Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.7 (DNA polymerase)
 17,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present paper reports on the induction of two cell surface markers on human lymphoid cells following herpes simplex virus (HSV) infection. While both primary and chronic infections of human lymphoid cells led to the induction of receptors for the Fc region of 7S IgG, chronic HSV infection was also characterized by the induction of surface-bound IgM. Surface and intracellular Fc receptors were detected in the human lymphoid cell line, Raji, infected with HSV types 1 and 2. Under optimal conditions with a multiplicity of infection (m.o.i.) of 50 to 100 p.f.u. per cell, this marker was inducible in only about 53% of the infected cells. Kinetic studies revealed the appearance of these receptors at around 5 h following HSV infection and they reached a plateau 16 to 18 h p.i. Interestingly, this Fc receptor expression (i.e. percentage of positive cells) was found to be similar in primary and chronically HSV-infected Raji cells. Both human leukocyte interferon and phosphonoacetic acid (PAA), an inhibitor of herpesvirus DNA polymerase activity, effectively inhibited Fc receptor synthesis during primary HSV-infection and these two agents suppressed its induction in chronically HSV-infected Raji (Raji-HSV) cells. This inhibitory or suppressive effect, particularly of PAA, suggests that this HSV-induced Fc receptor may represent a late virus function in the infected cell. Unlike primary HSV infection, about 80% of the chronically HSV-infected Raji cells were found to express surface-bound IgM. This IgM induction was suppressed by long-term interferon treatment but not with PAA-treatment. Superinfection studies of interferon and PAA-treated Raji-HSV cells indicate that only the former would develop Fc receptors suggesting a protective role of this IgM against superinfection by HSV.
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PMID:Studies on the induction of IgG-Fc receptors and synthesis of IgM in primary and chronically-infected lymphoid (Raji) cells by herpes simplex virus. 23 Feb 88

We have investigated the induction of Fc receptor (FcR) in different types of lymphoid cell lines (LCL) infected with herpes simplex virus (HSV). Subpopulations of certain of these LCL normally express FcR unrelated to herpetic infection. Differentiation of virus-induced FcR from that related to normal cell function was therefore possible. FcR detection was carried out by means of a rosette assay using ox erythrocytes coated with 7S immunoglobulin G (EA rosettes). Both HSV types 1 and 2 were found to induce FcR in B, T, and "null" (i.e., non-B, non-T) type LCL; however, in all the LCL tested, this HSV-induced FcR expression appeared to be more restricted in the responding T LCL than in responding B and null type LCL. In addition, kinetic experiments revealed that the time course of HSV-induced FcR expression differed among these LCL types tested. Interestingly, a number of LCL were resistant to HSV infection or restricted HSV gene expression, including expression of the viral products responsible for FcR induction. In all the responding HSV-infected LCL, induction of FcR always paralleled the expression of HSV antigens. Synthesis of HSV-induced FcR was shown to be inhibited by phosphonoacetic acid, an inhibitor of herpesvirus DNA polymerase activity, whereas FcR of non-HSV origin was found to be resistant to inhibitor. This would infer that HSV codes for an FcR which can be differentiated from that of cellular origin by using phosphonoacetic acid. Therefore, two different mechanisms of FcR synthesis may be suggested, one virus mediated and the second probably under cellular control. In addition, the data obtained using Epstein-Barr virus producer as well as isogeneic monoclonal cell lines, with and without the Epstein-Barr virus genome, indicated that the resident Epstein-Barr virus genome in the target cell did not have a detectable effect in the induction of FcR by HSV.
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PMID:Herpesvirus-lymphoid cell interactions: comparative studies on the biology of herpes simplex virus-induced Fc receptors in B, T, and "null" lymphoid cell lines. 624 24