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What do you think about the Swine Flu epidemic?
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Tatyana
Elite Mentor
We have had flu epidemics and pandemics since the time of Hippocrates.
It is nature's own biological warfare, natural selection of viruses.
It is no different from things like MRSA developing from Staph. aureus.
I did quite a bit of research and wrote an essay on influenza A virus for one of my immunology classes.
Ever since this essay, I have had the flu jab every year.
Sorry, the images/figures don't cut and paste.
With the human imunodeficiency virus and devastating the world population, it is difficult to believe that something as common and as easy to catch as 'the flu' kills more people each year than AIDS (Garfinkel and Katze, 1994). Influenza A is responsible for the most devastating plague ever recorded, the Spanish flu of 1918-20. Influenza A killed an estimated twenty million people, more people than the casualties of the First World War. As of 1994, an estimated three million people have developed full-blown AIDS (Voet and Voet, 1995).
Its annual outbreaks, the first recorded by Hippocrates in 412 BC, are occasionally interrupted by devastating worldwide infection called pandemics. Due to the viruses ability to continually infect the worlds' population, its structure, method of infection, and replication within its hosts have been intensely studied by virologists and other scientists.
The viruses that cause influenza belong to the family Orthomyxovirus, which are essentially avian viruses that have 'recently' crossed into mammals (Keen, 1999). There are three immunological classes belonging to the family Orthomyxovirus, but only influenza virus A represents the major infection to human beings as well as other mammals such as pigs, horses, aquatic mammals and birds.
The virions or virus particles of influenza virus are normally spherical and 80-120 nm in diameter but they can be filamentous, and several micrometers long (Inglis, 1992). The viral genome is unusual in that it consists of eight different sized strands of negative single stranded RNA. The eight viral RNAs code for the seven structural proteins, and three non-structural proteins that occur only in infected cells (Inglis, 1992). The RNA of the virus is covered with a protein coat called a nucleoprotein (NP) that forms a helical structure similar to the chromosomes of eukaryotic cells.
Associated with the nucleic acid are three polymerase polypeptides (PA, PB1 and PB2) that are responsible for RNA transcription (Jawetz, Melnick and Adelberg, 1991). This nuclear core, called a nucleocapsid, is surrounded by a protein coat composed of matrix protein (M1 and M2) that forms a shell underneath the viral lipid envelope. The viral envelope originates from the plasma membrane of the animal cells that they infect. Into this are inserted two glycoproteins, hemagglutinin (HA) and neuraminidase (NA), that appear as 'spikes' in electron microscopy. These spikes are used to name the different strains of influenza.
Various subtypes of the spikes have been discovered thus far, thirteen HA (H1-H13) and nine NA (N1-N9).
Only three subtypes of HA (H1-H3) and two subtypes NA (N1 and N2) had been thought to infect humans until the recent avian flu (H5N1) in Hong Kong in 1998(Cann, 1999).
Besides being of importance in the classification of influenza A viruses, hemagglutinin and neuramimidase have important functional roles. Hemagglutinin has been so named as it caused erythrocytes to agglutinate (clump together). The hemagglutinin spikes are 10 nm long, rod-shaped glycoproteins that bind the virus to the cell at specific receptor sites containing sialic acid (N-acetylneuramic acid), including the glycophorin A receptor on erythrocytes (Mims, Playfair, Roitt, Wakelin and Williams, 1998). Each virion has approximately five hundred hemagglutinin spikes (Voet and Voet, 1995).
Between the hemagglutinin spikes there are mushroom-shaped spikes of an enzyme called neuraminidase. This enzyme catalyses the cleavage of sialic acid and other sugar residues that are found in mucin (mucous) allowing the virus to be able to move through the mucous between and covering cells. Neuraminidase also destroys the hemagglutinin receptors, sialic acid, on the host cells, allowing the newly formed virus particles to be released, or bud, from infected cells. Each virion has approximately 100 neuraminidase spikes (Voet and Voet, 1995).
