Abstract
Lassa virus (LASV) is the causative agent of Lassa fever, a human hemorrhagic disease associated with high mortality and morbidity rates, particularly prevalent in West Africa. Over the past few years, a significant amount of novel information has been provided on cellular factors that are determinant elements playing a role in arenavirus multiplication. In this review, we focus on host proteins that intersect with the initial steps of the LASV replication cycle: virus entry and genome replication. A better understanding of relevant virus–host interactions essential for sustaining these critical steps may help to identify possible targets for the rational design of novel therapeutic approaches against LASV and other arenaviruses that cause severe human disease.
Highlights
The Arenaviridae family includes viruses carried by mammalian hosts, classified in the Mammarenavirus genus, and members that infect reptilian hosts, which belong to the Reptarenavirus and Hartmanivirus genera [1]
Lassa virus (LASV) is the causative agent of Lassa fever (LF), a human hemorrhagic disease transmitted through contact with infected rodents (Mastomys spp.)
Arenaviruses primarily attach to cells by binding of their surface GP to specific receptor/entry factors at the plasma membrane of host cells. α-DG was the first entry receptor discovered for LASV, as well as for other Old World (OW) and for Clade C New World (NW) arenaviruses [29,30], and its interaction with GP has been widely characterized [31]
Summary
The Arenaviridae family includes viruses carried by mammalian hosts, classified in the Mammarenavirus genus, and members that infect reptilian hosts, which belong to the Reptarenavirus and Hartmanivirus genera [1]. The C-terminal domain of NP harbors a functional 30 -50 exoribonuclease activity of the DExD/H-box protein family that has been shown to oppose the host type I interferon (IFN-I)-mediated immune response during viral infection. In this regard, NP is capable of degrading small viral doubled-stranded RNA fragments that could function as pathogen-associated molecular patterns, to prevent their recognition by cellular pattern recognition receptors (PRRs) [17,19,20,21]. Deepening the knowledge about relevant virus-host interactions essential for sustaining these early critical steps may help identify possible targets for the rational design of novel therapeutic approaches against LASV and other arenaviruses that cause severe human disease
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