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Query: EC:2.7.7.48 (
transcriptase
)
9,479
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Earlier we reported a reduction to 1/30th-1/100th of the original number of infectious particles in the infectious vesicular stomatitis virus (VSV) released from L cells treated with 10 or 30 reference units of
interferon
per ml. However, in these cultures virus particle production, as measured by VSV particle-associated viral RNA, virus nucleocapsid protein, and viral
transcriptase
, was inhibited by less than 10%. Data reported in this paper show that there was a significant reduction in glycoprotein and membrane protein of VSV particles released from
interferon
-treated cells. Evidence supporting the deficiency of glycoprotein in VSV released from
interferon
-treated cells was derived from electron microscopic studies. Under conditions where glycoprotein spikes or projections were clearly detectable on the surface of VSV released from cells not treated with
interferon
, very few spikes were observed on VSV released from
interferon
-treated cells. These results suggested that
interferon
-treated cells produced VSV particles with low infectivity and that this low infectivity may be related to the reduced amount of glycoprotein and membrane protein incorporated into such particles.
...
PMID:Interferon-treated cells release vesicular stomatitis virus particles lacking glycoprotein spikes: correlation with biochemical data. 615 48
Conditions of
interferon
production stimulation were studied in human tonsillar cell cultures exposed to natural and synthetic inducers : poly(I) . poly(C), phage f2
RNA replicase
, phytohemagglutinin and the low-molecular inducer gossypol (beta-aminoethyl sulfoxide Na). It has been shown that being inferior in the productivity per one cell to the continuous lymphoblastoid Raji and Namalva cell liness the tonsillar cell cultures, due to their high density, produce rather high
interferon
titers reaching hundreds of IU50/ml. The viability of the tonsillar cell cultures and their incubation at 37 degrees C during 24 hours are rather important for adequate
interferon
production.
...
PMID:[Stimulation of interferon formation by natural and synthetic inducers in cultures of human tonsil cells]. 615 81
Earlier, we reported a 30-200-fold reduction in the yield of infectious vesicular stomatitis virus (VSV) released from L cells treated with 10-30 reference units ml-1 of
interferon
(
IFN
); however, in these cultures virus particle production, as measured by VSV particle-associated viral RNA, virus nucleocapsid protein and viral
transcriptase
, was inhibited less than 10-fold. There was biochemical and morphological evidence of a significant reduction in glycoprotein (G) and membrane protein (M) of VSV particles released from
IFN
-treated cells. We compare here the effects of tunicamycin (TM) and
IFN
in L cells. Treatment with TM or
IFN
reduced the production of infectious VSV particles, decreased the amount of G and M proteins in VSV released from treated cells, and inhibited an early step in the formation of asparagine-linked oligosaccharide chains, the incorporation by membrane preparations from treated cells of N-acetylglucosamine into glycolipids with the properties of dolichol derivatives.
...
PMID:Interferon treatment inhibits glycosylation of a viral protein. 615 39
Interferon treatment of mouse cells chronically infected with Moloney leukemia virus (3T3/MLV) resulted in 97 per cent inhibition of infective virus release. The intracellular localization and distribution of virus reverse-
transcriptase
and group specific (gs) antigen were determined in
interferon
treated and control cells. Cytoplasm of infected cells was fractionated by isopycnic centrifugation on discontinuous sucrose gradients. Fractions were analysed for their chemical composition and characterized by the activity of membranal marker enzymes. The association and levels of viral antigens were determined in each fraction. Fractions enriched with 5' nucleotidase, specific enzyme marker for plasma membrane, were also enriched with viral proteins. In
interferon
treated cells, intracellular accumulation of viral proteins was specifically localized in the plasma membrane. Threefold increase in reverse-
transcriptase
level was the maximal accumulation found in purified plasma membranes. Intracellular enzyme levels in
interferon
treated cells were in accordance with the amount of cell associated infective virus particles. The small accumulation of viral proteins and infective virus particles was not sufficient to account for the great reduction in virus yield observed in the supernatants of the
interferon
treated cells. A possible role for
interferon
in modification of plasma membrane associated with virus assembly is postulated.
...
