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Encapsulating Materials Within VNPs
Published in Nicole F Steinmetz, Marianne Manchester, Viral Nanoparticles, 2019
Nicole F Steinmetz, Marianne Manchester
VLPs containing metallic nanoparticles or QDs are also promising candidates for biomedical applications such as imaging and therapy. This will be discussed in detail in Chapter 8; here one example is given to demonstrate the feasibility of these hybrid VLPs for imaging purposes. The above-described assembly protocol can be adapted to other viruses. Successful nanoparticle-templated VLP assembly has been demonstrated using coat proteins from an alphavirus (Goicochea et al., 2007) and Simian virus 40 (SV40) (Li et al., 2009), both of which are mammalian viruses. SV40 is a polyomavirus that infects humans and monkeys. Infections are mostly latent, but the virus has the potential for tumor transformation. SV40 is a double-stranded DNA virus. The non-enveloped capsid has icoashedral T = 7 symmetry and a diameter of 45 nm (The Universal Virus Database of the International Committee on Taxonomy of Viruses, ICTVdB, http://www.nbci.nlm.nih.gov/ICTVdb).
Other causes of mesothelioma not related to asbestiform mineral fibers
Published in Dorsett D. Smith, The Health Effects of Asbestos, 2015
Viruses such as SV40 and MC29 avian leukosis virus are important cofactors in mesothelioma production. SV-40 inactivates tumor-suppressor genes and has demonstrated oncogenic potential in animal models. It has a predilection for human epithelial cells, but its actual role in mesothelioma carcinogenesis is likely as a promoter with mineral fibers such as asbestos, rather than a primary cause of human mesothelioma. An estimated 62% of 92 million U.S. residents received the potentially SV40-contaminated Salk polio vaccine for the 8 years it was used (1955–1963); of these, at least one-fifth may have received live, infectious SV40-containing vaccine. In addition, although efforts were made to exclude SV40 from polio vaccines, the testing done was not rigorous enough to totally ensure that all cohorts born after 1963 were given SV40-free polio vaccines. For example, a major Eastern European manufacturer used a procedure that did not fully inactivate SV40 in oral poliovirus vaccine; these SV40-contaminated vaccines were produced from the early 1960s to about 1978 and were used throughout the world. (Comar M, Zancotta N, Pesel G et al. Asbestos and SV40 in malignant pleural mesothelioma from a hyperendemic area of North-Eastern Italy. Tumori 2012;98:210–4; Cleaver AL, Bhamidipaty K, Wylie B et al. Long-term exposure of mesothelial cells to SV40 and asbestos leads to malignant transformation and chemotherapy resistance. Carcinogenesis 2014;35(2):407–14.)
BK virus in kidney transplant recipients with graft dysfunction
Published in Egyptian Journal of Basic and Applied Sciences, 2023
Doaa Mohamed Riad, Wafaa Kamel Mowafy, Hazem Hamed Saleh, Essam Mahmoud El Sawy, Noha Tharwat Abou El-Khier
Urine cytology: Cytology smears from urine samples of case group were performed. Standard smears were prepared from fresh voided morning urine samples, fixed in alcohol, and stained with Papanicolaou stain. When positive for Decoy cells, the number of cells was counted (Figure 1).Renal graft biopsies: Renal graft biopsies were performed for all patients in the case group.Immunostaining with SV40 m-Ab: SV40 m-Ab from Santa Cruz Biotechnology (USA) was used.
Characterization of pulmonary responses in mice to asbestos/asbestiform fibers using gene expression profiles
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Naveena Yanamala, Elena R. Kisin, Dmitriy W. Gutkin, Michael R. Shurin, Martin Harper, Anna A. Shvedova
Both carcinogenic and non-carcinogenic health outcomes such as pleural fibrosis and plaques, pulmonary fibrosis, have been observed in asbestos workers. Much of our understanding regarding the mechanisms for induction of carcinogenic and non-carcinogenic outcomes is based upon studies involving the biological effects of asbestos/asbestiform fibers (Kane 1996; Oberdorster 1996; Sanchez et al. 2009; Sayan and Mossman 2016). The disease-causing potential of asbestos related exposures is governed by several factors, including (1) duration and frequency of exposures, (2) individual susceptibility and biopersistence, as well as (3) type, shape and surface characteristics of the fibers (Fubini and Fenoglio 2007; Kane 1996). However, not all fibers with similar characteristics have the potential to trigger similar pathogenic responses. For example, despite exhibiting almost identical size distributions, erionite and crocidolite asbestos fibers lead to differential carcinogenic outcomes (Andujar et al. 2016; Carbone et al. 2011; Carbone and Yang 2012; Wagner et al. 1985). The inhalation of fibrous erionite by rats produced mesothelioma in 96.6% of animals but no apparent lung cancers (Wagner et al. 1985). Crocidolite (in the same experiment at 10-fold higher dose than erionite) produced lung cancer in 3.6% of rats with no appearance of mesotheliomas. However prolonged exposures to high levels of crocidolite asbestos fibers was reported to induce mesothelioma in approximately 5% of humans, albeit requiring additional factors such as genetic predisposition and/or SV40 infection (Carbone, Kratzke, and Testa 2002; Carbone et al. 1994; Comar et al. 2012; Dogan et al. 2006). Additional individual risk factors, such as smoking and other pre-existing lung diseases, further complicate disease paradigms seen after asbestos exposures. While smoking combined with asbestos exposure did not appear to increase the risk of mesothelioma occurrence (Frost, Darnton, and Harding 2011; O’Reilly et al. 2007), it is known to enhance the risk of developing lung cancer that is greater than the individual risks from asbestos and smoking added together (Moller et al. 2014; NTP 2016). Moreover, both erionite and fibrous talc (asbestiform mineral fibers) are thought to be biopersistent. Yet erionite is a potent animal and human carcinogen while fibrous talc is not (Wild 2006). These studies indicate that morphology, fiber type/size/number and biopersistence are not the only critical factors/indicators that determine fiber-induced carcinogenesis (Boulanger et al. 2014).