtesy of the National Institute of Allergy and Infectious Diseases (NIAID) [1]
• 
  Antigenic Shift
  Click on the image to expand.
  Image courtesy of the National Institute of Allergy and Infectious Diseases (NIAID) [2]

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This page is about microbiologic aspects of the organisms. For clinical aspects of specific causative organisms: Template:Seealso Template:Seealso Template:Seealso

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The Orthomyxoviruses (ορθός, orthos, Greek for “straight”; μυξα, myxa, Greek for “mucus“)^[1] are a family of RNA viruses that includes six genera: Influenza virus A, Influenza virus B, Influenza virus C, Isavirus, Thogotovirus and Quaranjavirus. The first three genera contain viruses that cause influenza in vertebrates, including birds (see also avian influenza), humans, and other mammals. Isaviruses infect salmon; the thogotoviruses are arboviruses, infecting vertebrates and invertebrates, such as ticks and mosquitoes.^[2][3][4]

The three genera of Influenza virus, which are identified by antigenic differences in their nucleoprotein and matrix protein, infect vertebrates as follows:

• Influenza virus A infects humans, other mammals, and birds, and causes all flu pandemics
• Influenza virus B infects humans and seals
• Influenza virus C infects humans, pigs and dogs.

In a phylogenetic-based taxonomy, the category “RNA virus” includes the category “negative-sense ssRNA virus“, which includes the Order “Mononegavirales“, and the Family “Orthomyxovirus” (among others). The genera-associated species and serotypes of Orthomyxovirus are shown in the following table.

Group: ssRNA(-)

^[7]

There are three genera of influenza virus: Influenza virus A, Influenza virus B and Influenza virus C. Each genus includes only one species, or type: Influenza A virus, Influenza B virus, and Influenza C virus, respectively. Influenza A and C infect multiple species, while influenza B almost exclusively infects humans.^[8][9]

Influenza A viruses are further classified, based on the viral surface proteins hemagglutinin (HA or H) and neuraminidase (NA or N). Sixteen H subtypes (or serotypes) and nine N subtypes of influenza A virus have been identified.

Further variation exists; thus, specific influenza strain isolates are identified by a standard nomenclature specifying virus type, geographical location where first isolated, sequential number of isolation, year of isolation, and HA and NA subtype.^[10][11]

Examples of the nomenclature are:

1. A/Brisbane/59/2007 (H1N1)
2. A/Moscow/10/99 (H3N2).

The type A viruses are the most virulent human pathogens among the three influenza types and cause the most severe disease. The serotypes that have been confirmed in humans, ordered by the number of known human pandemic deaths, are:

• H1N1 caused “Spanish Flu” in 1918, “Swine flu” in 2009.^[12]
• H2N2 caused “Asian Flu”.
• H3N2 caused “Hong Kong Flu“.
• H5N1 is a pandemic threat.
• H7N7 has unusual zoonotic potential.^[13]
• H1N2 is endemic in humans and pigs.
• H9N2, H7N2, H7N3, H10N7.

Influenza B virus is almost exclusively a human pathogen, and is less common than influenza A. The only other animal known to be susceptible to influenza B infection is the seal.^[21] This type of influenza mutates at a rate 2–3 times lower than type A^[22] and consequently is less genetically diverse, with only one influenza B serotype.^[8] As a result of this lack of antigenic diversity, a degree of immunity to influenza B is usually acquired at an early age. However, influenza B mutates enough that lasting immunity is not possible.^[23] This reduced rate of antigenic change, combined with its limited host range (inhibiting cross species antigenic shift), ensures that pandemics of influenza B do not occur.^[24]

The influenza C virus infects humans and pigs, and can cause severe illness and local epidemics.^[25] However, influenza C is less common than the other types and usually seems to cause mild disease in children.^[26][27]

The virion is pleomorphic; the envelope can occur in spherical and filamentous forms. In general, the virus’s morphology is spherical with particles 50 to 120 nm in diameter, or filamentous virions 20 nm in diameter and 200 to 300 (–3000) nm long. There are some 500 distinct spike-like surface projections of the envelope each projecting 10 to 14 nm from the surface with some types (i.e. hemagglutinin esterase (HEF)) densely dispersed over the surface, and with others (i.e. hemagglutinin (HA)) spaced widely apart.

