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Zaire Ebola virus is one of the six known virus species in the Ebola virus genus. Four out of the six known Ebola virus species, including EBOV, can cause severe and often fatal hemorrhagic fever in humans and other mammals, known as Ebola virus disease (EVD). Ebola virus is the only member of the Zaire Ebola virus species, which belongs to the Ebola virus genus, filamentous virus family, and single negative chain virus order. The members of this species are collectively referred to as Zaire Ebola virus. The natural host of Ebola virus is believed to be bats, especially fruit bats, which mainly spread between humans and animals through bodily fluids.
Figure 1. Structure of Zaire Ebola Viru. (Marini G,et al, 2017)
The viral particles of Ebola virus (EBOV) are cylindrical/tubular in shape, and their genome consists of negative stranded RNA, including viral envelope, matrix, and nucleocapsid components. These cylinders typically have a diameter of about 80 nm, and their lipid bilayer surfaces protrude virus encoded glycoproteins (GP), forming 7-10 nm long protrusions. The length of the cylinder varies, usually up to 800 nm and sometimes up to 1000 nm. The outer envelope of the virus particle is formed by budding from specific areas of the host cell membrane, and GP protrusions are inserted into these areas during biosynthesis. The distance between individual GP molecules is about 10 nm. The viral proteins VP40 and VP24 are located between the envelope and nucleocapsid, i.e. in the matrix space. The center of the viral body structure is the nucleocapsid, which is composed of a series of viral proteins attached to a linear negative stranded RNA of 18-19 kb that does not have 3 '- polyadenylation or 5' – capping. The RNA is coiled in a spiral shape and complexed with NP, VP35, VP30, and L proteins; The diameter of the spiral is 80 nm.
The severe pathology of EBOV infection stems from direct cytopathic effects, and more importantly, the virus's ability to disrupt key host cell pathways. The key pathological targets and genes include:
| Diagnosis | Details |
| Cell Entry and Receptor Interaction | The cellular orientation of EBOV is largely determined by its glycoprotein (GP). The virus utilizes the "polysaccharide cap" and mucin like domain on GP to shield neutralizing epitopes. In order to enter, GP binds to host attachment factors such as C-type lectins on the surface of target cells (such as DC-SIGN, L-SIGN) and T cell immunoglobulin and mucin domain 1 (TIM-1) proteins. |
| Immune Evasion Through Viral Proteins | EBOV proteins VP35 and VP24 are the main immune antagonists. VP35 is a potent inhibitor of the RIG-I like receptor (RLR) pathway. It binds to double stranded RNA (a molecular pattern associated with viral pathogens) and masks its detection by host sensors such as RIG-I and MDA5. This directly inhibits the production of type I interferon (IFN - α/β) and weakens the antiviral state of neighboring cells. |
| Host Factors in Disease Severity: | Host genetic factors affect disease outcomes. The polymorphism of genes involved in immune response, such as those encoding TLR4, IL1B, and CD209 (DC-SIGN), is associated with susceptibility or resistance to severe EVD. The FERMT3 gene involved in platelet function is also associated with the severity of bleeding. |
Each viral particle contains a linear single stranded negative sense RNA molecule with a length of 18959 to 18961 nucleotides. Its 3 'end is not polyadenylation, and its 5' end is not capped. The virus genome encodes seven structural proteins and one non structural protein. The gene sequence is 3 '- leading sequence - NP - VP35- VP40- GP/sgP - VP30- VP24- L - tail sequence -5'; The leading sequence and tail sequence are non transcriptional regions that carry important signals for controlling the transcription, replication, and packaging of the viral genome into new viral particles. The NP, VP35, and L gene fragments of filamentous viruses have been identified as endogenous sequences in the genomes of various small mammals. Research has found that the 472 nucleotides at the 3 'end and 731 nucleotides at the 5' end required for viral "microgenome" replication are sufficient to complete the replication. Using third-generation sequencing technology, researchers can complete sample sequencing within 48 hours at the fastest. Like other RNA viruses, Ebola virus rapidly mutates in patients during disease progression and also mutates in local hosts.
The Ebola virus is cell-free and does not replicate through any type of cell division,on the contrary, they use a combination of host and virus encoded enzymes, as well as host cell structures, to produce multiple copies of themselves. Then, these molecules self assemble into viral macromolecular structures in the host cell. The virus completes a set of steps when infecting each individual cell. The virus attacks the host receptor by attaching surface protein aggregates of glycoproteins (GP) and is internalized into the host cell's large fusion. In order to penetrate cells, the viral membrane fuses with the vesicle membrane and the nucleocapsid is released into the cytoplasm. The encapsulated negative sense genome ssRNA was used as a template for synthesizing (3 '-5') polyadenylation monophosphate mRNA, and the mRNA was translated into a single viral protein using host cell ribosomes, tRNA molecules, etc. These viral proteins are processed: glycoprotein precursor (GP0) is cleaved into GP1 and GP2, and then highly glycosylated using cellular enzymes and substrates. These two molecules first assemble into a heterodimer, and then assemble into a trimer, forming a surface protein polymer.
In summary, the Zaire Ebola virus (EBOV) poses a significant threat to global public health due to its high mortality rate, ability to cause explosive outbreaks, and profound impact on infected individuals and communities. Its pathogenesis is a complex interaction between rapid, systemic viral replication and skilled disruption of the host immune system by the virus, mainly through targeting key innate immune pathways (RIG-I/MDA5 signaling and STAT1 nuclear translocation) such as VP35 and VP24 proteins. Identifying host factors such as NPC1 cholesterol transporter is crucial for virus entry, which is essential for understanding its lifecycle. However, challenges still exist, including ensuring fair access to these countermeasures, managing persistent viruses in survivors' bodies, and understanding natural hosts. Continuous monitoring, research on broad-spectrum antiviral drugs, and strengthening global health infrastructure are crucial for preventing future epidemics and ultimately achieving better results globally.
Reference
| Target | Cat. No. | Product Name | Host | Isotype | Application | |
| Zaire Ebola Virus Nucleoprotein | CABT-B290 | Anti-Zaire Ebola Virus Nucleoprotein monoclonal antibody, clone 2F7 | Mouse | IgG1 | WB | Inquiry |
| Zaire Ebola Virus VP24 Protein | CABT-B291 | Anti-Zaire Ebola Virus VP24 Protein monoclonal antibody, clone 0F9 | Mouse | IgG1 | WB | Inquiry |
| Zaire Ebola Virus VP35 Protein | CABT-B292 | Anti-Zaire Ebola Virus VP35 mAb, clone 7D6 | Mouse | IgG2a | WB, IP, IF | Inquiry |
| Zaire Ebola Virus VP35 Protein | CABT-B293 | Anti-Zaire Ebola Virus VP35 Protein (N-Terminal) monoclonal antibody, clone 20D8 | Mouse | IgG2b | WB | Inquiry |
| Target | Cat. No. | Product Name | Host | |
| GP1 | DAG-WT267 | Recombinant Zaire Ebola Virus glycoprotein 1 (GP1) [His] | HEK293 | Inquiry |
| GP1,2 | DAG-WT268 | Biotinylated Zaire Ebola Virus glycoprotein 1,2 (GP1,2) [His,Avi] | HEK293 | Inquiry |
| GP1 | DAG-WT269 | Recombinant Zaire Ebola Virus glycoprotein 1,2 (GP1,2) [His] | HEK293 | Inquiry |
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