To most of the world, Ebola Zaire haemorrhagic fever, also simply known as ‘the Ebola virus’ (EBOV) (Hayden, 2014), was relatively unknown until early 2014 when an outbreak in West Africa seemingly appeared out of nowhere. Yet outbreaks have been reported in primates, both human and non-human, since its discovery in 1976 (P. Ascenzi et al. 2008), and the outbreaks seem to be increasing in frequency. Several studies leave us with very little to no doubt that EBOV has caused severe die-offs among non-human primates (Bermejo et al. 2006; Caillaud et al. 2006), and is a great concern when considering biodiversity conservation of already threatened great apes. Unfortunately, …show more content…
2009). This essay will focus on Ebola Zaire haemorrhagic fever, looking into its microbiology, ecology, pathogenesis, immunology and finally how it affects wild …show more content…
Some lab experiments have shown that bats infected with another closely related filovirus; Marburg, shed the virus in their mouths through saliva. So it is possible that wild bats could spread Ebola Zaire in a similar way by leaving traces on fruit that later gets consumed by apes (Hayden, 2014).
Pathogenesis and immunology
Studies of Ebola under ideal conditions have been rare (Feldmann and Geisbert, 2011) and most of what we do know about EBOV comes from research done on rodents and non-human primates (P. Ascenzi et al. 2008). From this research and observations during epidemics it has so far been documented that the pathogenesis primarily involves immunosuppression, increased blood vessel permeability, and impaired coagulation (Meyers et al. 2014).
The Ebola virus enters through mucous membranes and breaches in the skin, affecting multiple cell types, especially those of the immune system and internal organs (Meyers et al. 2014). Here the characteristic GP gene’s main product – glycoprotein, mediates all steps in host cell entry (Wool-Lewis and Bate, 1998), from which point the Ebola Virus really starts to wreak