var _gaq _gaq = genome consists of single-stranded RNA mold. Virulence of influenza there are three main types, named A, B, C. The main difference lies in the proteins of the major capsid nucleocapside.Le caratteistiche conferitici are two proteins found in extensions known as the spike protein. One is called hemagglutinin, the other neuraminidase. The first is also the rincpale protein on the surface of the virus, is also the main site of AACC by antibodies. It is also the protein that shows increased genetic drift, and it is precisely the root cause of the continuing development of new strains, so every year we end up with new vaccines.
The influenza virus is a dangerous enemy. Normally the immune system fights viral infections by killing the virus for several days and causing the annoying symptoms of influenza. Each year, influenza vaccines activate the immune system to enable it to fight the most common flu viruses. About every twenty years, it appears that a new flu strain is much more virulent than those pitches, and then spread with great rapidity. This happened, for example, at the end of World War causing a pandemic (known as English), which has killed more than 20 million people, more than twice as many people who were death in war.
Hook the target and attack
The hemagglutinin is one of the factors that make the virus so effective. It 's a tip-shaped protein that extends out from the surface of the virus. In the active form shown here, 1ruz PDB file, the hemagglutinin consists of two different types of chains shown in blue and beige. The chains are blue the latching mechanism of the target, looking for particular sugar chains on the cell surface. When found, the hemagglutinin binds to, thus engaging the virus to the cell, then the chains beige begin the attack, as shown on the next page. The name
hemagglutinin refers to the ability of influenza virus to agglutinate red blood cells: the virus is covered with several hemagglutinin molecules that can bind many red blood cells, creating a lump so large as to be visible.
Subtypes hidden
The specificity and thus the hazard of each strain of influenza virus hemagglutinin depends on the particular type he has. They know more than a dozen subtypes of hemagglutinins. Three of these, called H1, H2 and H3 (H is the original English name of hemagglutinin), attacked the man because they are able to recognize specific sugars on the surface of some cells in our section respiratory infection that's why we started there when the flu. 
Other subtypes such as H5, attack glycoproteins found in the digestive system of birds. Most of these subtypes is not dangerous to humans and not even the threat of bird life and thus constitutes a kind of hidden reservoir of virus. A potential danger, however, may come from the exchange of genes between different strains.
Other subtypes such as H5, attack glycoproteins found in the digestive system of birds. Most of these subtypes is not dangerous to humans and not even the threat of bird life and thus constitutes a kind of hidden reservoir of virus. A potential danger, however, may come from the exchange of genes between different strains. The H5N1 bird flu virus that has come to the front pages during this period, which is decimating the bird population, but is not currently a real danger to humans because they do not have the right to hemagglutinin attack human cells. (The acronym refers to an N1 subtype of a second viral protein surface: neuraminidase that the virus uses to break away from the infected cell and spread the infection). However, there is the possibility that the virus could acquire a hemagglutinin-specific man, and then we can cause real problems. This might, for instance, by pigs. Indeed, the latter are susceptible to both avian viruses to humans that. In cases where a pig was infected simultaneously by both types of virus, they may exchange genes during infection. In this way you could create a new virus with the virulence of avian viruses and more with the ability to attack human cells.
The hemagglutinin shown here has been derived from the virus causing the pandemic that has killed so many people in 1918, the English. The DNA coding for this hemagglutinin was isolated from samples stored and the hemagglutinin was synthesized in the laboratory in accordance with such genetic information. We have obtained two crystal structures, the active form shown here (PDB file 1ruz), and a precursor of the hemagglutinin, not shown (PDB file 1rd8). 
The protein is attached to the viral membrane by a short filament protein that can not be seen in the crystal structure and that there is schematically represented by the segments beige below.
haemagglutinin in action 
The protein is attached to the viral membrane by a short filament protein that can not be seen in the crystal structure and that there is schematically represented by the segments beige below. The hemagglutinin is a ruthless molecular machine that engages and kills the cells. This process is accomplished in multiple steps.
In the first, the three binding sites on the top of the protein bind to sugars of some cell membrane glycoproteins shown in green in the top left of the figure (PDB file 1hge).
In the second step, the virus enters the cell by endocytosis, ie, the host cell as an endosome, intussusception of the cell membrane, which tries to digest the virus, creating an acid environment. The virus, however, resisted this attack, even the acid environment necessary for him to trigger the mechanism of its counterattack to the cell. Thanks to its acid, hemagglutinin opens and folds up taking a completely different structure. Slices of orange and red are usually tucked inside the protein, but are worn out in acid as shown in the middle of the figure above (PDB file 1htm, 1ibn, 2vir). The red portion is called fusion peptide, has a great affinity for membranes, it is part of the cell membrane and it clips securely to the virus.
In the third step, as shown on the right side of the figure (fike 1qu1 PDB), the portions are wrapped up as orange yellow contract and that makes the protein and forces the two membranes to approach almost to toccasi with each other. Finally, the two membranes fuse and the viral RNA enters the cell beginning the process of infection.
course viruses develop strategies to escape the attack of the antibodies and thus are born every year new strains still able to infect. One strategy is to change the arrangement of carbohydrates on the hemagglutinin surface. These carbohydrates are shown in green in Fig. If the virus adds a new carbohydrate at the point where the antibody is bound, in the future to prevent quell'anticorpo to bond and have made it ineffective.
PDB
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