PMID:Localization of reverse-transcriptase in interferon-treated mouse cells chronically infected with Moloney leukemia virus. 615 72
A 200-fold inhibition in the titer of infectious vesicular stomatitis virus (VSV) was produced in cultures of Ly cells treated with 30 reference units of
interferon
per milliliter. Virus particle production, as measured by VSV particle-associated
transcriptase
, or nucleocapsid protein was inhibited by a maximum of tenfold. The glycoprotein and membrane protein content was reduced in VSV derived from
interferon
-treated cells. Thus
interferon
-treated cells may have produced VSV particles with low infectivity, which may be related to the reduced amount of glycoprotein incorporated into such particles. These findings resemble those reported in
interferon
-treated cells infected with murine leukemia viruses.
...
PMID:Selective inhibition of glycoprotein and membrane protein of vesicular stomatitis virus from interferon-treated cells. 624 16
Carrier cultures of L cells infected with wild-type vesicular stomatitis virus (VSV0) were initiated without the use of defective-interfering particles or homologous
interferon
. The cloned viruses recovered from such carrier cultures after passage 21 were characterized as temperature-sensitive. Furthermore, these clones of the mutant showed restricted replication at permissive temperature in HEp-2 cell cultures as compared to the wild-type VSV0. This restrictive replication of the mutant in HEp-2 cells was not due to a defect in the expression of virion-associated primary
transcriptase
activity in vivo, but due to the marked reduction in virus-specific characterized may govern the synthesis of mutant virus-specific amplified RNA in HEp-2 cells.
...
PMID:Host restriction property of a vesicular stomatitis virus mutant isolated from carrier cultures. 627 Feb 62
The outer surface lipoproteins of Borrelia burgdorferi, OspA and OspB, stimulate the production of nitric oxide (NO) by murine bone marrow-derived macrophages from BALB/c, C3H/HeN, and C3H/HeJ mice. Gamma
interferon
(IFN-gamma) caused a three- to fivefold enhancement of this production of NO, and the L-arginine analog N-guanidino-monomethyl L-arginine inhibited it. Activation of transcription of the inducible NO synthase gene in stimulated macrophages was demonstrated by reverse transcriptase rapid PCR. Although IFN-gamma increased the amount of NO produced in macrophage cultures, it did not cause transcription of the inducible NO synthase gene greater than that seen with the Borrelia proteins. OspA and OspB also induced the production of high levels (40 to 150 ng/ml) of IFN-gamma in cultures of macrophages incubated with interleukin-2 (IL-2)-elicited cells from normal (T and NK cells) and scid (NK cells) mice but not in macrophages or IL-2-elicited cells cultured individually. This suggests that OspA stimulated macrophage production of cytokines, which, in turn, stimulated the production of IFN-gamma by NK and T cells. Reverse
transcriptase
rapid PCR demonstrated that OspA and sonicated B. burgdorferi stimulated production of several inflammatory cytokines in macrophage cultures, including IL-1, IL-6, IL-12, IFN-beta, and tumor necrosis factor alpha. As tumor necrosis factor alpha, IFN-beta, and IL-12 are potent activators of IFN-gamma production by T and NK cells, their presence in these cocultures could be responsible for the IFN-gamma production. Lymphocytes from infected C3H mice also produced IFN-gamma when stimulated with B. burgdorferi; thus, immune cells may also modulate NO responses. The generation of NO during infection with B. burgdorferi may be important, as NO has potent antimicrobial properties. NO can also be involved in pathological inflammatory processes in which its generation is detrimental to the host. Thus, the colocalization of B. burgdorferi lipoproteins, NO-producing cells, and regulatory cytokines may determine the outcome of infection.
...
