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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).
WHO: accessory after the fact?
Published in Théodore H MacDonald, David Player, Mathura P Shrestha, Sacrificing the WHO to the Highest Bidder, 2018
The danger of inadvertently constructing highly lethal pathogens was recently demonstrated by an Australian research team experimenting with a virus that is closely related to the smallpox virus. The team genetically engineered the mouse-pox virus in an attempt to create a fertility control vaccine to control mouse populations. The result was unintended and unforeseen – all of the mice infected with the new virus strain died, even those that had been vaccinated against mousepox. It turned out that the additional gene had the unanticipated effect of turning off the immune system of the mice, making them vulnerable to lethal infection by the otherwise harmless virus. The prospect of a genetically engineered smallpox virus overcoming vaccinations and the immune system is disturbing.
Medical theory, medical care, and preventive medicine
Published in Lois N. Magner, Oliver J. Kim, A History of Medicine, 2017
Another potential threat arises from the possibility of modifying other poxviruses and creating more virulent strains. Confirmation of this concept occurred in 2001, when researchers studying mousepox were able to make a virulent virus that could infect previously immunized mice. Scientists warned that, while it may not be true that any graduate student could create a dangerous genetically engineered virus on the kitchen counter with a blender and a face mask, it is possible that scientists in a rogue nation with illicit smallpox stocks could create genetically engineered bioweapons.
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
It is a lipid-conjugate of cidofovir with a higher efficacy in animal models owing to its improved oral bioavailability, lack of nephrotoxicity, and higher conversion rate to the active form [37–39]. The lipid moiety is removed upon entry into the cell via lipid uptake pathways, and the cidofovir becomes available to kinases for phosphorylation reactions. Brincidofovir efficacy was observed in mouse and rabbit models experimentally infected by the mousepox virus and rabbitpox virus, respectively [40–42]. Brincidofovir passed phase III of clinical trials (immunocompromised adults and children were recruited) to treat cytomegalovirus and adenovirus with only a few adverse effects [37]. In the case of a smallpox infection, the recommended dose for adults was 200 mg/week for three weeks [40]. Nonetheless, the efficacy of cidofovir and brincidofovir in MPXV infections is yet to be determined.
ECTV Abolishes the Ability of GM-BM Cells to Stimulate Allogeneic CD4 T Cells in a Mouse Strain-Independent Manner
Published in Immunological Investigations, 2019
Lidia Szulc-Dąbrowska, Piotr Wojtyniak, Justyna Struzik, Felix N. Toka, Anna Winnicka, Małgorzata Gieryńska
Mousepox is a severe disease with high mortality rates in susceptible strains of mice. Resistant strains are also susceptible to infection; however, they develop asymptomatic or subclinical disease with no mortality (Jacoby and Bhatt, 1987). Resistance and susceptibility to lethal mousepox are associated with polarized T helper cell (Th)1 or Th2 responses, respectively. Therefore, in resistant strains of mice, e.g. C57BL/6, strong Th1 response with interferon(IFN)-γ production determines protection and is associated with elevated NK cell activity and robust cytotoxic T lymphocyte (CTL) response. On the contrary, susceptible strains, e.g. BALB/c mice develop nonprotective Th2 response, which is associated with low IFN-γ production and weak activity of NK cells and CTLs, resulting in fulminant disease and death (Chaudhri et al., 2004). However, deficiencies in Th2 cytokine signaling exacerbate ECTV infection; therefore, factors determining resistance or susceptibility to mousepox seem to be more complex than just a Th1/Th2 balance (Sakala et al., 2015).