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=Family: **//Orthomyxoviridae//**= toc

Introduction
Orthomyxoviridae is a single stranded RNA enveloped virus that is spherical in shape. This family includes the influenza virus which causes illness and death to thousands of people each year. The purpose of this Wikispace is to provide information about what exactly Orthomyzoviridae is, how it functions, and how it is fought.

Definition:
 Orthomyxoviridae ‘Ortho’ is the Greek for straight and ‘Myxa’ is the Greek word mucus. Orthomyxoviridae contains 7 segments to 8 segments of linear negative-sense single stranded RNA. Orthomyxoviridae includes Influenzavirus(A, B, and C), Isa virus, and Thogoto virus.

**Morphology**



 * Orthomyxoviridae is an enveloped virus that comes in pleomorphic and filamentous forms and can be spherical or filamentous; 50-120 nm in diameter, or 20 nm in diameter; 200-300(-3000) nm long.
 * Surface projections of envelope consist of about 500 spikes (projecting 10-14 nm from the surface); dispersed evenly over all the surface that include haemagglutinin and neuraminidase with a ratio of about 4 to 1.
 * The nucleocapsid is enclosed within lipoprotein membrane.
 * Nucleocapsids filamentous have no clear modal length; 50-130 nm long; 9-15 nm in diameter.

Physical and Physiochemical Properties

 * The molecular mass (Mr) of virions is 250 x106.
 * Virions have a buoyant density in sucrose 1.17 to 1.2 g cm-3.
 * The sedimentation coefficient of the fastest or only component is 700 to 800 S20w.
 * Under in vitro conditions virions are very, sensitive in the presence of ions.
 * Virions are sensitive to treatment with heat, lipid solvents, non-ionic detergents, formaldehyde, oxidizing agents.
 * The infectivity is reduced after exposure to irradiation.

Chemistry
**Nucleic acids** They are 80-120 nm in diameter and 200-300(-3000) nm long. The genome of the orthomyxovirus consists of six to eight segments of linear, negative-sense, single-stranded RNA. The complete genome is 10000-14600 nucleotides long. The genome has terminally redundant sequences and they are repeated at both ends. The multipartite genome is encapsidated with each segment in a separate nucleocapsid, and the nucleocapsids are surrounded by one envelope. **Lipids** Lipids are present and located in the envelope. Virions are composed of 18-37% lipids by weight. The composition of viral lipids and host cell membranes are similar. The lipids are modified cellular lipids and are derived from plasma membranes.  **Proteins**
 * ** Protein ** || ** Function ** ||
 * ** PB1 ** || Transcriptase: cap binding ||
 * ** PB2 ** || Transcriptase: elongation ||
 * ** PA ** || Transcriptase: protease activity ||
 * ** HA ** || Haemagglutinin ||
 * ** NP ** || Nucleoprotein: RNA binding; part of transcriptase complex; nuclear/cytoplasmic transport of vRNA ||
 * ** NA ** || Neuraminidase: release of virus ||
 * ** M1 ** || Matrix protein: major component of virion ||
 * ** M2 ** || Integral membrane protein - ion channel ||
 * ** NS1 ** || Non-structural: nucleus; effects on cellular RNA transport, splicing, translation. Anti-interferon protein. ||
 * ** NS2 ** || Non-structural: nucleus+cytoplasm, function unknown ||
 * ** NEP ** || Nuclear Export Protein ||

Life Cycle
Virus attaches to cell's sialic acid, small sugar, receptor with its surface protein Haemagglutinin. The virus is then absorbed into the cell where a lysosome degrades the nucleocapsid releasing the viral negative sense RNA so that it can enter the nucleus. This (-) RNA is then transcribed into (+) mRNA which goes on to produce proteins for both the virus progeny along with RNA replication. Positive sense RNA is also made for the (-) RNA, and goes on to produce progeny (-) RNA. The (-) RNA progeny condenses to form a new nucleocapsid as is moves to the outer edge of the cell where it will bud off using the host cell membrane.

The picture to the left shows once again the structure of Orthomyzoviridae. The picture to the right shows the replication cycle within the cell. It is important to note that replication occurs within the cell nucleus.



Hosts
All types of vertebrates Influenza-mainly Humans, Birds, and Pigs

Taxonomy
Group V: Negative sense ssRNA viruses
 * Family: Orthomyxoviridae
 * Genus: Influenzavirus A
 * Genus: Influenzavirus B
 * Genus: Influenzavirus C
 * Genus:Thogotovirus
 * Genus: Isavirus

**Pathology**
The major and most devastating for of Orthomyzoviridae is the influenza virus.

Influenza virus is transmitted from person to person primarily in droplets released by sneezing and coughing. Some of the inhaled virus lands in the lower respiratory tract, and the primary site of the disease is the tracheobronchial tree, although the nasopharynx is also involved. The neuraminidase of the viral envelope may act on the N-acetylneuraminic acid residues in mucus to produce liquefaction. This liquified mucus may help spread the virus through the respiratory tract in concert with the mucociliary transport. The superficial mucosa suffers cellular destrcution and desquamation because of the infection of the mucosal cells.

