I enter the nerves of sick people and cause inflammation of the brain in humans and other animals. I operate in over 150 countries, with over 3 billion people living in the parts of the world where I operate. In 2015 alone, I caused approximately 17,400 deaths. I am the rage virus. I belong to the genus Lyssavirus, which is composed of RNA viruses of the family Rhabdoviridae, order Mononegavirales. Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay Like other lyssaviruses, I have a single-stranded RNA genome with a negative sense. I have two major structural components: a helical ribonucleoprotein (RNP) core and a surrounding shell. In my RNP, my genomic RNA is tightly enclosed within the nucleoprotein. My RNA genome encodes all 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 tightly arranged trimeric spikes on my surface. My matrix protein is associated with both the envelope and the RNP and may be the core protein of rhabdovirus assembly. Additionally, like other lyssaviruses, I have helical symmetry, giving me a cylindrical shape with a length of approximately 180 nm and a transverse diameter of approximately 75 nm. One of my ends is rounded or conical and my other end is flat or concave. My lipoprotein envelope bears button-like spikes composed of glycoprotein G. However, these spikes do not cover my planar extremity. Beneath my envelope is the membrane or matrix protein layer (M) which can be invaginated at the planar end. Once I'm in a muscle or nerve cell, I undergo replication. The trimeric spikes on the outside of my membrane interact with a cellular receptor, most likely being the receptor for acetylcholine (an organic chemical that functions as a neurotransmitter in the brains and bodies of many types of animals). The cell membrane then pinches during a process called pinocytosis and allows me to enter the cell via 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 strand of positive RNA, all of which come from my original negative-strand RNA, using free nucleotides in the cytoplasm. The five mRNA strands are then translated into their corresponding porteins (P, L, N, G and M proteins) which I maintain at 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 then is transported to the Golgi apparatus, where a sugar group is added to it (glycosylation). Where there is enough protein, my polymerase enzyme will begin to synthesize new negative RNA strands from the positive strand RNA template. These negative strands will then form complexes with my N, P, L and M proteins and then move towards the inner membrane of the cell, where my G protein has embedded itself in the membrane. My G protein then wraps itself around the NPLM protein complex, taking with it part of the host cell membrane, which will form the new outer shell of the virus particle that I will also become. At this point, the virus then exits the cell, creating a duplicate of me. From the entry point, I (a new version ofmyself as a virus) am neurotropic, traveling rapidly along neuronal pathways to the central nervous system. I usually first infect muscle cells near the site of infection, where I am able to replicate without being "noticed" by the host's immune system. Once enough of me has been replicated, the replicas and I begin to bind to acetylcholine receptors (p75NR) at the neuromuscular junction. After that, we (all replicated versions of me) then travel through the nerve cell axon via retrograde transport, because our P proteins interact with dyneins, which are proteins found in the cytoplasm of nerve cells. Once we reach the cell body, we quickly travel to the central nervous system (CNS), replicate in motor neurons, and finally reach the brain. Once the brain is infected, we travel centrifugally to the peripheral and autonomic nervous systems, eventually migrating to the salivary glands, where I (as the overall virus) are then ready to be transmitted to the next host. All warm-blooded species, including humans, have the possibility of becoming infected by me and developing symptoms. Additionally, I have also been adapted to grow in cells of poikilothermic (“cold-blooded”) vertebrates. Most animals infected by me have the ability to transmit the disease to humans. Of all the animals that can be infected, bats, monkeys, raccoons, foxes, skunks, cattle, wolves, coyotes, dogs, mongooses and cats pose the greatest risk for humans. Small rodents, such as squirrels, hamsters, guinea pigs, gerbils, chipmunks, rats, mice, and lagomorphs like rabbits and hares, are almost never infected by me and are therefore not known to transmit rabies to humans. I am usually present in the nerves and saliva of an animal showing signs of rabies. Therefore, the route of infection is usually, but not always, through a bite. In many cases, the infected animal is exceptionally aggressive, may attack without provocation, and exhibits otherwise unusual behavior as I modify the host's behavior in order to facilitate my transmission to other hosts. Transmission of my disease between humans is extremely rare, but a few cases have been recorded during transplants. During the phase where I travel to the host's nervous system after a bite, the virus cannot be easily detected and vaccination can still give cell-mediated immunity to prevent the onset of rabies. However, once I reach the brain, I quickly cause encephalitis, or inflammation of the brain due to infection. It is at this stage that symptoms begin. Once the patient becomes symptomatic, treatment is almost never effective and mortality exceeds 99%. Symptoms in humans usually appear one to three months after causing the infection; however, this time frame can vary from less than a week to more than a year. The time depends on how far 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 demonstrate hydrophobia (“fear of water”). Symptoms of hydrophobia include panic when 8%.