Abstract
Rabies is a lethal zoonotic disease caused by lyssaviruses, such as rabies virus (RABV), that results in nearly 100% mortality once clinical symptoms appear. There are no curable drugs available yet. RABV contains five structural proteins that play an important role in viral replication, transcription, infection, and immune escape mechanisms. In the past decade, progress has been made in research on the pathogenicity of RABV, which plays an important role in the creation of new recombinant RABV vaccines by reverse genetic manipulation. Here, we review the latest advances on the interaction between RABV proteins in the infected host and the applied development of rabies vaccines by using a fully operational RABV reverse genetics system. This article provides a background for more in-depth research on the pathogenic mechanism of RABV and the development of therapeutic drugs and new biologics.
Highlights
Rabies is a fatal zoonotic disease caused by lyssaviruses, such as rabies virus (RABV), which infects humans and other mammals [1]
The aim of this study is to summarize the interactions between RABV structural proteins and host cells and to review the progress in reverse genetics systems to better understand viral pathogenic mechanisms and to develop novel biologics [6–10]
Treatment with IFN-β neutralizing antibody improved the replication efficiency of Ni-CE in muscle cells, highlighting the importance of IFN antagonism. These results suggest that the P protein plays a key role in evading innate immune responses, rendering it a potential therapeutic target for RABV post-exposure prophylaxis (PEP) or anti-viral drugs
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The G protein is capable of inducing the production of virus neutralizing antibodies (VNA), and mediates cellular tropism and absorption by neuronal cells [4,5]. These five structural proteins work together to regulate viral replication, transcription, infection, and evasion of the host immune response. The aim of this study is to summarize the interactions between RABV structural proteins and host cells and to review the progress in reverse genetics systems to better understand viral pathogenic mechanisms and to develop novel biologics [6–10]. RABVstructural structuralproteins, proteins,N, N,P,P,M, M,G, G,and andLL(Figure (Figure1), 1),play playvital vitalroles rolesinin assembling mature virus particles.
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