The major glycoprotein (HA) is interposed irregularly by clusters of neuraminidase (NA), with a ratio of HA to NA of about 4–5 to 1.

Lipoprotein membranes enclose the nucleocapsids; nucleoproteins of different size classes with a loop at each end; the arrangement within the virion is uncertain. The ribonuclear proteins are filamentous and fall in the range of 50 to 130 nm long and 9 to 15 nm in diameter. They have a helical symmetry.

Viruses of this family contain 6 to 8 segments of linear negative-sense single stranded RNA.^[28]

The total genome length is 12000–15000 nucleotides (nt). The largest segment 2300–2500 nt; of second largest 2300–2500 nt; of third 2200–2300 nt; of fourth 1700–1800 nt; of fifth 1500–1600 nt; of sixth 1400–1500 nt; of seventh 1000–1100 nt; of eighth 800–900 nt. Genome sequence has terminal repeated sequences; repeated at both ends. Terminal repeats at the 5′-end 12–13 nucleotides long. Nucleotide sequences of 3′-terminus identical; the same in genera of same family; most on RNA (segments), or on all RNA species. Terminal repeats at the 3′-end 9–11 nucleotides long. Encapsidated nucleic acid is solely genomic. Each virion may contain defective interfering copies.

The following applies for Influenza A viruses, although other influenza strains are very similar in structure:^[29]

The influenza A virus particle or virion is 80–120 nm in diameter and usually roughly spherical, although filamentous forms can occur.^[30] Unusually for a virus, the influenza A genome is not a single piece of nucleic acid; instead, it contains eight pieces of segmented negative-sense RNA (13.5 kilobases total), which encode 11 proteins (HA, NA, NP, M1, M2, NS1, NEP, PA, PB1, PB1-F2, PB2).^[31] The best-characterised of these viral proteins are hemagglutinin and neuraminidase, two large glycoproteins found on the outside of the viral particles. Neuraminidase is an enzyme involved in the release of progeny virus from infected cells, by cleaving sugars that bind the mature viral particles. By contrast, hemagglutinin is a lectin that mediates binding of the virus to target cells and entry of the viral genome into the target cell.^[32] The hemagglutinin (H) and neuraminidase (N) proteins are targets for antiviral drugs.^[33] These proteins are also recognised by antibodies, i.e. they are antigens.^[14] The responses of antibodies to these proteins are used to classify the different serotypes of influenza A viruses, hence the H and N in H5N1.

Typically, influenza is transmitted from infected mammals through the air by coughs or sneezes, creating aerosols containing the virus, and from infected birds through their droppings. Influenza can also be transmitted by saliva, nasal secretions, feces and blood. Infections occur through contact with these bodily fluids or with contaminated surfaces. Flu viruses can remain infectious for about one week at human body temperature, over 30 days at 0 °C (Expression error: Missing operand for *. ), and indefinitely at very low temperatures (such as lakes in northeast Siberia). They can be inactivated easily by disinfectants and detergents.^[34][35][36]

The viruses bind to a cell through interactions between its hemagglutinin glycoprotein and sialic acid sugars on the surfaces of epithelial cells in the lung and throat (Stage 1 in infection figure).^[37] The cell imports the virus by endocytosis. In the acidic endosome, part of the haemagglutinin protein fuses the viral envelope with the vacuole’s membrane, releasing the viral RNA (vRNA) molecules, accessory proteins and RNA-dependent RNA polymerase into the cytoplasm (Stage 2).^[38] These proteins and vRNA form a complex that is transported into the cell nucleus, where the RNA-dependent RNA polymerase begins transcribing complementary positive-sense cRNA (Steps 3a and b).^[39] The cRNA is either exported into the cytoplasm and translated (step 4), or remains in the nucleus. Newly synthesised viral proteins are either secreted through the Golgi apparatus onto the cell surface (in the case of neuraminidase and hemagglutinin, step 5b) or transported back into the nucleus to bind vRNA and form new viral genome particles (step 5a). Other viral proteins have multiple actions in the host cell, including degrading cellular mRNA and using the released nucleotides for vRNA synthesis and also inhibiting translation of host-cell mRNAs.^[40]