PMID:Outer surface lipoproteins of Borrelia burgdorferi stimulate nitric oxide production by the cytokine-inducible pathway. 752 Apr 17
The purpose of this study was to determine whether human fibroblasts express CD40, a 50-kDa member of the tumor necrosis factor-alpha-receptor superfamily. CD40 is an important mitogenic receptor on B lymphocytes which regulates B lymphocyte proliferation and differentiation. Interestingly, CD40 mRNA was detected in human lung, gingival, synovial, dermal (foreskin), and spleen fibroblasts using the reverse-
transcriptase
polymerase chain reaction. Moreover, the CD40 protein was detected on cultured human fibroblasts using anti-CD40 mAbs (G28-5, EA-5) and flow cytometry and on fibroblasts in dermal tissue sections via in situ staining. In contrast to B lymphocytes, where CD40 expression is unregulated both by interleukin-4 and
interferon
(IFN-gamma), CD40 expression on cultured human fibroblasts could only be upregulated by IFN-gamma. IFN-gamma induced a 10-fold increase in CD40 mRNA and protein levels. Furthermore, via a two-color staining technique for CD40 expression and DNA content, IFN-gamma not only upregulated CD40 expression on cultured human fibroblasts, but also shifted fibroblasts into the G0/G1 phase of the cell cycle. This observation suggested that nonproliferating fibroblasts might display elevated levels of CD40. To test this hypothesis, CD40 expression was analyzed on fibroblasts in log phase growth vs fibroblasts which had reached confluency and were nonproliferating. Interestingly, confluent fibroblasts expressed higher levels of CD40 than fibroblasts in log phase growth. These data suggest that CD40 expression by human fibroblasts is related to cell growth. In summary, this report is the first to demonstrate that human fibroblasts from a variety of tissues display CD40. While the function of CD40 on fibroblasts is not yet known, it may facilitate fibroblast proliferation, an event important for tissue repair, and may facilitate inflammation via interaction with T lymphocytes and mast cells, which display the CD40 ligand.
...
PMID:CD40 expression by human fibroblasts. 755 83
We reported previously that murine L-929 cells expressing a human
interferon
(
IFN
)-gamma cDNA lacking a signal peptide sequence synthesize but fail to secrete human IFN-gamma and support viral replication at a reduced level. These cells also had elevated levels of
IFN
-inducible gene products. We show here that a similar response is seen in human cells expressing a mutated murine IFN-gamma cDNA. The ability of human IFN-gamma to induce gene expression in murine cells is shown to be due to the intracellular IFN-gamma rather than to clonal variation, induction of endogenous murine
IFN
, or alternative mediators of antiviral activity. We have used a murine cell line, Ltk-aprt-, which is resistant to both type I and II IFNs but responsive to combined treatment with both. Ltk-aprt- cells transfected with human IFN-gamma cDNA lacking a signal sequence support virus replication at the same level as control cells. However, unlike transfectants containing only the neoR selection gene, clones expressing the mutated human IFN-gamma gene show strong protection against viral infection and elevated levels of 2,5 A synthetase mRNA and MHC class I protein after treatment with IFN-beta alone. Reverse
transcriptase
-PCR rules out the induction of endogenous murine
IFN
expression as a mediator of these effects. Thus, expression of intracellular human IFN-gamma mimics treatment with extracellular murine IFN-gamma in permitting a synergistic response to IFN-beta. Given the inability of human IFN-gamma to bind to the murine cell-surface receptor our results show that intracellular IFN-gamma can activate certain responses independent of cell-surface binding.
...
PMID:Induction of gene expression by intracellular interferon-gamma: abrogation of the species specificity barrier. 757 13
Based on the antiviral effect of
interferon
on rotavirus replication the inhibitory effect of 2',5'-oligoadenylates on MRNA and double-stranded RNA synthesis was studied using an in vitro assay. The chemically synthesized oligonucleotides were used to determine several characteristics of the inhibitory effect, such as chain length, presence of phosphate residues at the 5'-end, and the 2',5'-phosphodiester bond itself. In vitro transcription was inhibited by oligos with 5 or more adenine residues at a final concentration of 100 microM or greater. This result makes rotavirus
transcriptase
different from other viruses in which the inhibitory effects are associated with dinucleotides and trinucleotides. The inhibitory effect was increased when the oligo contained a phosphate residue at the 5'-end; in this case, inhibition was also seen at lower oligo concentrations as well as at shorter oligo chain length. The study of the kinetics of inhibition showed that the inhibition by p(A2'p5')(3)3A was competitive with a Ki value of 256 microM. The effect of the oligonucleotides on the in vitro viral RNA replication showed that the 2',5'-oligoadenylates were not able to significantly inhibit the in vitro rotavirus RNA synthesis. The lack of inhibition in the in vitro assay was very peculiar since RNA transcription and replication involves the viral RNA polymerase, VP1.
...
PMID:Effect of interferon and 2',5'-oligoadenylates on rotavirus RNA synthesis. 760 12
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