THE ANTIVIRAL ACTION OF <i>THREO</i>‐β‐PHENYLSERINE

Dickinson, Loïs; Thompson, Mildred J.; Nicholson, Jackie

doi:10.1111/j.1476-5381.1957.tb01364.x

Cited by 10 publications

(4 citation statements)

References 21 publications

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“…The activity of p-phenylserine is probably directed against the intracellular multiplication of the rabies virus. Dickinson and Thompson (1957) found that ,8-phenylserine was acting during the first half of the latent period of influenza A virus multiplication in chorioallantoic membrane fragments. Furthermore, the addition of phenylalanine reversed the inhibition.…”

Section: Discussionmentioning

confidence: 97%

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The in vivo inhibition by β-phenylserine of rabies, myxoma, and vaccinia viruses

Pons

Preston

1961

Virology

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The daily intraperitoneal administration of 19-15 mg of ,%phenylserine protected rats against death from lethal amounts of rabies virus. The protective effect was most marked when the animals were treated for 3 days prior to the injection of the virus, although initiation of treatment 24 hours after the virus was injected also gave protection. The administration of nn-phenylalanine or nn-tyrosine in combination with p-phenylserine reversed the inhibition of rabies virulence. Rabies-infected animals protected with /3-phenylserine and challenged with a second injection of rabies virus 6-7 weeks later did not show any immunity. The xanthine oxidase activity of infected rat brain increased during the course of rabies. The increased activity paralleled the titer of virus in the brain. There was no alteration in the xanthine oxidase activity when animals injected with the virus were treated with @-phenylserine. P-Phenylserine inhibited the propagation of vaccinia virus in rabbit skin when the compound and virus were mixed prior to injection. The daily intraperitoneal injection of 75 mg of p-phenylserine delayed the development of myxomatosis in rabbits. The compound had no apparent effect on the multiplication of influenza A (PRS), eastern equine encephalitis, poliovirus (Lansing strain), or mouse encephalomyelitis (FA strain) viruses in mice. The compound was inactive also against influenza A virus in embryonated eggs.

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Section: Discussionmentioning

confidence: 97%

“…Inhibition p-Phenylserine inhibition of bacteria can be reversed by the addition of excess phen- ylalanine or tyrosine. Dickinson and Thompson (1957) showed that P-phenylserine inhibition of influenza A virus multiplication in chorioallantoic membrane fragments could be reversed by phenylalanine.…”

Section: Reversal Of P-phenylserinementioning

confidence: 99%

The in vivo inhibition by β-phenylserine of rabies, myxoma, and vaccinia viruses

Pons

Preston

1961

Virology

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“…methoxinine and ethionine (Ackermann, 1951 b) and phenylserine (Dickinson & Thompson, 1957) have been found to inhibit virus growth in tissue culture in concentrations tolerated by the tissue; their activity was annulled by the corresponding natural amino acids. This suggested that virus-infected cells needed more of certain amino acids than did uninfected cells.…”

Section: Discussionmentioning

confidence: 99%

“…in de-embryonated eggs Ackermann (1951 b) reported ethionine, and Dickinson & Thompson (1957) p-phenylserine, to delay growth of influenza A in isolated chorio-allantoic membrane and to be antagonized by the analogous natural amino acids (methionine and phenylalanine, respectively). In view of the results obtained here on amino acid uptake it was of interest to test these two compounds for ability to delay growth of influenza B in de-embryonated eggs.…”

Section: Action Of M-)-phenylserine and Dl-ethionine On Growth Of Injmentioning

confidence: 99%

The Effect of Infecting the Cells of the De-embryonated Egg with Influenza Virus on their Uptake of Glucose and Amino Acids

Mills¹

1958

Journal of General Microbiology

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SUMMARY:A method was found for infecting all the cells of the de-embryonated hen's egg with influenza B virus (strain Lee). Infected cells took up more glucose from the culture medium than did uninfected cells. Neither infected nor uninfected cells took up any of six amino acids, given singly. A mixture of thirteen amino acids was taken up well, and to the same extent, by infected and uninfected cells. When cysteine, histidine or methionine was omitted from this mixture, the remaining amino acids were taken up better by uninfected cells than by infected cells; when any other amino acid (arginine, glutamhe, isoleucine, leucine, lysine, phenylalanine , threonine, tryptophan, tyrosine, valine) was omitted there was no significant difference in uptake by infected and uninfected cells. In this system, ethionine delayed multiplication of influenza virus, but p-phenylserine did not. These results are consistent with an increased requirement of the infected cell in this system for cysteine, histidine and methionine.Amino acid analogues, e.g. methoxinine and ethionine (Ackermann, 1951 b) and phenylserine (Dickinson & Thompson, 1957) have been found to inhibit virus growth in tissue culture in concentrations tolerated by the tissue; their activity was annulled by the corresponding natural amino acids. This suggested that virus-infected cells needed more of certain amino acids than did uninfected cells. In turn, knowledge of increased needs for amino acids by virus-infected cells might act as a guide to other amino acid analogues capable of inhibiting virus growth. The present work reports a search for such increased needs by measuring the uptake of amino acids by normal and virus-infected cells.For this work it seemed advisable to use a uniform population of cells and a non-cytopathogenic virus. The cells of the de-embryonated hen's egg, which are said to be very uniform (Henle, 1953), and influenza B virus, strain Lee, were chosen. Lee virus has the added advantage that it gives rise to 'incomplete' virus less readily than do other strains of influenza virus (Fazekas de St Groth & Graham, 1954), so avoiding possible complications from this cause. To make any effect of infection as clear as possible it was necessary to infect all the exposed cells; it also seemed likely that decreasing the concentration of internal metabolites by starvation might make effects of infection on uptake clearer. In view of this, preliminary studies were made to find the effect of starvation on virus production and the conditions necessary for infecting all the cells. A study of the effect of infection on glucose uptake similar to those of Ackermann (1951 a) and Bauer (1953), made as a preliminary to work on amino acid uptake, is also reported here.

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Genetic Studies with Influenza A Virus

Simpson¹

1964

Novartis Foundation Symposia

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THE ANTIVIRAL ACTION OF THREO‐β‐PHENYLSERINE

Cited by 10 publications

References 21 publications

The in vivo inhibition by β-phenylserine of rabies, myxoma, and vaccinia viruses

The in vivo inhibition by β-phenylserine of rabies, myxoma, and vaccinia viruses

The Effect of Infecting the Cells of the De-embryonated Egg with Influenza Virus on their Uptake of Glucose and Amino Acids

Genetic Studies with Influenza A Virus

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