Negative-sense vRNAs that form the genomes of future viruses, RNA-dependent RNA transcriptase, and other viral proteins are assembled into a virion. Hemagglutinin and neuraminidase molecules cluster into a bulge in the cell membrane. The vRNA and viral core proteins leave the nucleus and enter this membrane protrusion (step 6). The mature virus buds off from the cell in a sphere of host phospholipid membrane, acquiring hemagglutinin and neuraminidase with this membrane coat (step 7).^[41] As before, the viruses adhere to the cell through hemagglutinin; the mature viruses detach once their neuraminidase has cleaved sialic acid residues from the host cell.^[37] After the release of new influenza virus, the host cell dies.

Orthomyxoviridae viruses are one of the only RNA viruses that replicate in the nucleus. This is because the machinery of orthomyxo viruses cannot make their own mRNAs. They use cellular RNAs as primers for initiating the viral mRNA synthesis in a process known as cap-snatching.^[42] Once in the nucleus, the RNA Polymerase Protein PB2 finds a cellular pre-mRNA and binds to its 5′ capped end. Then RNA Polymerase PA cleaves off the cellular mRNA near the 5′ end and uses this capped fragment as a primer for transcribing the rest of the viral RNA genome in viral mRNA.^[43] This is due to the need of mRNA to have a 5′ cap in order to be recognized by the cell’s ribosome for translation.

Since RNA proofreading enzymes are absent, the RNA-dependent RNA transcriptase makes a single nucleotide insertion error roughly every 10 thousand nucleotides, which is the approximate length of the influenza vRNA. Hence, nearly every newly manufactured influenza virus will contain a mutation in its genome.^[44] The separation of the genome into eight separate segments of vRNA allows mixing (reassortment) of the genes if more than one variety of influenza virus has infected the same cell (superinfection). The resulting alteration in the genome segments packaged into viral progeny confers new behavior, sometimes the ability to infect new host species or to overcome protective immunity of host populations to its old genome (in which case it is called an antigenic shift).^[14]

Mammalian influenza viruses tend to be labile, but can survive several hours in mucus.^[45] Avian influenza virus can survive for 100 days in distilled water at room temperature, and 200 days at 17 °C (Expression error: Missing operand for *. ). The avian virus is inactivated more quickly in manure, but can survive for up to 2 weeks in feces on cages. Avian influenza viruses can survive indefinitely when frozen.^[45] Influenza viruses are susceptible to bleach, 70% ethanol, aldehydes, oxidizing agents, and quaternary ammonium compounds. They are inactivated by heat of 133 °F (Expression error: Missing operand for *. ) for minimum of 60 minutes, as well as by low pH <2.^[45]

Vaccines and drugs are available for the prophylaxis and treatment of influenza virus infections. Vaccines are composed of either inactivated or live attenuated virions of the H1N1 and H3N2 human influenza A viruses, as well as those of influenza B viruses. Because the antigenicities of the wild viruses evolve, vaccines are reformulated annually by updating the seed strains. However, when the antigenicities of the seed strains and wild viruses do not match, vaccines fail to protect the vaccinees. In addition, even when they do match, escape mutants are often generated. Drugs available for the treatment of influenza include Amantadine and Rimantadine, which inhibit the uncoating of virions by interfering with M2, and Oseltamivir (marketed under the brand name Tamiflu), Zanamivir, and Peramivir, which inhibit the release of virions from infected cells by interfering with NA. However, escape mutants are often generated for the former drug and less frequently for the latter drug.^[46]

Dog flu

• Hoyle, L. (1969). “The Influenza Viruses”. Virology Monographs. Springer-Verlag. 4. ISBN 3-211-80892-2. ISSN 0083-6591. OCLC 4053391.

