Target intelligence / Profile preview

Filoviridae (Filovirus) (FILO)

Target
FILO
Molecular classification
Virus, Pathogen, Negative-strand RNA virus
01

Overview

Filoviruses, members of the family Filoviridae, are filamentous, enveloped, single-stranded, negative-sense RNA viruses that cause severe and often fatal hemorrhagic fevers in humans and non-human primates. The family includes highly lethal pathogens such as the Ebola virus (EBOV) and Marburg virus (MARV), which are characterized by case fatality rates ranging from 25% to 90%. The viral lifecycle is driven by several essential proteins that serve as therapeutic targets: the surface glycoprotein (GP), which facilitates attachment to host cell receptors like Niemann-Pick C1 (NPC1) and endosomal fusion, and the large (L) protein, which acts as an RNA-dependent RNA polymerase (RdRp) for genome replication and transcription. Treatment strategies generally involve neutralizing the glycoprotein with monoclonal antibodies, such as the FDA-approved cocktails Inmazeb and Ebanga, or inhibiting the viral polymerase with small-molecule nucleotide analogs like remdesivir and favipiravir. Despite the success of these targeted therapies, the rapid mutation rate and high virulence of filoviruses necessitate the continued development of broad-spectrum or pan-filovirus inhibitors.

Other names
FiloviridEbolavirusMarburgvirusHemorrhagic fever virusCueva-like virus
02

Mechanism of action

Neutralization of the viral surface glycoprotein (GP) to block host cell entry and fusion; competitive inhibition of the viral RNA-dependent RNA polymerase (L protein) to terminate RNA synthesis and replication; inhibition of endosomal processing and cysteine proteases required for glycoprotein priming.

03

Biological functions

Viral replicationViral entryHost cell attachmentImmune evasionRNA synthesisViral buddingViral assemblyTranslation
04

Disease associations

Ebola Virus Disease (EVD)Marburg Virus Disease (MVD)Viral Hemorrhagic FeverInfection
05

Safety considerations

Rapid viral mutation leading to therapeutic escape and drug resistanceAntibody-dependent enhancement (ADE) of viral infectionCytokine storm and severe systemic inflammatory response syndromeSpecies-specificity of monoclonal antibodies limiting cross-protectionSafety risks associated with handling live virus (BSL-4 requirement)
06

Interacting drugs

Remdesivir

8 more in the full profile.

07

Biomarkers

Viral load (RT-PCR)Soluble glycoprotein (sGP) levelsAspartate aminotransferase (AST)Alanine aminotransferase (ALT)Pro-inflammatory cytokines (IL-6, TNF-alpha)D-dimer levels

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