Ebola and Marburg haemorrhagic fever

Abstract

Ebolaviruses and Marburgviruses (family Filoviridae) are among the most virulent pathogens for humans and great apes causing severe haemorrhagic fever and death within a matter of days. This group of viruses is characterized by a linear, non-segmented, single-stranded RNA genome of negative polarity. The overall burden of filovirus infections is minimal and negligible compared to the devastation caused by malnutrition and other infectious diseases prevalent in Africa such as malaria, dengue or tuberculosis. In this paper, we review the knowledge gained on the eco/epidemiology, the pathogenesis and the disease control measures for Marburg and Ebola viruses developed over the last 15 years. The overall progress is promising given the little attention that these pathogen have achieved in the past; however, more is to come over the next decade given the more recent interest in these pathogens as potential public and animal health concerns. Licensing of therapeutic and prophylactic options may be achievable over the next 5-10 years.

Fig. 1.

(A) A schematic illustration of a filovirus particle is presented. Four proteins are involved in the formation of the ribonucleoprotein complex: polymerase or large protein (L), nucleoprotein (NP), virion structural protein 30 (VP30), VP35. The glycoprotein (GP) is a type I trans membrane protein and is anchored with the carboxy-terminal part in the virion membrane. The soluble GP (sGP) is a non-structural glycoprotein secreted from infected cells and is only secreted by Ebolaviruses. VP40 and VP24 are membrane-associated proteins. (B) Schematic representation of Ebola virus (EBOV) and Marburg virus (MARV) genomes.

Fig. 2.

Reported outbreaks or isolated cases of haemorrhagic fever caused by marburgviruses (MARV, represented in green) and Ebolaviruses (EBOV, TAFV, SUDV, and BDBV, represented in red) in Africa.

Fig. 3.

Pathogenesis model, based on findings with EBOV (Zaire ebolavirus). Viruses enter the body through lymphatic and/or blood vessels. Dendritic cells and macrophages are the first cells to be infected by filoviruses. The virus spreads from the initial site of infection to secondary lymphoid organs and liver where intense replication takes place in other cells of the host organisms (hepatocytes, endothelial cells, fibroblasts and epithelial cells). The extensive infection of antigen-presenting cells (APC) leads to altered inflammatory responses and uncontrolled release of mediators. This contributes to the pathogenesis by attracting inflammatory responses followed by further and uncontrolled release of mediators.