Rabies virus: Structure, Pathogenesis and Modes of transmission
Rabies is caused by Rabies virus. It belongs to Rhabdoviridae family. The viruses included in this family are rod shaped, enveloped, single stranded RNA virus. They infect mammals, reptiles, birds, fishes, insects and plants. Rhabdoviruses infecting mammals are included in two genera:
Lyssavirus- Rabies, Lagos bat virus, Mokola, Duvenhage, Australian bat
Vesiculovirus- Vesicular stomatitis virus and related virus
Out of these, only rabies virus is medically important member of the genus Lyssavirus.
Structure of Rabies virus
Rabies virus is a bullet shaped, negative-sense, non-segmented, single-stranded RNA virus measuring approximately 60 nm × 180 nm. It is composed of an internal protein core or nucleocapsid, containing the nucleic acid, and an outer envelope, a lipid-containing bilayer covered with transmembrane glycoprotein spikes. Beneath the envelop lies the matrix (M) protein layer which may be invaginated at the planar end. The virus genome encodes five proteins associated with either the ribonucleoprotein (RNP) complex and the viral envelope. The L (RNA dependent RNA polymerase or transcriptase), N (nucleoprotein), and NS (transcriptase-associated) proteins comprise the RNP complex, together with the viral RNA. These aggregate in the cytoplasm of virus-infected neurons form Negri bodies, the characteristic histopathological finding of rabies virus infection. The M (matrix) and G (glycoprotein) proteins are associated with the lipid envelope. The G protein forms the knob like protrusions that cover the outer surface of the virion envelope and is the only rabies virus protein known to induce virus-neutralizing antibody.
Modes of transmission: Rabies in human is most often transmitted by the bite of rabid dogs. It can also be transmitted
- By contact with the saliva of rabid animals (licking)
- By inhalation of aerosolized virus (Bat caves)
- By transplantation of infected tissue (e.g. cornea)
Multiplication of Rabies virus
Replication of rabies virus is believed to be similar to that of other negative-stranded RNA viruses. The virus first attaches to the host cell membranes via G protein, it then penetrates cytoplasm by fusion or pinocytosis, and ribonucleoprotein core is uncoated into the neuronal cell. The core initiates primary transcription of the five complementary messenger RNAs by using the virion-associated RNA-dependent RNA polymerase. Each RNA is then translated into individual viral proteins (L, N, NS, M and G). After viral proteins are synthesized, replication of the genomic RNA continues with the synthesis of full length, positive-stranded RNA, which acts as a template for the production of progeny negative-stranded RNA.
Human infection occurs usually by the bite of rabid animals. The virus present in the saliva of animal is deposited in the wound. Viral multiplication takes place in the muscles, connective tissues or nerves for 48-72 hrs. It then penetrates the nerve endings and travel by retrograde of axonal transport in the nerve cell towards spinal cord and brain. The movement of virus in axon is passive, at a speed of about 3mm/hr. Once the virus reaches the spinal cord, virus ascends rapidly to the brain where it multiples and spreads along the nerve trunks to various highly innervated parts of the body (skin of head & neck, salivary glands, retina, cornea, nasal mucosa, adrenal medulla , renal parenchyma and pancreatic acinar cells). Virus multiplies in salivary glands and is shed in saliva which plays a vital role in transmission of virus and its survival in nature.
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