Rabies

Rabies

·         Rabies viruse is a neurotropic viruse, responsible for the fatal disease RABIES among humans and several other animals

·         Its transmission occurs through the saliva of the infected animals. The virus is classified as follows

Ø  Group-ss RNA (-ve)

Ø  Order-monomegavirale

Ø  Family-rhabdoviridae

Ø  Genus-lyssaviruse

Ø  Species-rabies

·         Structure of rabies viruse: the viruse is bullet shaped with a length of about 180 nm and cs diameter of 75 nm.

·         One end of the viruse is conically rounded and other end is planar.

·         The genome is surrounded by a  lipoprotein envelope which poses spike like glycoprotein gene

·         The spike do not cover the planar end of the virion.

·         Beneath the envelope is the matrix protein layer wahich may invaginated at the planar end

·         The core consist hellcally arranged ribonucleoprotein

·         The genome is unsemented, linear single stranded RNA with –ve sense .

·         The RNA genome encodes 5 genes: the order of these genes 3’NMPGL-E is highly conserved.

·         The genes code for five different protein:

1.       N- nucleoprotein

2.       P-phospho protein

3.       M-matrix protein

4.       G-glycoprotein

5.       L-viral RNA polymerase

·         All the transcripltion or the replication events occur inside the cytoplasm in the specialized viruse factory known as NEGRI BODY.

·         The negri body are 2 to 4 nanometer in diameter and are typical for rabies infection.

·         Negri bodies are used as a definite histological proof for the viral infection.

·         Infection: infevtion of human beings are through bite of an infected animal, such as the incected dog, cat, bat, etc….

·         From the wound the viruse tracels quickly long the neural pathways to the CNS.

·         The exact molecular mechanism of this transportation is still unknown, although the binding of p protein from rabies viruse to the dyenin light chain protein have been shown in several cases of pathogenesis.

·         The protein also acts as an interferon antagonist.

·         In this way the p protein also decreases the immune system response of the host cell.

·         From the CNS the virus travels to the other organs.

·         The salivary glands and the tissues of the mouth receives high concenteation of the virus.

·         Thus allosing its further transmission ans secondary infection.

·         Life cycle:

·         After the receptor binding, the rabies viruse wnters into the host cell therough endosomal transport pathway inside the wndosome.

·         The low ph value induces the membrane fusion .

·         Thus enabling the viral genome to reach the cytosol.

·         Both receptor binding and membrane fusion os catalysed by the glycoprotein gene which plays a critical role in the pathiogenesis.

·         Any mutant viruse without gene protein cannot propagate.

·         Now the viral genome is transmited by P-L polymerase.

·         The p protein is essential co factor for the 2_polymerase.

·         The enzyme is responsible for formation of new viral protein molecules.

·         This viral polymarasse can only recognize ribonucleoprotein and canot use free RNA as template.

·         Later on the activity of polymerase switches to replication in oreder to produce the full length +ve strand RNA copies i.e. co,plementory RNA

·         These complementary RNAs are used to make new –ve strand genomes and are used as template.

·         Thay are packsged togehetr with protein which proceeed to form virus.

·         Rabies is essentially ans  overwhwlming encephalomyletis. In humans the incubation period from the time of infection varies from 6 days to a year, but is basically sbout 3-8 weels.

·         The development of symptoms and the length of the incubation period depens upon the severiety snd the site of bite.

·         It has been seen that only about 5-15% of human bitten byb rabid animals show rabies symnptoms.

·         Symptoms in humans include severe headache and high fever with alternating stages of excitement and depressions.

·         Patient have difficulty in swallowing and slight muscular stimuli in throat and chest.

·         Death usually  follows paralysis.

·         The moratality rate in rabies is about 100 percent.

·         If a person is biteen by rabid animal the long period of the incubation allows time for measures to be taken to prevent the viruse from reaching the CNS.

·         These measures include a combination of passive immunization and active immunization.

·         The active immunization includes the administration of rabies vaccins to stimulat the longer lasting production of the antibodies by t he patient.

·         Laboratory confirmation of rabies of the animal which has botten the patient is done by one of the following gmethods:

1.       Detection of rabies virus antigen in clinical specimen by the use of the fluorescent antibodies.

2.       Isolation of virus from the urine, saliva, spinal fluid of tissues by ennoculation into the brain of mice.

3.       Demonstration of the inclusion bodies i.e. the negri bodies in the nerve cels of the brain

·         In all the above cases the negative results do not exclude rabies and for theis reason the animal should not be killed but kept under observation for atleasr two weeks.

If the animal shows the symptoms of rabies, the human victim must be vaccinated.