The hemagglutinin and neuraminidase spikes are essential to viral infection and release. They are also the proteins constituting the antigens, or the targets for the immune system antibodies. They have been intensely studies and the structure has been determined to the amino acid level. HA is transcribed on ribosomes associated with the endoplasmic reticulum and then is further processed in the Golgi apparatus. This protein is then cleaved into two subunits, HA1 and HA2 that remain bound together by a disulphide bridge, called a dimer. HA1 and HA2 are separated by a cleavage furrow, which is the site of attachment of the sialic acid. Three of these dimers form the hemagglutinin spike (Jawetz, Melnick and Adelberg, 1991).
Neuraminidase is made of four identical monomers, called a tetramer. Each of the viral protein monomers contains a highly conservative active site, which cleaves the sialic acid (Jawetz, Melnick and Adelberg, 1991).
Viral infection can be divided into several steps, attachment, penetration, uncoating, replication, assembly and release. Influenza virions are transmitted in aerosols, tiny airborne droplets laden with virions, or from contact with contaminated hands or surfaces.
These are inhaled and deposited on the respiratory epithelium, specifically ciliated epithelial cells. The virus attaches via the hemagglutinin spikes to sialic acid on the surface of the plasma membrane of the cell. The receptor bound virus is brought into the cell by endocytosis in coated pits into endocytotic vesicles and finally endosomes. These endosomes are acidified by the cell. In the low pH environment of the endosome, the HA spikes are cleaved which causes a conformational change in the hemagglutinin. This change activates HA2 which causes the fusion of the viral lipid envelope with the endosome lipid membrane (Cann, 1999). The viral nucleocapsid is released into the cellular cytoplasm in a process called uncoating.
Once the virion has been uncoated, sequences in the NP protein result in the translocation of the nucleocapsid into the nucleus where transcription occurs. Transcription mechanisms used by orthomyxoviruses differ from other RNA viruses in that it occurs in the nucleus. The negative configuration of influenza virus A's RNA must first be transcribed, by the three polymerase polypeptides (PB1, PB2 and PA) that are associated with each segment of the viral genome, into a positive sense strand. Two types of positive sense RNA are made.
Viral mRNAs are transported into the cytoplasm where it uses host ribosomes to translate viral structural proteins such as hemagglutinin, neuraminidase, matrix proteins, and capsomeres (Cann, 1999). Viral cRNA remains in the nucleus where it codes for the synthesis of progeny negative sense RNA vRNA (viral RNA) (Voet and Voet, 1995).
Once all of the viral components have been transcribed, the assembly of virions can occur. Most of the proteins made in the cytoplasm remain in the cytoplasm. The envelope glycoproteins, hemagglutinin and neuraminidase that have been translated from viral mRNA, are inserted into areas of the host cell membrane. The nucleoprotein moves back into the nucleus and associates with the newly synthesised vRNA to form new nucleocapsids (Cann, 1999). Once associated, the nucleocapsid moves back into the cytoplasm and toward the cell membrane. The new nucleocapsids join with the glycoproteins in the membrane and bud through it. The newly formed virions are now free to infect other cells.
The viral life cycle does not occur without an immunological response from the host organism. Innate immune mechanisms restrict the early stages of infection and delay the spread of the virus. These defences include interferon, natural killer cells and macrophages. Natural killer cells appear within two days of viral infection and destroy infected cells early in the virus replication cycle before new virions appear (Roitt, Brostoff and Male, 1998).
Interferon (IFN) is a cytokine made by virus infected cells or activated T-cells that inhibits viral reproduction. This cytokine is able to do this by slowing protein synthesis in the infected cell by coding for various proteins. While most of the proteins have not been identified, RNA-activated protein kinase (PKR) is thought to have an important role in halting the shutdown of protein synthesis. PKR is normally present in cells and is thought to function as a tumour suppresser.
This enzyme phosphorylates one of the ribosomal initiation factors in eukaryotic cells, which prevents them from transcribing mRNA. As viruses require high levels of protein synthesis, they have developed mechanisms to avoid this immunological response. Viruses normally code for an enzyme that binds to PKR to prevent its activation. Influenza virus A is unique in that it uses the hosts own products and mechanism in halting the interferon response. This enzyme, a protein kinase named p58, is thought to be an oncogene that inhibits the activation of PKR, therefore viral protein synthesis is able to proceed (Garfinkel and Katze, 1994).
