Presentation on theme: "RABIES Kiki Turner & Kate Hewitt. History of Rabies The virus has been around for centuries, the first written record of a case was in 1930 BC. In."— Presentation transcript:
History of Rabies The virus has been around for centuries, the first written record of a case was in 1930 BC. In 1960 the virus was isolated. Louis Pasteur was the one to isolate the virus.
Characteristics of Rabies The virus is able to replicate in all warm blooded animals, but also ones of poilkilothermic vertebrates The virus causes inflammation of the brain It is caused by a bite from an infected animal Rabies makes its way up to the brain by following peripheral nerves
Structure of Rabies The virus is bullet shaped and is 180 nanometers long and 75 nanometers wide. It is made up of proteins like the matrix protein, glycoproteins, and ribonucleoproteins. The virus has a helical ribonucleoprotein core, encased in a membrane called the envelope. It has cocentric layers. The virus is firmly twisted, enclosed in RNA
Host Cells and Rabies The virus is first transmitted by an infected animal biting another mammal. The virus enters the cytoplasm of its chosen cell via pinocytosis. Membranes fuse, releasing the virus into the cytoplasm. Once the virus is in the body, it enters the peripheral nervous system, and travels along nerves toward the central nervous system. The host cells for Rabies are the brain and spinal cord cells. The Rabies virus survives by forcing its host cell find another host for it.
Rabies Genome The rabies virus contains ssRNA. Rabies is has nonsegmented, negative-stranded RNA. The Rabies genome codes for five proteins: nucleoprotein, phosphoprotein, matrix protein, glycoprotein, and polymerase.
Rabies Genome Replication/Translation Genome replication takes place in the cytoplasm. Messenger RNA must be transcribed to permit virus replication. “A viral-encoded polymerase (L gene) transcribes the genomic strand of rabies RNA into leader RNA and five capped and polyadenylated mRNAs, which are translated into proteins. The intracellular ratio of leader RNA to N protein regulates the switch from transcription to replication. When this switch is activated, replication of the viral genome begins. The first step in viral replication is synthesis of full- length copies (postive strands) of the viral genome. When the switch to replication occurs, RNA transcription becomes "non-stop" and stop codons are ignored. The viral polymerase enters a single site on the 3’ end of the genome, and proceeds to synthesize full-length copies of the genome. These positive strands of rabies RNA serve as templates for synthesis of full-length negative strands of the viral genome.” - http://www.cdc.gov/rabies/virus.htmlhttp://www.cdc.gov/rabies/virus.html
Rabies assembly and exit For the assembly process, the proteins come together to form an RNP-m core. This core migrates along the plasma membrane toward glycoproteins and begins to coil. From this, the completed virus is formed from the plasma membrane, within the central nervous system. The rabies virus instructs its host cell to create new rabies cell components, as described above. The parts gather, and the cell overfills, lysing/bursting and setting the newly created rabies cell free.
Symptoms The primary symptoms of rabies are flu-like symptoms for anywhere from two weeks to two years. Others are slight or partial paralysis, insomnia, confusion, hallucinations, paranoia, anxiety, cerebral dysfunction, The later stages include hydrophobia (trouble swallowing due to paralysis) and the inability to quench thirst which then results in foaming of the mouth. Rabies can be fatal.
Treatments Treatment is a post-exposure round of shots. After bite, patients are given one dose of immunoglobin and five doses of rabies vaccines over 28 days. Half of the immunoglobin is injected into the immediate area of the bite, while the other half is injected into the arm or leg. The rabies vaccine is given as soon after the bite as possible, and then on days 3, 7, 14, and 28.
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