Rabies lyssavirus (RABV) (RABV)

Rabies lyssavirus (RABV) is a bullet-shaped, negative-sense, single-stranded RNA virus belonging to the Rhabdoviridae family and is the primary causative agent of rabies [1, 14, 18]. It is a highly neurotropic pathogen typically transmitted through the saliva of infected animals via bites or scratches, progressing from the site of inoculation to the central nervous system through retrograde axonal transport [14, 17, 19]. Once the virus reaches the brain, it causes acute, progressive encephalitis that is almost invariably fatal without prior vaccination or timely post-exposure prophylaxis [1, 9, 16]. Therapeutically, Rabies lyssavirus is targeted primarily through its surface glycoprotein (G), which mediates receptor binding and membrane fusion, and its large protein (L), which functions as the RNA-dependent RNA polymerase [2, 5, 10, 11]. The G protein is the main target for neutralizing antibodies found in vaccines and rabies immunoglobulins (RIG), while the L protein serves as a target for experimental antivirals like ribavirin and favipiravir [2, 14, 16]. Despite established protocols for pre- and post-exposure prevention, there remains no effective treatment for symptomatic rabies, highlighting a critical gap in clinical research [1, 3, 15].

Other names

Rabies virusRABVLyssavirus rabiesRabies lyssavirus 1

The mechanisms of action include: 1) Neutralization of viral particles by binding to the surface glycoprotein (G) to block cell entry [5, 10, 11]; 2) Inhibition of the viral RNA-dependent RNA polymerase (L protein) to prevent genome replication and transcription [2, 14, 16]; 3) Inhibition of viral membrane fusion during the early stages of infection [10, 16]; and 4) Induction of protective immune responses through active and passive immunization [1, 6].