As influenza infection proceeds, the adaptive immune response activates cytotoxic T cells, helper T cells and antiviral antibodies, specifically immunoglobulin G and immunoglobulin A (IgG and IgA)(Roitt, Brostoff and Male, 1998). IgA is mainly produced at mucosal surfaces where it serves to prevent reinfection. IgG acts against the hemagglutinin and neuraminidase surface proteins and restricts the spread of the virus to neighbouring cells and tissues by neutralising virus infectivity (Roitt, Brosnoff and Male, 1998). While antibodies limit influenza virus A spread and reinfection, it is strain specific and is readily avoided by the virus.
One of the characteristics of influenza virus A is its ability to change. Small mutations that occur on a regular basis on hemagglutinin and neuraminidase spikes result in antigenic drift that the adaptive immune system, specifically memory B-cells, will have no response to. Antigenic drift occurs when amino acid substitutions occur due to random point mutations. These mutations occur when selective pressure on the virus is brought about by an increase in immunity in the host population (Voet and Voet, 1995).
In addition to this drift, a new strain of influenza virus A seems to appear every ten to forty years to which no one has immunity (Jawetz, Melnick and Adelberg, 1998). This is due to antigenic shift, in which there is a sudden major change in the HA and/or NA antigens.
Influenza virus A is susceptible to antigenic shift because of its genome and as it has the ability to infect a variety of mammals. Influenza virus A has eight separate strands of genetic material, RNA, which is considered to be less 'stable' than DNA and therefore more likely to mutate. The separate strands could easily be mixed in an animal infected with two strains of influenza. Deadly viral strains of influenza appear to occur where human, birds and swine live in close quarters. These conditions have long existed in Hong Kong, where several of the world's pandemics have appeared to originate.
Influenza virus A continues to infect approximately thirty percent of the world's population each year (Roitt, Brosnoff and Male, 1998). While most people do not die directly from influenza, the secondary complications like bacterial pneumonia and encephalitis lead to a high mortality rate in susceptible and immunologically compromised individuals. A pandemic may not function in this way. During the Spanish flu of 1918-20, the majority of the fatalities were healthy young people between the ages of twenty and forty-five. The influenza virus killed by damaging the lung tissue to such an extent that the patient died by drowning.
Influenza virus A is one of the most prevalent unconquered infectious diseases of the twentieth century.
Despite being one of the most intensely studied viruses, its chameleon-like nature with its ability to change its coat, has led to constant monitoring of the animals it infects, and the need to predict a new vaccination each year. Unlike other infectious viruses, such as polio, influenza virus A will likely never be eliminated because of its repository in other animals, and because of its ability to mutate into new antigenic strains.
The 1998 Hong Kong flu (H5N1) had the potential to be as devastating as the Spanish flu pandemic. It was seen as a wake up call, an imminent warning that the next pandemic is overdue. It is believed that the H5N1 virus can only be transmitted directly from birds to humans. This is the first known example of cross species infection (Laver, 1999).
The current fear of virologists and epidemiologists is that the deadly H5N1 flu may have been contracted by someone visiting Hong Kong during the epidemic. In this age of global travel, it would be easy for this carrier to meet with a virus that is easily transmitted. The combination of the two could be the genesis of the new pandemic. The question then is not 'if' another deadly global pandemic like the Spanish flu arises, but when.
It is nature's own biological warfare, natural selection of viruses.
It is no different from things like MRSA developing from Staph. aureus.
I did quite a bit of research and wrote an essay on influenza A virus for one of my immunology classes.
Ever since this essay, I have had the flu jab every year.
Sorry, the images/figures don't cut and paste.
With the human imunodeficiency virus and devastating the world population, it is difficult to believe that something as common and as easy to catch as 'the flu' kills more people each year than AIDS (Garfinkel and Katze, 1994). Influenza A is responsible for the most devastating plague ever recorded, the Spanish flu of 1918-20. Influenza A killed an estimated twenty million people, more people than the casualties of the First World War. As of 1994, an estimated three million people have developed full-blown AIDS (Voet and Voet, 1995).
