Abstract
Rabies has affected mankind for several centuries and is one of the oldest known zoonoses. It is peculiar how little is known regarding the means by which rabies virus (RABV) evades the immune response and kills its host. This review investigates the complex interplay between RABV and the immune system, including the various means by which RABV evades, or advantageously utilizes, the host immune response in order to ensure successful replication and spread to another host. Different factors that influence immune responses—including age, sex, cerebral lateralization and temperature—are discussed, with specific reference to RABV and the effects on host morbidity and mortality. We also investigate the role of apoptosis and discuss whether it is a detrimental or beneficial mechanism of the host’s response to infection. The various RABV proteins and their roles in immune evasion are examined in depth with reference to important domains and the downstream effects of these interactions. Lastly, an overview of the means by which RABV evades important immune responses is provided. The research discussed in this review will be important in determining the roles of the immune response during RABV infections as well as to highlight important therapeutic target regions and potential strategies for rabies treatment.
Highlights
Rabies has afflicted mankind for centuries [1], and there have been several significant advances towards the prevention and elimination of rabies—such as the development of the first rabies vaccine by Louis Pasteur [2,3]—relatively little is understood regarding the means by which rabies virus (RABV) infects, spreads, evades the immune system, and kills
RABV is able to sequester a variety of initial innate immune responses in the early stages of infection, which leads to the sequestration or hindering of any subsequent adaptive immune responses
There has been a dramatic increase in the number of new and developing viral therapeutic options including RNA-based therapies such as RNA interference (RNAi), aptamers and microRNA-based therapies
Summary
Rabies has afflicted mankind for centuries [1], and there have been several significant advances towards the prevention and elimination of rabies—such as the development of the first rabies vaccine by Louis Pasteur [2,3]—relatively little is understood regarding the means by which rabies virus (RABV) infects, spreads, evades the immune system, and kills. How does RABV evade, or utilize, the immune system in order to successfully replicate and spread? We discuss the question of immune evasion and exploitation by addressing multiple aspects of the virus as well as the responses of the immune system to RABV infection. We provide a comprehensive summary and some of our own insights in order to highlight gaps or inconsistencies that may be addressed in future studies
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