Abstract
The earliest studies demonstrating inhibition of viral growth by guanidine were published approximately 20 years ago (Rightsel et al. 1961). Soon after the initial discovery, mutants that were either resistant to or dependent upon guanidine were described (Lonno et al. 1963; Nakano et al. 1963). In general, growth of many members of the Picornaviridae family, which comprises a large number of lipid-free animal viruses that contain single-stranded RNA genomes, is susceptible to inhibition by guanidine (Caliguiri and Tamm 1973). Included among the sensitive picornaviruses are the three strains of poliovirus, coxsackieviruses, echoviruses, rhinoviruses, and foot-and-mouth disease virus (FMDV). Echoviruses 6, 7, 8, 12, and coxsackievirus B6 are resistant to the compound (Crowther and Melnick 1961). Orthomyxoviruses, paramyxoviruses, reoviruses, most togaviruses, and animal viruses that contain DNA are also naturally resistant to guanidine. Replication of Sindbis and Semliki Forest viruses of the Alphavirus genus of the togavirus family (Friedman 1970) and two plant viruses, tobacco necrosis (Varna 1968) and tobacco mosaic virus (TMV; Dawson 1975) are sensitive to the inhibitor.
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Tershak, D.R., Yin, F.H., Korant, B.D. (1982). Guanidine. In: Came, P.E., Caliguiri, L.A. (eds) Chemotherapy of Viral Infections. Handbook of Experimental Pharmacology, vol 61. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-68487-6_8
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