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Order Mononegavirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
The Filoviridae family contains variously shaped, often filamentous viruses (shown in Figure 31.1b) and consists of 6 genera with 11 species (Kuhn et al. 2019). Several filovirus representatives, such as various variants of EBOV of the genus Ebolavirus and Marburg virus (MARV) of the genus Marburgvirus, are pathogenic for humans and highly virulent. The natural hosts for filoviruses could be bats, as for Ebola- and Marburgviruses, whereas others may infect fish.
Classification of Hemorrhagic Fevers
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
The name Filoviridae has been suggested to include the genus Filovirus of which the type species is the Marburg virus and the other member is Ebola virus.4 Another proposal is that both these viruses be included in the rhabdovirus group. However, it has been noted that the major features which distinguish these viruses from the rhabdoviruses are the particle length, the unique proteins and a central axial channel of diameter significantly smaller than that of the rhabdoviruses. The classification is still under review.
Chemical and Biological Threats to Public Safety
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Viral hemorrhagic fevers (VHF) are a clinically related group of viral diseases with a diverse etiology. The family of Filoviridae includes the Marburg and Ebola viruses. Similarly, the family of Bunyaviridae includes the hantavirus and bunyavirus (which primarily causes encephalitis in humans). All are RNA viruses endemic in Africa and with the exception of the bunyavirus, cause severe or fatal hemorrhagic fevers. The condition is characterized by acute onset of fever, headache, generalized myalgia, conjunctivitis, and severe prostration, followed by various hemorrhagic symptoms. The organism facilitates the destruction of endothelial cells, leading to vascular injury and increased capillary permeability, leukopenia, and thrombocytopenia. Antiviral therapy has not been shown to be clinically useful.
The role of sialic acid-binding immunoglobulin-like-lectin-1 (siglec-1) in immunology and infectious disease
Published in International Reviews of Immunology, 2023
Shane Prenzler, Santosh Rudrawar, Mario Waespy, Sørge Kelm, Shailendra Anoopkumar-Dukie, Thomas Haselhorst
Ebola viruses belong to the Filoviridae family and consist of many strains which are capable of causing hemorrhagic fever [27]. Ebola viruses also utilize dendritic cells and macrophages to disseminate to the lymph nodes, liver and spleen [88]. Ebola virus dendritic cell entry involves several steps requiring multitude of receptors. DC-SIGN mediates attachment of the Ebola virus to dendritic cells by glycoprotein recognition, meanwhile TIM/TAM receptors bind phosphatidylserine on the membrane of virus facilitating viral cell entry by means of apoptotic mimicry [89–91]. From here Ebola viruses enters the cell after macropinocytosis and the viral glycoprotein is cleaved using cellular proteases like cathepsin B [27, 92]. The cleavage allows for glycoprotein recognition by endosome receptor Niemann-Pick C1, which allows the virus to enter the cytoplasm [93, 94]. It was recently discovered that in a similar way to HIV-1, ebola virus buds from host cells and incorporates GM1 gangliosides which bind Siglec-1 [27]. The role of Siglec-1 in attachment and entry of Ebola virus is poorly understood, but it has been shown that anti-Siglec-1 antibodies are able to hinder viral entry and that Siglec-1 is more prominent to the entry of the virus than other well-known receptors like DC-SIGN [27]. Currently, there are studies underway to create vaccines for Zaire ebolavirus (ZEBOV), which is the species responsible for a recent outbreak in West Africa. However, there are other species which will not be covered by vaccine efforts and Siglec-1 may represent an important therapeutic target [27].
The roles of epidermal growth factor receptor in viral infections
Published in Growth Factors, 2022
So far, there is no specific drug to treat DENV infection. Bekerman et al. (2017) have revealed the antiviral activity of combined treatment of erlotinib and sunitinib in two DENV-infected IFN-α/β and IFN-γ receptor-deficient murine models, AG129 and AG-B6. Erlotinib is a reversible EGFR inhibitor approved for the treatment of metastatic NSCLC and pancreatic cancer, whereas sunitinib is an ATP-competitive multitargeted tyrosine kinase inhibitor approved for the treatment of renal cell carcinoma, gastrointestinal stromal tumour, and pancreatic neuroendocrine tumour (Shukla et al. 2009; Blumenthal et al. 2012). Prophylactic and daily combined treatment of erlotinib and sunitinib at 30 mg/kg respectively resulted in 11-fold reduction in DENV viremia in infected AG-B mice. This combined treatment also reduced morbidity and mortality in AG-129 and AG-B6 mice infected with lethal DENV inoculum. In addition to DENV, Bekerman et al. also demonstrated that the combined treatment inhibited Ebola virus (EBOV) infection in vivo. EBOV is one of the members of family Filoviridae that causes haemorrhagic fever associated with 50–90% human mortality. It is an enveloped virus that consists of non-segmented, single stranded and negative-sense RNA genome (Lee et al. 2008). Prophylactic and daily treatment of erlotinib and sunitinib at 45 and 5 mg/kg respectively reduced morbidity and mortality in EBOV-infected mice, as evidenced by greater weight gain and 50% survival (Bekerman et al. 2017). However, little is known on the role of EGFR in EBOV infection.
Repurposing of well-known medications as antivirals: hydroxychloroquine and chloroquine – from HIV-1 infection to COVID-19
Published in Expert Review of Anti-infective Therapy, 2020
Sara Naghipour, Mahsa Ghodousi, Sara Rahsepar, Sepideh Elyasi
The Filoviridae family includes Ebola and Marburg viruses. CQ becomes highly concentrated in tissues such as the adrenal glands, liver, spleen, and kidneys – tissues suffering extensive necrosis in fatal filoviral infections. Since the glycoprotein of Filoviruses is the only protein involved in initiating infection and cytotoxicity, inhibiting its glycosylation could potentially (1) inhibit EboV tropism for a wide range of host cells and organs; (2) lead to the production of noninfectious or less infectious virus and (3) decrease Ebov pathogenicity. Therefore, it saves time for the adaptive immune response, which normally fails in fatal cases. A steady state CQ plasma concentration of at least 1 μg/mL or a whole blood concentration of 16 μM/L must be achieved and be sustained until the patients’ viremia becomes undetectable [54]. However, the studies in this field are limited to in vitro and in vivo researches on CQ, mostly with controversial findings (Table 6) [55–60].