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Biosecurity in the Life Sciences
Published in Kezia Barker, Robert A. Francis, Routledge Handbook of Biosecurity and Invasive Species, 2021
Limor Samimian-Darash, Ori Lev
Around 1998–1999, a group of Australian scientists experimented with clinical mousepox (ectromelia virus) to develop an artificial strain that would cause infertility in mice. However, by adding a mouse gene involved in immune response to the mousepox virus, the scientists created a new violent strain that killed most of the mice, even those genetically immune to or vaccinated against mousepox. The scientists first informed the Australian government and military of their discovery yet soon afterwards went on to publish the results of their study in Journal of Virology. The mousepox virus itself, it was noted, poses no threat to humans. However, as humans possess an immune-system gene similar to the one used in the study, scientists expressed worries about the possibility of unethical use of these findings, mainly in the sense of turning human viruses into weapons (Broad, 2001; Jackson et al., 2001).
Cidofovir and Brincidofovir
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Graciela Andrei, Robert Snoeck
While CDV required 40–50 μM to inhibit the replication of vaccinia virus Copenhagen strain or cowpox virus Brighton strain by 50%, BrinCDV was active at 0.6–0.8 μM, resulting in a 58- to 75- fold increase in activity for BrinCDV (Kern et al., 2002). In addition, the EC50 values for BrinCDV in a plaque reduction assay in human foreskin fibroblast ranged from 0.2 to 1.2 μM for different vaccinia virus strains compared to 10–46 μM for CDV. BrinCDV inhibits the replication of other poxviruses at substantially lower concentrations compared to CDV (EC50 values for BrinCDV and CDV, respectively, were 0.10 and 27.3 μM for variola Bangladesh strain, 0.5 and 12 μM for ectromelia virus, 0.5 and 39 μM for rabbitpox virus, and 0.0016 and 0.98 μM for orf virus) (Dal Pozzo et al., 2007; Hostetler, 2009). BrinCDV proved efficacious and superior to CDV in the treatment of poxvirus infections in several animal models of infection, including lethal models of vaccinia virus and cowpox virus, both when the drug was given prophylactically and therapeutically (Quenelle et al., 2004b; Smee et al., 2004b; Table 216.3). Marked activity of BrinCDV was found in a lethal aerosol challenge model with ectromelia virus (the causative agent of mousepox) infection in mice (Buller et al., 2004; Parker et al., 2008a; Parker et al., 2008b). BrinCDV was also effective in the treatment of monkeypox virus infection in STAT1-deficient mice (Stabenow et al., 2010).
The discovery of novel antivirals for the treatment of mpox: is drug repurposing the answer?
Published in Expert Opinion on Drug Discovery, 2023
Ahmed A. Ezat, Jameel M. Abduljalil, Ahmed M. Elghareib, Ahmed Samir, Abdo A. Elfiky
NIOCH-14 is a chemically synthesized precursor of tecovirimat [50]. It has a potent activity against several orthopoxviruses and is easier to synthesize when compared to tecovirimat [51]. In vivo evaluation of NIOCH-14 in a mouse model intranasally infected with the Infectious Ectromelia virus showed no significant differences in survival rate compared to the tecovirimat-treated group [50]. Of note, 100% survival was found when NIOCH-14 was administered up to 2 days after infection. Significant reductions in viral titers in lungs and nose specimens were also observed. However, the survival dropped to 60% when the treatment was delayed to 6 days post-infection. Similar findings were also observed in mouse models infected with MPXV or smallpox [50]. Its efficacy was also documented in the marmot model infected with MPXV when administered at 40 mg/kg once per day [50].
Tuberculosis vaccine BCG: the magical effect of the old vaccine in the fight against the COVID-19 pandemic
Published in International Reviews of Immunology, 2022
Ashok Aspatwar, Wenping Gong, Shuyong Wang, Xueqiong Wu, Seppo Parkkila
BCG might protect mice from Japanese encephalitis infection [44]. The mice vaccinated with BCG when infected with the causative virus showed a delay in the appearance of clinical symptoms and increased survival compared with the control group mice [44]. Notably, many other studies have demonstrated that the mice vaccinated with BCG develop resistance against viral infections. These studies include the mice injected with nonviable Mtb Jamaica cells associated with oil-droplet emulsions (WCV). These mice showed a very high resistance to the injection of Encephalomyocarditis virus (EMCV) [45,46]. It has been shown that BCG also protects the mice from Ectromelia virus by enhanced production of interferon in peritoneal exudate cells and spleen cells [47,48]. In another study, the mice were inoculated with BCG intravenously and challenged with Encephalomyocarditis virus, Murine hepatitis virus 1, Murine hepatitis virus 2, Herpes simplex virus, foot-and-mouth disease virus, and A0 and A2 influenza viruses. In most cases, the mouse inoculated with BCG exhibited significantly higher resistance to lethal infections compared to the control mice [40]. In a murine model of severe combined immunodeficiency (SCID) with disseminated candidiasis, BCG vaccination led to an increased survival, which was partially dependent on NK cells [52,53].
Deficiency of Selected Cathepsins Does Not Affect the Inhibitory Action of ECTV on Immune Properties of Dendritic Cells
Published in Immunological Investigations, 2020
Magdalena Bossowska-Nowicka, Matylda B. Mielcarska, Justyna Struzik, Agnieszka Jackowska-Tracz, Michał Tracz, Karolina P. Gregorczyk-Zboroch, Małgorzata Gieryńska, Felix N. Toka, Lidia Szulc-Dąbrowska
Orthopoxviruses belong to the Poxviridae family and are linear, double-stranded DNA (dsDNA) viruses with a size of 130–360 kbp. However, only about half of the virus genes are essential for replication. Some orthopoxviruses, like vaccinia virus (VACV), monkeypox virus (MPXV) and cowpox virus (CPXV), have evolved ability to infect a very broad range of animals (including mammals, birds, reptiles and insects), but others, like variola virus (VARV) and ectromelia virus (ECTV) are very restricted to their natural hosts, human and mouse, respectively (Lefkowitz et al., 2006; Smith and Kotwal, 2002; Zehender et al., 2018). Since the eradication of smallpox (caused by VARV) in 1979 and cessation of vaccinations, the world population is increasingly becoming susceptible to poxvirus infection. Zoonotic poxviruses have been reported in the last two decades, e.g., emerging human MPXV in Africa, North America and United Kingdom, CPXV infection in cats and exotic animals and humans, cases of VACV infection in humans in South America and India (Essbauer et al., 2010; Vaughan et al., 2018). There are no antiviral treatments to all these poxvirus infections and the current vaccine against smallpox, although effective, has some safety concern. Hence, it calls for maintained efforts to find potential therapeutic targets of poxviruses and improve safety of the existing vaccine. Understanding the biology of poxviruses may lead to determination of their unique immune evasion strategies exploited especially in their natural hosts.