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Filovirus was first reported and named Marburg contagion in 1967 during an outbreak of viral haemorrhagic fever (HF) in Frankfurt (Germany) and Belgrade( Yugoslavia). Infection with pathogenic filoviruses results in a severe acute complaint characterized by the rapid-fire onset of generalized symptoms similar as fever, headache and myalgia, as well as frequent gastrointestinal symptoms, which in severe cases progresses to a systemic infection that results in multiorgan failure and in numerous cases death. In 1976, Ebola contagion (EBOV) was determined to be the cause of outbreaks of viral HF in the Sudan and Congo. The Ebola contagion has caused numerous casualties in recent times. Ebola haemorrhagic fever causes deadly complaint in humans andnon-human primates performing from infection with the Ebola contagion rubric of the family Filoviridae.
Ebola viruses are non-segmented negative-sense RNA viruses. The proteins encoded in the genome are the nucleoprotein NP, the polymerase cofactor VP35, the matrix protein VP40, the non-structural soluble glycoprotein sGP, the structural glycoprotein GP1,2, the transcriptional activator VP30, the nucleocapsid-associated protein VP24 and the polymerase L. Attachment of virions at the cell surface is followed by uptake via macropinocytosis into endolysosomes. Subsequently, the virus envelope fuses with the endolysosomal membrane and RNP complexes are released into the cytoplasm, where they relax and become transcriptionally active. Primary transcription is facilitated by viral RNP complex proteins brought into the cell, and viral mRNAs are translated into proteins by host ribosomes. The newly synthesized viral proteins facilitate secondary transcription and genome replication, copying the viral genomic RNA (vRNA) through an antigenomic intermediate (cRNA). Newly formed RNP complexes condense into a packaging-competent form and are transported to budding sites.
Fig 1. Ebola virus genome structure and life cycle.
(Source: Nature Review Microbiology, 2019)
Targeting the entry process. Targeting the entry process is the furthest developed avenue of development of antivirals against filoviruses. Current efforts focus on the development of cross-protective antibodies targeting multiple filovirus species, which would be beneficial not only because it would reduce the number of therapies that would have to be developed for use in humans but also because it would potentially allow deployment against novel pathogenic filoviruses. Small-molecule entry inhibitors have also been extensively investigated, and the vast majority of candidate therapeutic compounds are directed against this process.
Targeting the viral RNA synthesis machinery. Strategies to target viral RNA synthesis include both representatives that directly target viral components of the RNA synthesis machinery and those that target cellular contributors to the RNA synthetic process. Both approaches have shown considerable potential.
Targeting morphogenesis and budding. In contrast to entry and viral RNA synthesis, few compounds targeting morphogenesis or budding have been identified, and no compound is known to be protective in an animal model. However, despite the low number of identified drugs, theoretical considerations suggest a number of antiviral targets in morphogenesis and budding that could be exploited for therapy.
References
| Target | Cat. No. | Product Name | Expression System | Tag/Conjugate | Application | |
| BEBOV GPDTM | DAGB178 | Bundibugyo Glycoprotein (minus the Transmembrane Region) [His] | Insect cells | His | WB | Inquiry |
| EBOV VLP | DAGB179 | Ebola virus-like particles | Insect cells | Unconjugated | WB | Inquiry |
| EBOV VP40 | DAGB183 | Ebola virus VP40 matrix protein | E. coli | Unconjugated | ELISA, WB | Inquiry |
| rREBOV GPDTM | DAGB187 | Reston Ebolavirus Glycoprotein (minus the Transmembrane Region) [His] | Insect cells | His | WB | Inquiry |
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