Immunogenicity, Pathogenesis, and Host’s Immuno-Responses to Marburg Virus Infection

Due to the sudden emergence and burnout nature of Marburg virus (MARV) outbreaks, little is known about MARV's pathogenicity and immunogenicity. These gaps in knowledge are limiting our understanding of the disease and the implementation of cost-effective prevention and control measures including case management through safe and effective therapeutic modalities. Therefore, this review aims to synthesize and summarize evidence about pathogenicity, immunogenicity, and virulence in humans towards MARV. Upon infection, MARV rapidly disseminates throughout various tissues, provoking severe cellular injury, particularly in lymphatic organs, the liver, kidneys, and the gastrointestinal tract. The virus takes advantage of host cells by avoiding immune responses, mainly by disrupting the function of dendritic cells and blocking the signaling pathways for interferon. As a result, patients experience profound immune dysregulation characterized by early lymphocyte depletion and a shift towards pro-inflammatory cytokine release, resulting in a cytokine storm that can lead to hemorrhagic septic shock. Additionally, adaptive immune responses, including antibody production, are impaired, further complicating recovery and increasing susceptibility to severe disease outcomes. Understanding these intricate host-pathogen interactions is critical for developing effective therapeutic strategies and vaccines against MARV. Continuing research is essential to explain the mechanisms of immune evasion and to identify potential intervention points for improving patient outcomes.