Rabies has been around since 2,300 B.C. and is a zoonotic neurotropic viral disease that affects all warm-blooded animals. Rabies virus falls under the family Rhabdovirus and is caused by Lyssaviruses. The genus Lyssavirus contains seven genotypes that all produce rabies-like viruses. There are variants for rabies virus transmission that can vary from various geographical areas. The rabies virus is a single stranded, negative-sense, bullet shaped, enveloped, RNA genome that encodes five genes: nucleoprotein, phosphoprotein, matrix protein, glycoprotein, and the viral RNA polymerase. The nucleoprotein is one of the most important genes and has a vital role in replication and transcription. If the nucleoprotein is not phosphorylated, both the replication and transcription process will be reduced. Glycoprotein is another important gene, which is an antigen responsible for the induction of virus-neutralizing antibodies. The rabies virus attacks both the brain and central nervous system and is excreted via the saliva. In most cases a clinical rabies infection will result in death. In 1885, Louis Pasteur created the first vaccine for rabies. Rabies occurs in more than 150 countries and almost 55,000 people die because of rabies each year. In most countries, canine rabies is the cause for the majority human rabies cases.
Viral Characteristics and Their Relationship to Clinical Signs and Disease Control
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Rhabdoviruses are stable in the environment (especially when the pH is alkaline). The rabies virus is able to persist in frozen temperatures, although, it can easily be inactivated by detergent-based disinfectants, chemicals, and ultraviolet radiation. There are a wide variety of reservoirs for the rabies virus, which vary throughout the world such as raccoons, skunks, and bats. In the natural hosts of rabies, the virus can persist and shed for an extent amount of time, without causing disease.
The transmission of rabies occurs through the bite of a rabid animal or by virus-infected saliva contaminated scratch wound. The virus enters the peripheral nerves through sensory or motor nerve endings. The virus binds to either nerve or muscle cells via a nicotinic acetylcholine receptor located in the neuromuscular junction. The virus enters the host by fusion of the viral envelop to the cell membrane of a host cell. The virus remains at the site of inoculation for an extended period of time while replicating in the muscle cells. Replication occurs within the cytoplasm but is slow-acting since the rabies virus does not stop host cell protein and nucleic acid synthesis. This whole process occurs without causing clinical signs and is considered the incubation period.
The prodromal phase occurs before the onset of clinical disease and is characteristic of a change in the animalââ‚¬â„¢s temperament. The neuronal infection of the viral genome travels down the axons by retrograde transport and is delivered to the central nervous system. During the prodromal phase, the virus spreads to the brain, and magnifies the amount of virus by infecting the Schwan cells. Infection of the brain leads to encephalitis. Once the virus reaches the limbic system of the brain it begins to replicate extensively. This causes the clinical fury to occur due to the release of cortical control of behavior. The virus spreads from the central nervous system to the salivary glands via peripheral nerves. The rabies virus budding takes place at the intracytoplasmic membranes of infected neurons as well as the plasma membranes of the salivary gland epithelial cells. The virus is detectable in the brain if an animal can transmit the rabies virus via its saliva.
Prevention & Control
In humans, rabies is almost 100% fatal, and that is why it is important to take preventative measures. Controlling rabies in wildlife populations is difficult. There is a vaccine-rabies glycoprotein recombinant virus vaccine available and also an oral vaccine that can be distributed in baits that are effective. Vaccinating dogs and cats is the most effective method to prevent rabies transmission. Another preventative measure is to quarantine or euthanize an animal that has been bitten by a suspected rabid animal.
Pre-exposure vaccinations are given to high-risk groups such as veterinarians, animal handlers and other people who have an increased chance of being in contact with rabies virus. The pre-exposure vaccinations prevent clinical rabies after exposure. Pre-exposure vaccination requires three inoculations of inactivated rabies vaccine. Post-exposure prophylaxis prevents the virus from entering the nerves by reducing viral load at the exposure site. Post-exposure prophylaxis involves one immunization of rabies immune globin and five immunizations of inactivated rabies virus based vaccine within the 28 days period. The inactivated rabies virus vaccine works by stimulating both the humoral and cell-mediated cytotoxic immune system to produce virus-neutralizing antibodies to protect against the lethal virus.
Research on Rabies
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Researchers are trying to create a novel rabies vaccine that will provide protection from a single dose. By the use of recombinant and reverse genetics there was a development of replication deficient vectors where one of the five essential rabies virus genes was deleted. Thus the virus could no longer complete its lifecycle effectively. Researchers are also trying to create a live virus vaccine in order to produce both effective innate and adaptive immunity.