What Is Type A Flu – Influenza A virus (IAV) causes influenza in birds and some mammals and is the only alphainfluzavirus species in the Orthomyxoviridae virus family.
All subtypes of the influenza A virus have been isolated from wild birds, although the disease is rare. Some isolates of the influenza A virus cause serious disease in poultry and rarely in humans.
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Viruses are sometimes transferred from wild waterfowl to poultry, and this can cause an outbreak or pandemic of human influenza.
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Influenza A viruses are single-stranded negative segmented RNA viruses. The different subtypes are labeled according to the H number (hemagglutinin type) and N number (neuraminidase type). There are 18 different H-recognized antibodies (H1 to H18) and 11 different N-recognized antibodies (N1 to N11).
Each virus subtype has evolved into different entities with different pathological profiles; some are pathological to one species but not others, some are pathological to several species.
A refined and purified influenza A vaccine has been developed for humans and many countries are stockpiling to allow rapid administration to the population in the event of an avian influenza pandemic. Bird flu is sometimes called bird flu and bird flu colloquially. In 2011, researchers announced the discovery of an effective antibody against all types of influenza A virus.
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Influenza A viruses are RNA viruses that are divided into subtypes based on the type of two proteins on the surface of the virus:
N = neuraminidase, the enzyme that cleaves the glycosidic bonds of sialic acid monosaccharide (formerly known as neuraminic acid).
Hemagglutinin is involved in virus recognition and binding to target cells, as well as the infection of the cell with RNA. Neuraminidase, on the other hand, is essential for the further release of daughter virus particles produced in an infected cell so that they can spread to other cells.
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Different influenza viruses encode different hemagglutinin and neuraminidase proteins. For example, the H5N1 virus is an influenza A subtype that has a type 5 hemagglutinin (H) protein and a type 1 neuraminidase (N) protein. There are 18 known types of hemagglutinin and 11 known types of neuraminidase, so theoretically 198 different combinations of these proteins can be used.
Certain variants are identified and named according to the isolates they resemble, and are therefore assumed to share a common ancestor (for example, like the Fujian influenza virus); according to their typical host (for example, human influenza virus); according to their subtype (for example H3N2); and according to their terms (for example LP, pathological low). Thus, influenza caused by a virus similar to the A/Fujian/411/2002(H3N2) isolate is known as Fujian influenza, human influenza, and H3N2 influenza.
Variants are sometimes named after the species (host) to which the strain is endemic or to which it has adapted. The main differences referred to in this convention are:
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Most of the known strains are extinct strains. For example, the strain that caused the Hong Kong flu is no longer in the annual H3N2 flu subtype.
Annual influenza (also called “seasonal flu” or “human flu”) causes about 36,000 deaths and more than 200,000 hospitalizations in the United States each year. In addition to this number of people, the flu costs a total of more than $10 billion in the United States each year.”
The trivalent influenza vaccine, which is updated annually, consists of components of the surface glycoprotein hemagglutinin (HA) of H3N2, H1N1 and B influenza viruses.
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Measured resistance to the standard antiviral drugs amantadine and rimantadine in H3N2 increased from 1% in 1994 to 12% in 2003 to 91% in 2005.
“Modern H3N2 human influenza viruses are now endemic in pigs in southern China and H5N1 avian viruses may reoccur in this intermediate host.”
In 2011, FI6, an antibody directed at the hemagglutinin protein, was discovered. FI6 is the only known antibody that is effective against all 16 subtypes of the influenza A virus.
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Transmission electron microscopy (TEM) reconstruction of the 1918 pandemic influenza virus. The lower structure protects the remnants of the cell membrane used to amplify the virus.
The image shows elliptical particles that represent the smallest particles produced by the flu virus. Cleaning methods often deform particles without proper fixation protocols, leaving them with a “spherical” appearance.
Filamentous or medium-sized particles simply extend along the longitudinal axis on opposite sides of the gome segments.
