A comparative analysis of Marburg virus-infected bat and human models from public high-throughput sequencing data.

Abstract

Marburg virus (MARV) disease (MVD) is an uncommon yet serious viral hemorrhagic fever that impacts humans and non-human primates. In humans, infection by the MARV is marked by rapid onset, high transmissibility, and elevated mortality rates, presenting considerable obstacles to the development of vaccines and treatments. Bats, particularly Rousettus aegyptiacus, are suspected to be natural hosts of MARV. Previous research reported asymptomatic MARV infection in bats, in stark contrast to the severe responses observed in humans and other primates. Recent MARV outbreaks highlight significant public health concerns, underscoring the need for gene expression studies during MARV progression. To investigate this, we employed two models from the Gene Expression Omnibus, including kidney cells from Rousettus aegyptiacus and primary proximal tubular cells from Homo sapiens. These models were chosen to identify changes in gene expression profiles and to examine co-regulated genes and pathways involved in MARV disease progression. Our analysis of differentially expressed genes (DEGs) revealed that these genes are mainly associated with pathways related to the complement system, innate immune response via interferons (IFNs), Wnt/β-catenin signaling, and Hedgehog signaling, which played crucial roles in MARV infection across both models. Furthermore, we also identified several potential compounds that may be useful against MARV infection. These findings offer valuable insights into the mechanisms underlying MARV's pathophysiology and suggest potential strategies for preventing transmission, managing post-infection effects, and developing future vaccines.