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The article reports on the Yersinia pestis, a causative agent of bubonic plague, excrete L-aspartic acid at the expense of exogenous L-glutamic acid during expression of the low-calcium response. It discusses that the results of enzymic analysis provided suggest that a previously defined deficiency of aspartese (AspA) accounts for the phenomenon rather than an elevated oxaloacetate pool. It infers that the only known distinction between most sequenced isolates of aspA from Y. A study on the Yersinia pestis is presented.

The article discusses a study which showed that herpes simplex virus co-infection-induced Chlamydia trachomatis persistence is not mediated by any known persistence inducer or anti-chlamydial pathway. A tissue-culture model of Chlamydia trachomatis/herpes simplex virus type-2 (HSV-2) co-infection indicates that viral co-infection stimulates the formation of persistent chlamydiae. Luminex assays indicate that interferon (IFN)-gamma, interferon-alpha and tumor necrosis factor (TNF)-alpha are not released from co-infected cells while semiquantitative reverse transcriptase polymerase chain reaction (RT-PCR) studies show that IFN-beta, IFN-gamma, indoleamine 2,3-dioxygenase, lymphotoxin-alpha and inducible persistence is not stimulated by any persistence-associated cytokine.