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A virus particle (also called a virion) is 80-120 nanometers in diameter, so the smallest virions take on an elliptical shape.
The length of each particle varies greatly because influenza is pleomorphic and can span several micrometers to produce filamentous virions.
Confusion about the nature of influenza virus pleomorphy stems from the belief that laboratory-adapted strains usually lose the ability to form filaments.
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Despite these different shapes, the location of all influenza A viruses is similar. They all consist of a viral rim with two major types of proteins wrapped around a central core.
The two major proteins found on the outside of viral particles are hemagglutinin (HA) and neuraminidase (NA). HA is a protein that mediates the binding of the virion to target cells and the delivery of the viral gene to the target cell. NA participates in the release of abundant unproductive sites of attachment that remain in the mucosa
In addition, they are also antigenic proteins that can bind the host’s antibodies and trigger an immune response. Influenza A viruses are classified into subtypes based on the types of these two proteins on the surface of the viral periphery. There are 16 known subtypes of HA and 9 subtypes of NA, but only H 1, 2 and 3 and N 1 and 2 are commonly found in humans.
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The central core of the virion contains the viral gome and other viral proteins that package and protect the genetic material. Unlike the genomes of most organisms (including humans, animals, plants, and bacteria), which are composed of double-stranded DNA, many viral genomes are composed of a different single-stranded nucleic acid called RNA. But unusually for viruses, the genome of the influenza A virus is not a single piece of RNA; rather, it consists of segmented pieces of negative-sense RNA, each containing one or two GEs that encode the product of the GE (a protein).
The term negative-sense RNA simply means that the RNA genome cannot be directly translated into protein; it must first be transcribed into positive sse RNA before it can be translated into protein products. The compartmentalized nature of Gome allows base genes to be exchanged between different types of viruses.
The Influza A virus base is 13,588 bases long and is contained in eight RNA segments that encode at least 10 but up to 14 proteins, depending on the strain. The suitability or effectiveness of alternative ge products may vary:
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Viral gome RNA segments have additional basic sequences at their ds-termini that allow them to hydrogen bond with each other.
The viral (-) to gome (vRNA) can only be transcribed after the PB2 protein binds to the host RNAs, allowing the PA subunit to cut a few nucleotides after the cap. This host-derived cap and accompanying nucleotides act as a primer to initiate viral transcription. Transcription proceeds along the vRNA until a few uracil bases are reached, initiating stuttering, in which the infectious viral mRNA is polyallylated to produce a mature transcript for nuclear export and translation at the host machinery.
RNA synthesis occurs in the nucleus of the cell, while protein synthesis occurs in the cytoplasm. Once the viral proteins are assembled into virions, the assembled virions leave the nucleus and move towards the cell membrane.
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The host cell membrane has patches of viral transmembrane proteins (HA, NA, and M2) and an underlying M1 protein layer that helps the assembled virions pass through the membrane, releasing proviruses into the extracellular fluid.
Influenza A virus subtypes were thought to have diverged about 2,000 years ago. Influenza A and B viruses are thought to have diverged from a common ancestor about 4,000 years ago, and the ancestors of influenza A and B viruses and the ancestor of influenza C are thought to have diverged from a common ancestor about 8,000 years ago. long ago.
If there are lesions in any of the eight RNA strands that make up the gome that prevent replication or expression of the ge esstial, the virus is not viable when it infects a single cell (single infection). However, when two or more damaged viruses infect the same cell (multiple infection), viable prophylaxis can be produced, provided that the eight gummy segments are preserved in at least one undamaged copy. This means that reactions can happen over and over again.
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Upon infection, the influenza virus triggers a host response involving increased production of reactive oxygen species, which can damage the virus.
Although viral persistence is normally vulnerable to oxidative damage under natural conditions, multiple reactivation is likely to be selectively beneficial as a type of repair process. It has been suggested that multiple reactivations associated with segmented RNA genomes may be similar to earlier
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