Abstract

Rabies virus is a strictly neurotropic virus that propagates in the nervous system (NS) of the infected vector host from the site of entry (usually due to a bite) up to the site of exit (salivary glands). Successful achievement of the virus cycle relies on the preservation of the neuronal network. Once rabies virus has entered the NS, its progression is not interrupted by the host defense mechanisms, which are inefficient. This might result from the intrinsic capacity of this virus to (1) evade the innate immune response launched by the infected neurons, (2) eliminate the protective T cells migrating into the NS and (3) limit the inflammation in NS tissues. In addition, by targeting the NS that has the striking capacity to centrally control the immune response, the infection also benefits from disarmed host defenses. The successful adaptation of the virus to the mammalian NS may explain why rabies is fatal in almost all cases.

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