Rabies Virus (RABV) Infection

Structure and genome

RABV has a bullet-shaped morphology with a length of about 180 nm and a cross-sectional diameter of about 75 nm, with a rounded or tapered end and a flat or concave end. Its genome is a single-stranded negative-sense RNA, nearly 12,000 nucleotides in length, encoding five viral proteins, including nucleoprotein (N), phosphoprotein (P), matrix protein (M), glycoprotein (G), and polymerase (L). The primary structure of its viral particles consists of an envelope and a helical ribonucleoprotein core (RNP). In the RNP, the genomic RNA is tightly wrapped by the nucleoprotein, while the phosphoproteins and polymerase are also bound to the RNP. The matrix proteins, on the other hand, are considered to be the core molecules for the assembly of RABV particles and are interconnected with the viral envelope. In addition, glycoproteins form about 400 trimeric spines that are tightly arranged on the viral surface and are responsible for the viral invasion process, as well.

Neuroinvasion Mechanism of RABV

The virus attaches itself to host cell surface receptors to enter cells during the early phases of RABV infection. Nicotinic acetylcholine receptors (nAChRs) are one known RABV receptor that has been found in research, supporting the idea that muscle cells are where the virus first infects cells. RABV particles enter the central nervous system via neuromuscular junctions (NMJs). After entering primary motor neurons, the virus utilizes retrograde axonal transport mechanisms to propagate to the central nervous system, where it replicates and assembles within the neuronal cell bodies.

Once inside the central nervous system, RABV demonstrates a strict preference for neurons, primarily transmitting between neurons via synaptic crossing. This process continues until RABV is widely distributed in the central nervous system, leading to behavioral changes and facilitating the virus's transmission to new hosts. Furthermore, RABV can spread from the central nervous system to various neural exterior organs, including the skin and salivary glands.

Figure 2. Lectin-Mediated Endocytosis and Transport Pathways of RABV within Neurons
(Source: Liu X, et al. 2022)

Rabies Prevention and Control

To protect high-risk populations, such as veterinarians and animal handlers, countries all around the world have implemented rabies immunization programs. Rabies vaccinations and rabies immune globulin are examples of prompt post-exposure prophylaxis (PEP) measures that can effectively prevent the virus's spread and infection.

Rabies outbreaks still happen all over the world, especially in underdeveloped nations, despite the fact that the prevalence of the disease has considerably decreased due to the widespread availability of rabies vaccines. In order to prevent and manage the spread of rabies, public health authorities' efforts—such as vaccinating animals, increasing public awareness, and setting up efficient monitoring and response mechanisms—remain vital.

To conclude, Rabies virus is a highly lethal virus with a complex and highly specific infection mechanism. RABV employs advanced biological mechanisms to successfully bypass the human immune system and proliferate quickly, posing considerable public health risks. However, current research into RABV yields new insights and approaches for rabies prevention, treatment, and control. Public attention and scientific preventive measures will be critical to limiting the spread of rabies.

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