Its annual outbreaks, the first recorded by Hippocrates in 412 BC, are occasionally interrupted by devastating worldwide infection called pandemics. Due to the viruses ability to continually infect the worlds' population, its structure, method of infection, and replication within its hosts have been intensely studied by virologists and other scientists.
The viruses that cause influenza belong to the family Orthomyxovirus, which are essentially avian viruses that have 'recently' crossed into mammals (Keen, 1999). There are three immunological classes belonging to the family Orthomyxovirus, but only influenza virus A represents the major infection to human beings as well as other mammals such as pigs, horses, aquatic mammals and birds.
The virions or virus particles of influenza virus are normally spherical and 80-120 nm in diameter but they can be filamentous, and several micrometers long (Inglis, 1992). The viral genome is unusual in that it consists of eight different sized strands of negative single stranded RNA. The eight viral RNAs code for the seven structural proteins, and three non-structural proteins that occur only in infected cells (Inglis, 1992). The RNA of the virus is covered with a protein coat called a nucleoprotein (NP) that forms a helical structure similar to the chromosomes of eukaryotic cells.
Associated with the nucleic acid are three polymerase polypeptides (PA, PB1 and PB2) that are responsible for RNA transcription (Jawetz, Melnick and Adelberg, 1991). This nuclear core, called a nucleocapsid, is surrounded by a protein coat composed of matrix protein (M1 and M2) that forms a shell underneath the viral lipid envelope. The viral envelope originates from the plasma membrane of the animal cells that they infect. Into this are inserted two glycoproteins, hemagglutinin (HA) and neuraminidase (NA), that appear as 'spikes' in electron microscopy. These spikes are used to name the different strains of influenza.
Various subtypes of the spikes have been discovered thus far, thirteen HA (H1-H13) and nine NA (N1-N9).
Only three subtypes of HA (H1-H3) and two subtypes NA (N1 and N2) had been thought to infect humans until the recent avian flu (H5N1) in Hong Kong in 1998(Cann, 1999).
Besides being of importance in the classification of influenza A viruses, hemagglutinin and neuramimidase have important functional roles. Hemagglutinin has been so named as it caused erythrocytes to agglutinate (clump together). The hemagglutinin spikes are 10 nm long, rod-shaped glycoproteins that bind the virus to the cell at specific receptor sites containing sialic acid (N-acetylneuramic acid), including the glycophorin A receptor on erythrocytes (Mims, Playfair, Roitt, Wakelin and Williams, 1998). Each virion has approximately five hundred hemagglutinin spikes (Voet and Voet, 1995).
Between the hemagglutinin spikes there are mushroom-shaped spikes of an enzyme called neuraminidase. This enzyme catalyses the cleavage of sialic acid and other sugar residues that are found in mucin (mucous) allowing the virus to be able to move through the mucous between and covering cells. Neuraminidase also destroys the hemagglutinin receptors, sialic acid, on the host cells, allowing the newly formed virus particles to be released, or bud, from infected cells. Each virion has approximately 100 neuraminidase spikes (Voet and Voet, 1995).
The hemagglutinin and neuraminidase spikes are essential to viral infection and release. They are also the proteins constituting the antigens, or the targets for the immune system antibodies. They have been intensely studies and the structure has been determined to the amino acid level. HA is transcribed on ribosomes associated with the endoplasmic reticulum and then is further processed in the Golgi apparatus. This protein is then cleaved into two subunits, HA1 and HA2 that remain bound together by a disulphide bridge, called a dimer. HA1 and HA2 are separated by a cleavage furrow, which is the site of attachment of the sialic acid. Three of these dimers form the hemagglutinin spike (Jawetz, Melnick and Adelberg, 1991).
Neuraminidase is made of four identical monomers, called a tetramer. Each of the viral protein monomers contains a highly conservative active site, which cleaves the sialic acid (Jawetz, Melnick and Adelberg, 1991).
