I enter the nerves of sick people and cause inflammation of the brain in humans and other animals. I am present in more than 150 countries, with more than 3 billion people in the regions of the world living where I live. In 2015 alone I caused approximately 17,400 deaths. I am the rabies virus. I belong to the Lyssavirus genus, which is composed of RNA viruses of the Rhabdoviridae family, order Mononegavirales. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay Like other Lyssaviruses, I have a negative-sense single-stranded RNA genome. I have two main structural components: a helical ribonucleoprotein (RNP) core and a surrounding shell. In my RNP, my genomic RNA is tightly enclosed by the nucleoprotein. My RNA genome encodes five genes: nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G), and viral RNA polymerase (L). The order of my five genes is highly conserved. My glycoprotein forms about 400 trimeric spikes that are neatly arranged on my surface. My matrix protein is associated with both the envelope and the RNP and may be the central protein of rhabdovirus assembly. Furthermore, like other Lyssaviruses, I have a helical symmetry, which gives me a cylindrical shape with a length of approximately 180 nm and a cross-sectional diameter of approximately 75 nm. One of my ends is rounded or conical and the other end is planar or concave. My lipoprotein envelope bears knob-shaped spikes composed of glycoprotein G. However, these spikes do not cover my planar extremity. Underneath my envelope is the membrane protein layer or matrix (M) which can be invaginated at the planar end. Once I am inside a muscle or nerve cell, I undergo replication. The trimeric spikes on the outside of my membrane interact with a cellular receptor, the most likely of which is the acetylcholine receptor (an organic chemical that functions in the brains and bodies of many types of animals as a neurotransmitter). The cell membrane then pinches in a procession known as pinocytosis and allows me to enter the cell through an endosome. Using the acidic environment of the endosome, I then simultaneously bind to its membrane, releasing my five proteins and single-stranded RNA into the cytoplasm. The L protein I released then transcribes five strands of mRNA and one positive strand of RNA, all of which come from my original negative strand of RNA, using free nucleotides in the cytoplasm. The five mRNA strands are then translated into their corresponding gateins (P, L, N, G, and M proteins) which are retained in free ribosomes in the cytoplasm. Some of my proteins require post-translational modifications. For example, my G protein travels through the rough endoplasmic reticulum, where it undergoes further folding, and is then transported to the Golgi apparatus, where a sugar group is added to it (glycosylation). Where there are enough proteins, my polymerase enzyme will begin to synthesize new negative strands of RNA from the template of the positive strand of RNA. These negative strands will then form complexes with my N, P, L, and M proteins and then travel to the inner membrane of the cell, where my G protein has incorporated itself into the membrane. My G protein then wraps itself around the NPLM protein complex bringing with it part of the host cell membrane, which will form the new outer envelope of the viral particle that I will also become. At this point, the virus sprouts from the cell, creating a duplicate of me. From the entry point, I (a new version of myself as a virus) amneurotropic and travel rapidly along neural pathways to the central nervous system. I usually first infect muscle cells close to the site of infection, where they are able to replicate without being "noticed" by the host's immune system. Once enough of me has been replicated, I and the replicas begin to bind to acetyl choline receptors (p75NR) on the neuromuscular junction. After doing so, we (all replicated versions of me) then travel down the axon of the nerve cell via retrograde transport, as our P proteins interact with dyneins, which are proteins found in the cytoplasm of the nerve cells. Once we reach the cell body, we travel rapidly to the central nervous system (CNS), replicating in motor neurons and finally reaching the brain. After the brain is infected, we travel centrifugally to the peripheral and autonomic nervous systems, eventually migrating to the central nervous system. salivary glands, where I (as a virus in general) am ready to be transmitted to the next host. All warm-blooded species, including humans, have the potential to become infected with me and develop symptoms. Furthermore, I have also been adapted to grow in cells of poikilothermic ("cold-blooded") vertebrates. Most of the animals infected by me have the ability to transmit the disease to humans. Of all the animals that pose a possibility of infection, bats, monkeys, raccoons, foxes, skunks, cattle, wolves, coyotes, dogs, mongooses, and cats pose the greatest risk to humans . Small rodents, such as squirrels, hamsters, guinea pigs, gerbils, chipmunks, rats, mice, and lagomorphs such as rabbits and hares, are almost never infected by me, and therefore are not known to transmit rabies to humans. They are usually present in the nerves and saliva of an animal showing signs of rabies. Therefore, the route of infection is usually, but not always, via a bite. In many cases, the infected animal is exceptionally aggressive, may attack without provocation, and displays otherwise unusual behavior because I have modified the host's behavior to facilitate my transmission to other hosts. Transmission of the virus between humans is extremely rare, but some cases have been recorded through transplant surgeries. During the phase in which it travels to the host's nervous system after a bite, the virus cannot be easily detected and vaccination can still ensure cell-mediated immunity to prevent the onset of rabies. However, after reaching the brain, it quickly causes encephalitis, or inflammation of the brain due to infection. This is the stage where symptoms begin. Once the patient becomes symptomatic, treatment is almost never effective and mortality is greater than 99%. Symptoms in humans typically appear one to three months after I cause the infection; however, this time period can range from less than a week to more than a year. The time depends on the distance I have to travel along the nerves to reach the central nervous system. Early symptoms may include fever and tingling at the site of exposure, followed by mild or partial paralysis, terror, abnormal behavior, confusion, anxiety, paranoia, agitation, insomnia, and hallucinations progressing to delirium and coma. During the later stages of my infection, any infected mammal may also exhibit hydrophobia (“fear of water”). When experiencing hydrophobia, symptoms include showing panic when presented with liquids to drink, difficulty swallowing, and an inability to quench one's thirst. When you suffer from hydrophobia, saliva production increases significantly and attempts to drink, or 8%.