The effect of virus infection on pyruvate metabolism

https://doi.org/10.1016/0006-3002(57)90336-0Get rights and content

Abstract

E. coli cells infected with T2 or T7 virus accumulate pyruvate during the metabolism of l-serine or lactate. This was shown to be due to a markedly reduced ability of virus-infected cells to metabolize pyruvate as compared with uninfected cells. When cells are first infected with T2 and then with T7, pyruvate continues to be utilized at the reduced rate characteristic of T2 infection, indicating that the effect of virus is on intracellular control mechanisms for pyruvate metabolism.

During viral adsorption and penetration, materials “leak” from the infected cells which have the ability to stimulate pyruvate metabolism in diluted cell-free extracts. In addition, cocarboxylase appears to be more labile in extracts from T2-infected cells as compared with extracts from normal cells. These facts may account for the reduced rate of oxidation of pyruvate in phage-infected cells. The present results are discussed in relation to other known metabolic effects of virus infection.

References (14)

  • S.S. Cohen

    J. Biol. Chem.

    (1948)
  • A.B. Pardee et al.

    J. Biol. Chem.

    (1952)
  • J. Szulmajster et al.

    Biochim. Biophys. Acta

    (1952)
  • T.E. Friedemann et al.

    J. Biol. Chem.

    (1943)
  • S.B. Barker et al.

    J. Biol. Chem.

    (1941)
  • O.H. Lowry et al.

    J. Biol. Chem.

    (1951)
  • J. Monod et al.

    Ann. inst. Pasteur

    (1947)
There are more references available in the full text version of this article.

This work was performed under contract No. AT (30-1)-1045 with Division of Biology and Medicine of the Atomic Energy Commission.

View full text