Viral infection can be divided into several steps, attachment, penetration, uncoating, replication, assembly and release. Influenza virions are transmitted in aerosols, tiny airborne droplets laden with virions, or from contact with contaminated hands or surfaces.
These are inhaled and deposited on the respiratory epithelium, specifically ciliated epithelial cells. The virus attaches via the hemagglutinin spikes to sialic acid on the surface of the plasma membrane of the cell. The receptor bound virus is brought into the cell by endocytosis in coated pits into endocytotic vesicles and finally endosomes. These endosomes are acidified by the cell. In the low pH environment of the endosome, the HA spikes are cleaved which causes a conformational change in the hemagglutinin. This change activates HA2 which causes the fusion of the viral lipid envelope with the endosome lipid membrane (Cann, 1999). The viral nucleocapsid is released into the cellular cytoplasm in a process called uncoating.
Once the virion has been uncoated, sequences in the NP protein result in the translocation of the nucleocapsid into the nucleus where transcription occurs. Transcription mechanisms used by orthomyxoviruses differ from other RNA viruses in that it occurs in the nucleus. The negative configuration of influenza virus A's RNA must first be transcribed, by the three polymerase polypeptides (PB1, PB2 and PA) that are associated with each segment of the viral genome, into a positive sense strand. Two types of positive sense RNA are made.
Viral mRNAs are transported into the cytoplasm where it uses host ribosomes to translate viral structural proteins such as hemagglutinin, neuraminidase, matrix proteins, and capsomeres (Cann, 1999). Viral cRNA remains in the nucleus where it codes for the synthesis of progeny negative sense RNA vRNA (viral RNA) (Voet and Voet, 1995).
Once all of the viral components have been transcribed, the assembly of virions can occur. Most of the proteins made in the cytoplasm remain in the cytoplasm. The envelope glycoproteins, hemagglutinin and neuraminidase that have been translated from viral mRNA, are inserted into areas of the host cell membrane. The nucleoprotein moves back into the nucleus and associates with the newly synthesised vRNA to form new nucleocapsids (Cann, 1999). Once associated, the nucleocapsid moves back into the cytoplasm and toward the cell membrane. The new nucleocapsids join with the glycoproteins in the membrane and bud through it. The newly formed virions are now free to infect other cells.
The viral life cycle does not occur without an immunological response from the host organism. Innate immune mechanisms restrict the early stages of infection and delay the spread of the virus. These defences include interferon, natural killer cells and macrophages. Natural killer cells appear within two days of viral infection and destroy infected cells early in the virus replication cycle before new virions appear (Roitt, Brostoff and Male, 1998).
Interferon (IFN) is a cytokine made by virus infected cells or activated T-cells that inhibits viral reproduction. This cytokine is able to do this by slowing protein synthesis in the infected cell by coding for various proteins. While most of the proteins have not been identified, RNA-activated protein kinase (PKR) is thought to have an important role in halting the shutdown of protein synthesis. PKR is normally present in cells and is thought to function as a tumour suppresser.
This enzyme phosphorylates one of the ribosomal initiation factors in eukaryotic cells, which prevents them from transcribing mRNA. As viruses require high levels of protein synthesis, they have developed mechanisms to avoid this immunological response. Viruses normally code for an enzyme that binds to PKR to prevent its activation. Influenza virus A is unique in that it uses the hosts own products and mechanism in halting the interferon response. This enzyme, a protein kinase named p58, is thought to be an oncogene that inhibits the activation of PKR, therefore viral protein synthesis is able to proceed (Garfinkel and Katze, 1994).
As influenza infection proceeds, the adaptive immune response activates cytotoxic T cells, helper T cells and antiviral antibodies, specifically immunoglobulin G and immunoglobulin A (IgG and IgA)(Roitt, Brostoff and Male, 1998). IgA is mainly produced at mucosal surfaces where it serves to prevent reinfection. IgG acts against the hemagglutinin and neuraminidase surface proteins and restricts the spread of the virus to neighbouring cells and tissues by neutralising virus infectivity (Roitt, Brosnoff and Male, 1998). While antibodies limit influenza virus A spread and reinfection, it is strain specific and is readily avoided by the virus.
