Rabies virus (RABV) is a neurotropic, enveloped, single-stranded RNA virus. It belongs to the Rhabdoviridae family, genus Lyssavirus. RABV infection causes rabies in humans and other animals. Rabies causes inflammation of the brain in humans and other mammals. Early symptoms of rabies include fever and tingling at the site of exposure, followed by one or more symptoms such as fear of water, violent movements, confusion, uncontrolled excitement, inability to move parts of the body, and loss of consciousness. The mortal rate is nearly 100% once the symptoms appear. It causes about 24,000 to 60,000 deaths all over the world each year. RABV has a wide range of natural hosts as well as other many rhabdoviruses. Many mammalian species have been reported to be infected by RABV in the wild, such as humans, dogs, cats, etc. In laboratory, it has been found that cell cultures from mammals, birds, reptiles and insects can also be infected by RABV.
Fig.1 RABV particles under electron microscopy
The RABV genome is a single-stranded, negative-sense RNA with a length of nearly 12k nt. It encodes five viral proteins including: nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G) and polymerase (L). RABV virion has two main structural components including an envelope and a helical ribonucleoprotein core (RNP), which is the same as all other rhabdoviruses. RABV genome is tightly packed up by the nucleoprotein in the RNP. Phosphoprotein and polymerase are associated with the RNP too. The matrix protein is believed to be the central molecule for the assembly of RABV particles, and also associated with the envelope of RABV. Shape of RABV particle is like a bullet, with a size of about 180 nm and a cross-sectional diameter of about 75 nm. One end of the virion is concave and the other end is conical.
Fig.2 Life cycle of RABV.
RABV enters the host cells through the endosomal transport pathway. Low pH within the endosomal promotes the fusion of membrane and thus enabling the viral genome to the cytosol. Transcription of viral genome is then performed by the P-L polymerase, and regulated by protein M along with the cis-acting sequences on the viral genome. Protein M also plays an important role in the replication of genome RNA. These new negative-sense RNA and protein N are then assembled into new RNPs to form the new virus.
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