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Mechanisms of Immune Sensing in Lassa Virus Infection

Tremmel Masaki

Lassa fever, an endemic viral hemorrhagic fever in West Africa, poses a substantial threat to human health due to its ability to cause outbreaks and its high fatality rate. The immune system's ability to detect and respond to Lassa virus (LASV) infection is critical in controlling the spread of the virus within the host. This article provides an overview of the mechanisms involved in immune sensing during LASV infection, focusing on the innate and adaptive immune responses. The innate immune system recognizes viral RNA through pattern recognition receptors (PRRs) such as Toll-like receptor 3 (TLR3), retinoic acid-inducible gene I (RIG-I), and melanoma differentiation-associated protein 5 (MDA5). These sensors initiate signaling cascades that lead to the production of type I interferons and proinflammatory cytokines, contributing to the host's antiviral defenses. In the adaptive immune response, cytotoxic T lymphocytes (CTLs) and B cells play essential roles in eliminating infected cells and generating long-term immunity. Despite the host's immune defenses, LASV has evolved strategies to evade detection and subvert the immune response, leading to persistent infections in some cases. Understanding these evasion mechanisms is crucial for the development of effective therapeutic strategies against Lassa fever.