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Rabies is caused by an enveloped, negative-sense, single-stranded RNA virus from the genus Lyssavirus in the family Rhabdoviridae.

It is transmitted from the saliva of an infected mammal through bites, skin scratches, or contact with mucous membranes like the eyes.

The virus enters muscle cells through receptor-mediated endocytosis, where it replicates slowly. The viral genome encodes a phosphoprotein that helps block type I interferon signaling and weakens early antiviral defenses.

The virus then buds from infected muscle cells and binds to neuronal receptors at the neuromuscular junction, allowing it to enter motor neurons.

Within the neurons, it travels backward along the axon via retrograde transport, gradually advancing toward the spinal cord and brain.

Once it reaches the central nervous system, the virus replicates extensively, leading to severe neuronal dysfunction.

Infected neurons activate immune responses, leading to inflammation that intensifies with increasing viral load and associated tissue damage.

The virus spreads through cranial nerves to highly innervated tissues, especially the salivary glands, which helps it spread to a new host.