**1. Introduction**

Rabies, an RNA virus from the genus Lyssavirus, also known as RABV, is a lethal pathogen to several species [1]. The evolutionary history of the virus suggests that its most recent ancestor likely diverged into two descendants, one infecting bats, the other infecting dogs. Once domesticated dogs became infected in the Old World, humans became the next target. Evolutionary biology tells us that rabies likely did not exist in the New World prior to the settlement of Europeans but was common throughout Europe, Asia, and Africa well before the discovery of the Americas [2].

RABV is transmitted through the saliva of an infected individual into the bloodstream of a healthy individual, typically via a bite, but possible through other wounds or ocular route. Upon infection, there are two ways the virus may manifest: furious and paralytic. Furious rabies often presents itself with bouts of anxiety, irritability, phobias, and many other symptoms that will later be discussed. Paralytic rabies has some common symptoms with furious rabies, however, paralysis is the most notable symptom just prior to death [3].

According to the CDC in 2015, nearly 60,000 human deaths occurred on average each year. Statistically, this can be interpreted as 1 human death every nine minutes [4]. Despite its large impact globally, the virus is relatively diminutive. The rabies virus has evolutionarily reduced its single-stranded RNA genome to only five genes. These genes encode five proteins, three of which make up the ribonucleoprotein (RNP) complex; the other two form the virus's envelope [5].

While the rabies virus has been heavily researched, lives continue to be lost. There is a great understanding of the epidemiology of the virus, however little is understood about the pathogenesis. Herein, the findings regarding the diagnosis, clinical course, treatment, and prevention of the rabies virus are summarized as well as data gaps in research and understanding of this pathogen.
