Virus-mutant

Gubareva LV, Kaiser L, Matrosovich MN, Soo-Hoo Y, Hayden FG (2001) Selection of influenza virus mutants in experimentally infected volunteers treated with oseltamivir, J Infect Dis 183 523-531... 

Palese P, Tobita K, Ueda M, Compans RW (1974b) Characterization of temperature sensitive influenza virus mutants defective in neuraminidase. Virology 61 397 10 Pegg MS, von Itzstein M (1994) Slow-binding inhibition of sialidase from influenza virus, Biochem Mol Biol Int 32 851-858... 

Mutations Much of our knowledge of viral reproduction and how it is regulated has depended on the isolation and characterization of virus mutants. Several kinds of mutants have been studied in viruses host-range mutants, plaque-type mutants, temperature-sensitive mutants, nonsense mutants, transposons, and inversions. 

Nonsense mutations change normal codons into nonsense codons. In viruses, nonsense mutations are recognized because hosts are available that contain suppressors able to read nonsense codons. The virus mutant will be able to grow in the host containing the suppressor, but not in the normal host. 

Cross-resistance - Cross-resistance has been observed between zanamivir-resistant and oseltamivir-resistant influenza virus mutants generated in vitro. 

Frykberg, L., S. Palmieri, H. Beug, T. Graf, M.J. Hayman, and B. Vennstrom, Transforming capacities of avian erythroblastosis virus mutants deleted in the erbA or erbB oncogenes. Cell, 1983. 32(1) 227-38. 

Palase P, Tobita K, Ueda M, Compans RW. Characterization of temperature sensitive influenza virus mutants defective in neuraminidase. Virology 1974 61 397-410. 

Kool M, Voncken JW, van Lier FL, Tramper J, Vlak JM (1991), Detection and analysis of Autographa californica nuclear polyhedrosis virus mutants with defective interfering properties, Virology 183 739-746. 

Moreau, M.-C. Inhibition of a vesicular stomatitis virus mutant by rifampin. J. Virol. 

Vrati, S., Faragher, S. G., Weir, R. C., and Dalgamo, L. (1986). Ross River virus mutant with a deletion in the E2 gene Properties of the virion, virus-specific macromolecule synthesis, and attenuation of virulence for mice. Virology 151, 222-232. 

A hepatitis B virus mutant associated with an epidemic of fulminant hepatitis. New Engl. J. Med. 1991 324 1705-1709... 

The isolation of drug-resistant virus mutants in the laboratory and the determination of their patterns of crossresistance may be useful to clarify the mechanisms of selective drug action. Indeed, one of the best ways to determine the overall mechanism of action of an antiviral drug is via drug resistance. The fact... 

It is possible that the virus mutant selected under the pressure of a certain drug is a mixture of two or more populations of virus. It has been found that the HSV-1 mutants arising under the selective pressure of HPMPC or HPMPA are not pure populations. Thus, plaque-purified virus must be prepared, and the drug-susceptibility profile of a few classes of compounds should be determined as well as the mutations in the drug-targeted viral gene that are associated with the resistant phenotype. 

Mechanisms Amantadine and rimantadine inhibit the first steps in replication of the influenza A and rubella viruses (Figure 49-1). These steps involve viral adsorption to the host cell membrane, penetration into the cell via endocytosis. and viral particle uncapping. The inhibitory action of these drugs may be due to their alkaline reaction, which raises the endo-somal pH. At low concentrations, amantadine also binds to a specific protein in the surface coat of the influenza virus to prevent fusion. Drug-resistant influenza A virus mutants can emerge and infect contacts of patients in treatment. 

Read GS, Frenkel N (1983) Herpes simplex virus mutants defective in the virion-associated shutoff of host polypeptide synthesis and exhibiting abnormal synthesis of alpha (immediate early) viral polypeptides. J Virol 46 498-512... 

ElA can also induce apoptosis in p53-null cells (Saos-2) and, thus, in a p53-independent manner. With virus mutants that lack ElB expression, it was recently shown that the 243R form of El A is able to induce apoptosis (Chiou and White 1997) however, conflicting data suggest that 243R can only induce apoptosis in a p53-dependent manner (Teodoro et al. 1995). The mechanism of apoptosis induction by ElA independent of p53 is not well understood. In the absence of other viral products, 243R is capable to activate a cascade of cysteine proteases. 

Kempkes, B., Spitkovsky, D., Jansen-Durr, R, Ellwart, J.W., Kremmer, E., Delecluse, H.J., Rottenberger, C., Bornkamm, G.W. and Hammerschmidt, W., B-cell proliferation and induction of early G1-regulating proteins by Epstein-Barr virus mutants conditional for EBNA2. Embo. J., 14, 88-96 (1995). 

Tanaka, K., Chowdhury, K., Chang, K. S. S., Israel, M., and Ito, Y., 1982, Isolation and characterization of polyoma virus mutants which grow in murine embryonal carcinoma and trophoblast cells, EMBO J. 1 1521-1527. 

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