One of the characteristics of influenza virus A is its ability to change. Small mutations that occur on a regular basis on hemagglutinin and neuraminidase spikes result in antigenic drift that the adaptive immune system, specifically memory B-cells, will have no response to. Antigenic drift occurs when amino acid substitutions occur due to random point mutations. These mutations occur when selective pressure on the virus is brought about by an increase in immunity in the host population (Voet and Voet, 1995).
In addition to this drift, a new strain of influenza virus A seems to appear every ten to forty years to which no one has immunity (Jawetz, Melnick and Adelberg, 1998). This is due to antigenic shift, in which there is a sudden major change in the HA and/or NA antigens.
Influenza virus A is susceptible to antigenic shift because of its genome and as it has the ability to infect a variety of mammals. Influenza virus A has eight separate strands of genetic material, RNA, which is considered to be less 'stable' than DNA and therefore more likely to mutate. The separate strands could easily be mixed in an animal infected with two strains of influenza. Deadly viral strains of influenza appear to occur where human, birds and swine live in close quarters. These conditions have long existed in Hong Kong, where several of the world's pandemics have appeared to originate.
Influenza virus A continues to infect approximately thirty percent of the world's population each year (Roitt, Brosnoff and Male, 1998). While most people do not die directly from influenza, the secondary complications like bacterial pneumonia and encephalitis lead to a high mortality rate in susceptible and immunologically compromised individuals. A pandemic may not function in this way. During the Spanish flu of 1918-20, the majority of the fatalities were healthy young people between the ages of twenty and forty-five. The influenza virus killed by damaging the lung tissue to such an extent that the patient died by drowning.
Influenza virus A is one of the most prevalent unconquered infectious diseases of the twentieth century.
Despite being one of the most intensely studied viruses, its chameleon-like nature with its ability to change its coat, has led to constant monitoring of the animals it infects, and the need to predict a new vaccination each year. Unlike other infectious viruses, such as polio, influenza virus A will likely never be eliminated because of its repository in other animals, and because of its ability to mutate into new antigenic strains.
The 1998 Hong Kong flu (H5N1) had the potential to be as devastating as the Spanish flu pandemic. It was seen as a wake up call, an imminent warning that the next pandemic is overdue. It is believed that the H5N1 virus can only be transmitted directly from birds to humans. This is the first known example of cross species infection (Laver, 1999).
The current fear of virologists and epidemiologists is that the deadly H5N1 flu may have been contracted by someone visiting Hong Kong during the epidemic. In this age of global travel, it would be easy for this carrier to meet with a virus that is easily transmitted. The combination of the two could be the genesis of the new pandemic. The question then is not 'if' another deadly global pandemic like the Spanish flu arises, but when.
Viruses constantly mutate, making them extremely adaptable. Tatyana threw out some good fact based numbers. I'm glad these numbers point out the absolute ludacracy of people freaking out about swine flu, avian flu, mad cow disease, etc. It just feeds into irrational fear that of course, is not fact based. The scary thing about the spanish flu strain was that it killed young and otherwise healthy adults. The flu generally is only detrimental to the elderly, the very young, or persons who already have compromised immune systems. With the swine flu, unless you come in contact with someone who is already infected (very unlikely), handle or come into contact with live pigs who are carrying the virus (even more unlikely), and don't have a compromised immune system, you probably shouldn't spend too much time worrying about it. Remember how absolutely ga ga everybody went about mad cow disease? I'm sure a great number of people went to their refrigerators and threw out their poultry when this swine flue "pandemic" started. Oh yes, mother nature has ways of taking us down a notch or two every once in awhile.
PICK3
New member
knot to mention something like 33k peeps a year buy it from regular flu in the U.S. every year
Creepusmaximus
New member
I simply don't care and I took Pick3's led and screwed a Mexican chick while eating a ham sandwich.
Whole thing is over blown.
Whole thing is over blown.
Razorguns
Well-known member
Nah. Before that, Simon will vote off the wrong person off American Idol. Riots will ensure, and people will kill each other in the streets. Mankind will end.
Dinosaurs, new smart ones, will then make their triupmhant return.
r