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• Viralzone: Orthomyxoviridae
• ICTV

For more information about seasonal human influenza virus that is not associated with animal exposure, see Influenza

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yazan Daaboul, M.D.

Swine influenza should be differentiated from the following diseases or pathogens that cause upper or lower respiratory tract infection or flu-like illness, such as other influenza viruses, such as human or swine influenza, other viral, bacterial, fungal, and parasitic agents that are typically associated with nasopharyngeal and respiratory tract infections, and non-infectious causes, such as asthma, chronic obstructive pulmonary disease (COPD), drug adverse effects, and cardiac causes.

Influenza should be differentiated from the following diseases or pathogens that cause upper or lower respiratory disease or flu-like symptoms:^[1][2]

• Other influenza viruses, such as human influenza or avian influenza
• Other infectious agents, including viruses, bacteria, fungi, and parasites, that are typically responsible for respiratory illness
  • Anthrax (caused by B. anthracis)
  • Arenaviruses
  • Cytomegalovirus (CMV)
  • Chlamydia pneumoniae
  • Coronaviruses (responsible for SARS and MERS)
  • Dengue fever
  • Echoviruses
  • Ebola virus infection
  • Hantavirus pulmonary syndrome
  • Herpes viruses
  • HIV disease
  • Histoplasmosis and other fungal causes of respiratory disease
  • Human metapneumovirus
  • Malaria
  • Measles
  • Parainfluenza virus
  • Poliovirus infection
  • Q fever
  • Rhinovirus
  • Respiratory syncytial virus
  • Other bacterial causes of nasopharyngeal and respiratory infection, such as S. pneumoniae, S. aureus, H. influenzae, M. pneumoniae, M. tuberculosis, L. pneumophila.

• Asthma
• Bronchiectasis
• Chronic obstructive pulmonary disease and emphysema
• Drugs, such as interferons, monoclonal antibodies, bisphosphonates, and chemotherapeutic agents
• Hematologic malignancies (leukemias and lymphomas)
• Myocarditis
• Metal fume fever
• Pericarditis
• Pulmonary embolism
• Vaccinations (typically transient and mild flu-like illness)

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Swine influenza usually occurs in outbreaks/pandemics, and the incidence may vary greatly from one year to another. The 2009 H1N1 global infection rate was 11% to 21%. During the 2009 swine influenza outbreak, the incidence in the USA was approximately 18,000 per 100,000 individuals (a total of 60 million cases) with approximately 265,000 hospitalizations reported. The worldwide case fatality rate is unknown, but is thought to range from 15,000 (initial reports) to 500,000 when patients with no healthcare access were counted. Individuals of all age groups may be affected by swine influenza. There is no gender or racial predilection to the development of swine influenza.

• Swine influenza usually occurs in outbreaks/pandemics, and the incidence may vary greatly from one year to another.
• The 2009 H1N1 global infection rate was 11% to 21%.^[1]
• During the 2009 swine influenza outbreak, the incidence in the USA was approximately 18,000 per 100,000 individuals (a total of 60 million cases) with approximately 265,000 hospitalizations reported.^[2]

• The exact case fatality rate is unknown.
• During the 2009 swine influenza outbreak, initial reports stated that a total of 15,000-18,000 individuals died worldwide, the majority of whom were under 65 years of age.^[3] However, reports published three years later speculated that more than 280,000 – 500,000 individuals may have died due to the 2009 swine influenza. The initial underestimation was thought to be caused by not counting individuals with no access to healthcare in developing countries.^[4][5][6]

• Individuals of all age groups may be affected by swine influenza.^[7]
• Compared to the elderly, younger individuals are at higher risk of developing swine influenza. It is thought that older individuals may have a higher degree of cross-protection against influenza infection.^[7]
• Small children and the elderly are at higher risk of developing swine flu-related complications.

There is no gender predilection to the development of swine influenza.

There is no racial predilection to the development of swine influenza.

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