Infectivity of influenza virus particles is preserved depending on temperature, pH and salinity of the water, and UV irradiation. At 4°C, the half-life of infectivity is about 2-3 weeks in water. Due to the conformation of the lipid bilayer, survival under normal environmental conditions should be shorter. Infectivity of the influenza virus particle is easily inactivated by all alcoholic disinfectants, chlorine and aldehydes. As far as is known, temperatures above 70°C will destroy infectivity in a few seconds.

Host
Interferon appears in respiratory secretions shortly after viral titers reach their peak level, and may play a role in the subsequent reduction in viral shedding. Interferon does this by slowing protein production, destroying RNA, and increases antigen presentation both within the infected cells and the neighboring cells.

Antibody usually is not detected in serum or secretions of the virus until it has progressed past the initail infection. Local antibodies appear to be responsible for the final clearing of virus from secretions. T cells and antibody-dependent cell-mediated cytotoxicity also participate in clearing the infection.

Antibody is the primary defense in immunity to reinfection. IgG antibody, which predominates in lower respiratory secretions, appears to be the most important. The IgG in these secretions is derived from the serum, which accounts for the close correlation between serum antibody titer and resistance to influenza. IgA antibody, which predominates in upper respiratory secretions, is less persistent than IgG but also contributes to immunity.

Only antibody directed against the hemagglutinin is able to prevent infection. A sufficient titer of anti-hemagglutinin antibody will prevent infection. Lower titers of anti-hemagglutinin antibody lessen the severity of infection. Anti-hemagglutinin antibody administered after an infection is under way reduces the number of infectious units released from infected cells, presumably because the divalent antibody aggregates many virions into a single infectious unit. Antibody directed against the neuraminidase also reduces the number of infectious units (and thus the intensity of disease), presumably by impairing the action of neuraminidase against N-acetylneuraminic acid residues in the virion envelope and thus promoting virus aggregation. Antibody directed against nucleoprotein has no effect on virus infectivity or on the course of disease.

Viral
Since Orthomyzoviridae is a single stranded negative sense RNA it is easily recognized within the body. It is easily recognized because RNA within the body is rare to begin with let alone single stranded (-) RNA. Because the (-) RNA has to use several of its own components, the host can respond to it quicker.

Orthomyxoviridae's influenza strains have two proteins that are mainly responsible for its differentiation and ability to successfully infect host. There are 16 types for haemagglutinin, H, and 9 types of neuraminidase, N. There are three H types that successfully infect and transfer to other humans. If an other H type was to gain access and spread to other humans it would become an epidemic. The reason it would be an epidemic is because it would such a change from what the body is normally accustomed to that it would know how to fight back.

The is able to mutate at a high rate because it because not have a set template for replication. Without a template any errors that occur when the RNA is being replicated will not be corrected and will be replicated in progeny RNA. Once replicated, if it produces a useful RNA strand, the host most find a new way to fight the virus. The host response to the virus causes the virus to mutate faster to find a way to prolong its existence through antigenic drift. The virus's ability to spread to other vertebrates also plays to its advantage and allows it to mutate within a different host. This antigenic drift can turn into antigenic shift if it switches to a different H or N class than is normally in a found within a host. This normally happens within a different host. This allows for brand new strains of the virus to be made and transferred easily.

Orthomyxoviridae also contains a protein within it that allows it to combat and interfer with interferon signaling in the cell. This lessens the effect of the immune response to the virus, and allows the virus to spread to more cells easily.

Important Members
[|Influenza virus A] [|Influenza virus B] [|Influenza virus C] [|Isa virus] [|Thogoto virus]

Areas of Impact
This virus is easily spread and is constantly mutating which gives it the potential to be devastating to a community, and easily become an epidemic, especial influenza. Hospital receive millions of patients every year due to influenza strains. Because influenza spreads so easily flu shots are given out everywhere around "Flu Season" to help prevent the spread of this virus. Millions of dollars are spent each year on flu shots and flu vaccines which puts a high demand on manufacturers and researchers to find and produce the best vaccines. New vaccines have to be made each year do to the virus's ability to mutate so rapidly. There are also flu medicines that you can take as well which have a haemmaglutinin or neuraminidase inhibitor to either prevent the cell from entering the cell or prevent it from budding off. The prevalence of influenza has caused a great increase for scientific study of the virus, hospital visits, and the production of new antiviral medication form manufactures.

Hello my name is Derrick Shire and I am a Biology pre-Med major with a minor in chemistry at the University of Saint Francis Fort Wayne. I have made this Wikispace for my virology class that I am currently enrolled in. I enjoy long walks on the beach, laying on a blanket under the stars, and curling up next to a warm fire. I have been bungee jumping, spelunking in uncharted caves, and white water rafting. I actually really like this class and I can say the alphabet backwards in less than five seconds. Finally I enjoy schmoozing.

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