INFLUENZA is also known as grippe or flu, an infectious disease. A number of viruses are found responsible for causing flu. These viruses belong to orthomyxoviridae family. Due to its structural protein such as internucleotide protein and matrix protein, the virus are divided into three types INFLUENZA A, INFLUENZA B, INFLUENZA C. Two proteins namely hemagluttinin and neuraminidase helps the virus influenza A to bind to any cell and cause the viral infection [1, 2]. Among these types influenza A is responsible for causing flu in human beings. Entry into to the body is through mouth and nose. The virus is covered by a coat which encloses seven to eight ssRNA. Influenza has sloppy character which means that influenza from one strain can incorporate genetic material from other strain. The organism which easily gets infected by any type of influenza becomes mixing site for all the influenza virus and leads to the formation of novel strain. Cytotoxic T lymphocytes (CTLs) which is specific for conserved viral antigens has the capacity to respond to different strains, in contrast to antibodies, which are generally strain-specific. The mechanism to generate such CTLs in vivo usually requires endogenous expression of the antigen, which occurs in the case of virus infection. This resulted in the generation of nucleoprotein-specific CTLs and protection from a subsequent challenge with a heterologous strain of influenza A virus. Based on their antigencity influenza A are also sub-divided (sub divided into ???) and currently the class H1N1 and H3N2 are in circulation (where in circulation??) [1, 2, 4, 5].
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Fig.1: Influenza virus A
Fig.2: 3-D model of influenza virus 
There are RNA viruses which lead to influenza in human and also in animals and birds. Influenza is found more severe than common cold and has lead to a mortality rate of 0.1% in human . Influenza has been divided into two types known as conventional influenza and seasonal influenza. Seasonal influenza occurs in winter [2, 3]. In history, it has been found that there were times when flu over breaks was severe. It is predicted that the situation becomes severe when there is no immunity against a virus strain. It was in 1933 when influenza virus was identified. It is reported that in 1918, there was wide cut break in which morbidity due to influenza ranged from 2% to 20% [2,6,9]. In April 2009, in Mexico a new strain was found against which the humans were having no immunity. It quickly spread throughout the world so fast that the WHO declared this new flu strain (termed novel H1N1 influenza A swine flu, often shortened to H1N1 or swine flu) as the cause of a pandemic on June 11, 2009. This was the first declared flu pandemic in 41 years [6,11].
Genetics of influenza virus:
The influenza A virus is an enveloped particle containing eight separate gene segments of single stranded, negative sense RNA which code for seven viral and three non structural proteins. Only two of the viral proteins, the haemagluttanin and neuraminidase are found on the surface of the virion. Both are anchored in the viral membrane and project out from viral surface, both are glycosylated and both exhibit major and minor changes in antigenecity during the evolution of new virus strains. The primary and secondary structural changes associated with antigenic reactions are to be established [5, 6]. Peptide maps and nucleotide sequences (150 to 300 residues long) from the 3'end of the neuraminidase gene have been used to partially characterize antigenic shift and drift but whole sequences are required if .(the sentence is incomplete)
Fig.3: Genetics of influenza virus (rather give explanation for this diagram)
Structure of influenza virus:
Influenza virion is around 200nm in diameter. Its envelope has "spikes" of haemogglutanin and neuraminidase. The helical ribonucleic protein is not often seen . ONLY THIS MUCH INFORMATION FOR STRUCTURE? WHAT ABOUT THE EXPLANATIONS OF THE PARTS OF THE VIRUS AS IN DIAGRAM??
Fig.4: Structure of influenza virus
Molecular structure of Haemogluttanin acid (HA) molecule:
Haemogluttanin acid is found in membrane of the virus and structurally it is homotrimeric membrane glycoprotein. It is cylindrical in shape and is approximately 13.5 nanometers long. These three identical monomers are combined and constructed into a central Î± helix coil; three spherical heads contain the sialic acid binding sites. HA monomers are synthesized and then cleaved by protease into HA1 and HA2 subunits [1, 5].
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Two proteins from HA1 and HA2 fuse to form a single protein which allows fusion to change the confirmation that allows viral infectivity.
Arginine is removed and the two domains combine to form a double bonded disulphide protein domain
(WHAT IS TRANSLATED) Translated in cell as a single protein
Haemagluttinin as a trimmer with receptor binding pockets.
Fig.5: Shows the pathway for the formation of HA (haemagluttanin acid)
* Influenza B virus is responsible for causing disease in human and it is found in human only.
MECHANISM OF VIRUS CAUSING INFLUENZA
Fig.1: Pathway showing the pathogenecity of influenza virus
The virus attaches itself to the host cell wall with the help of attachment site on surface of the virus known as virus receptor. The receptor sites on the host cell surface known as host cell receptor [3, 6]. Cells lacking receptor for a certain virus are resistant to the virus and so cannot be infected . The attachment can be blocked by antibody molecules that bind to the viral attachment sites or host cell receptors to influenza haemagglutinin. There are 16 known haemagglutinin types H1 to H16. HA (haemogluttaminic acid) binds to the sialic acid which is present on the surface of the target host cells . HA are proteins that possess specific affinity for certain sugar molecules. Since carbohydrates moieties exist in most animal cell membranes, they may attach themselves to receptor groups if the specific structure of the latter is suitable. Haemaglutinins or lectins can be characterized and detected by their capability of agglutinating the red blood cells. The interaction of haematogglutinin with the glycoprotein on the cell surface is manifested in vitro by agglutination of cells. [1, 6, 6]. Entry of the cell is guided by the binding of virus receptor protein to host receptor protein (HA spikes) to mucoproteins containing N-acetylnuraminic acid groups. After binding, the particle is engulfed by endocytosis via coated pits into endocytotic vesicles and finally endosomes. After the virion attaches to sialic-acid (neuraniminc acid) containing receptors on the cell surface, the formation of this complex and the virus is engulfed in the cell which is known as endocytosis. After entering the cell, the endosomal vesicles contain virus particles that move towards the cell nucleus. Now there is a fusion peptide on the HA is formed that insert in the endosomal membrane and fuses with the membrane of virus. When this occurs the viral RNA is released in the environment. Then this RNA material is sent to the cell nucleus where the RNA replication starts. The viral RNAs are not naked, but bound to a number of viral proteins. One of these proteins is M1 protein. If RNAs bind to M1 protein, they fail to enter the nucleus. Then that time they uses anew protein on their cell surface known asM2 .these viral protein forms a channel in the membrane that actively pumps proton from the endosome into the interior of the virion. These proton lower the pH in the interior of the virion, releasing the viral RNAs from M1. In this way RNA can enter the nucleus . Viruses have this characteristic feature to replicate widely throughout the body without causing any disease symptoms, if they do not cause significant cell damage or death. Although retroviruses (e.g. HIV) do not generally cause cell death, being released from the cell by budding rather than by cell lysis, they cause persistent infections and may be passed to offspring if they infect the germ line.Â Conversely, most other viruses, referred to as virulent viruses, ultimately damage or kill their host cell by several mechanisms, including inhibition of synthesis of host cell macromolecules, causing damage to cell lysosomes, altering the cell membrane the cell membrane, development of inclusion bodies, and induction of chromosomal aberrations[4,5,6].
Fig.6: Process occurring in the endosome
Fig.8: Process of replication of virus inside the host cell.
Influenza A rarely causes death. Infection with influenza is common among human population. So there comes the need for preventing this flu from spreading in large mass. This can be performed at cell level. After studying the mechanism of pathogenesis of influenza it can be suggested that any modification done in the virus or receptors of the virus can control the infection from flu viruses.
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