Marburg virus is one of two viruses classified in the genus Marburgvirus (family Filoviridae) and the causative agent of Marburg virus disease, a severe hemorrhagic fever. It has a non‑segmented, negative‑sense single‑stranded RNA genome of about 19 kilobases encoding seven structural proteins. The virus was first identified in 1967 during simultaneous outbreaks of hemorrhagic fever in laboratory workers in Marburg and Frankfurt, Germany, and Belgrade, Yugoslavia, who were exposed to tissues from African green monkeys imported from Uganda.
Classification, Biology and Ecology
Marburg virus particles are filamentous and enveloped, containing a helical nucleocapsid composed of the nucleoprotein (NP), virion proteins VP35 and VP30, the matrix protein VP40, the glycoprotein (GP), the minor matrix protein VP24 and the RNA‑dependent RNA polymerase (L). Along with Ravn virus, Marburg virus constitutes the species Marburg marburgvirus within the genus Marburgvirus, distinct from the Ebolavirus genus. The genomic organization mirrors that of ebolaviruses, but phylogenetic analyses show separate lineages. The natural reservoir of Marburg virus is believed to be the Egyptian fruit bat (Rousettus aegyptiacus), as viral RNA and antibodies have been detected in these bats, and experimental infection shows asymptomatic replication. Human infections occur through prolonged exposure to bat‑inhabited caves or mines, or via direct contact with infected primates or human patients. After an incubation period of 2‑21 days, Marburg virus disease presents with abrupt fever, chills, headache, myalgia, followed by vomiting, diarrhea, rash and bleeding. Case fatality rates vary from around 23 % to over 80 %, depending on the outbreak and access to medical care. There are no licensed specific antivirals; treatment is supportive, and monoclonal antibodies and vaccines are under development.
Historical Outbreaks and Clinical Importance
The first known outbreak in 1967 involved 31 cases and seven deaths among laboratory staff processing monkey kidneys for polio vaccine production. Intensive infection control halted the outbreak, and research identified a new filovirus. Sporadic cases occurred in South Africa (1975) and Kenya (1980, 1987). A major outbreak began in 1998 in Durba, Democratic Republic of the Congo, linked to gold miners frequenting bat‑infested caves, causing more than 150 cases with high mortality; a genetically distinct strain, later named Ravn virus, co‑circulated. The largest outbreak occurred in Angola in 2004–2005, resulting in over 250 cases and a case fatality of about 88 %. Subsequent outbreaks have been reported in Uganda (2007, 2012, 2017), Guinea (2021) and Ghana (2022), often associated with cave or mine exposures. Human-to-human transmission occurs through direct contact with blood or bodily fluids of infected individuals. Rapid diagnosis, isolation, barrier nursing and safe burial practices are critical to control spread. Experimental vaccines, including vesicular stomatitis virus vectors expressing Marburg glycoprotein, have shown protective efficacy in non‑human primates and are being evaluated in humans.
Marburg virus remains a significant zoonotic pathogen with the potential to cause explosive outbreaks of hemorrhagic fever. Continued surveillance of bat reservoirs, rapid case detection and advancement of vaccines and therapeutics are key components of preparedness.
Related Terms: Ravn Virus, Zaire Ebolavirus, Sudan Ebolavirus, Bundibugyo Ebolavirus, Crimean‑Congo Hemorrhagic Fever Virus