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At least 883 records · Page 49Linked to original sources
PubMed1996

DNA sequences responsible for specificity of DNA packaging and phage growth interference of bacteriophages T3 and T7.

T3 and T7 phages package recombinant plasmids carrying DNA necessary for DNA packaging (the pac sequences) of T3 and T7, respectively. Packaging is specific between T3 and T7. The pac sequence has a bipartite structure, consisting of target sequences for processing of concatemeric DNA (pac C) and its left side flanking sequence containing a promoter for phage RNA polymerase (pac B). To determine the sequences responsible for the specificity of plasmid DNA packaging, plasmids chimeric for the pac B and pac C sequences of T3 and T7 were constructed. Analysis of packaging of the chimeric plasmid DNAs showed that pac B is responsible for the packaging specificity of T3 and T7 DNAs. Plasmids carrying the genetic right end of T3 and T7 DNA interfered with the growth of T3 and T7 phages, respectively. Interference was specific between T3 and T7. pac B and sequences between pac B and pac C, but not pac C, were responsible for the interference. The specificity of interference was determined by pac B and sequences responsible for interference were partially defined.

Bacteriophage T3↗
PubMed2000

Co-infection of HHV-6 and HHV-8 is rare in primary effusion lymphoma.

The presence and distribution of Epstein-Barr virus (EBV), as well as human herpesvirus-6 and-8 (HHV-6 and HHV-8) was investigated by polymerase chain reaction in 191 samples from a variety of lymphoproliferative disorders. HHV-6 DNA was detected in 18% (30 of 169) of non-HHV-8 related lymphoproliferative disorders, with the highest frequency in AIDS-related lymphomas (8 of 25, 32%). In contrast, HHV-6 DNA was present in less than 5% (1 of 22) of HHV-8 related lymphoproliferative disorders [21 primary effusion lymphomas (PEL), and 1 cases of Castleman disease]. As compared to HHV-6, EBV DNA was frequently detected in PEL (11 of 19 samples, 58%). This study suggests that transformation to PEL is not enhanced by HHV-6, furthermore HHV-6 and -8 may interfere with each other.

Castleman Disease↗
PubMed1982

From interference to interferon: a brief historical introduction.

The idea that a substance mediating interference was released from cells upon contact with inactivated influenza A virus emerged from an abortive attempt at showing that interference was initiated by passage of only part of the virus into the cell, from previous knowledge about interference, and from the use of a simple technique allowing easy separation of fluid and tissue.

History, 20th Century↗
PubMed1980

Antibiotics that specifically block translation in virus-infected cells.

Several antibiotics including anthelmycin, blasticidin S, destomycin A, gougerotin, hygromycin B and edeine complex, known to powerfully block translation in cell-free systems, did neither inhibit protein synthesis in intact mouse L and 3T6 cells, nor in hamster BHK 21 cells, due to failure to cross the cell plasma membrane. However, after viral infection, these antibiotics exhibited a marked blockade of translation, that is related to the permeability changes induced by viral infection. The inhibition of protein synthesis by hygromycin B in virus-infected cells was studied over the time course of infection, both in encephalomyocarditis virus-infected mouse L cells and in Semliki forest virus-infected hamster BHK cells. We have observed that the entry of hygromycin B into virus-infected cells parallels the inhibition of cellular protein synthesis, i.e., the cells became permeable to this antibiotic at the time the shut-off of host translation occurred. A marked inhibition of picornavirus RNA synthesis by hygromycin B was also noticed, likely as a consequence of the inhibition of the viral replicase synthesis. Finally, a reduction in the virus yield by treatment of virus-infected cells with several antibiotics is also described. All these observations are considered in the context of the interference of viral infection with cellular functions and the potential use of inhibitors non-permeable to normal cells as antiviral agents.

Aminoglycosides↗
PubMed1983

Viral inhibition of lymphocyte mitogenesis: interference with the synthesis of functionally active T cell growth factor (TCGF) activity and reversal of inhibition by the addition of same.

We have investigated the mechanisms whereby co-incubation of several types of virus particles with human lymphoid cells in the presence of T cell lectins leads to inhibition of the proliferative response that otherwise ensues. The data indicate that, in the absence of infection, such inhibition can be reversed by the addition to cultures of relatively high concentrations of fluids rich in T cell growth factor (TCGF) activity. The ability of these fluids to achieve such reversal of inhibition is both concentration- and time-dependent. Addition of the factor to virus co-incubated cells more than 26 hr after culture initiation does not restore responsiveness. We have also shown that virus co-incubated cultures are deficient with respect to their ability to synthesize detectable levels of TCGF activity in the presence of phytohemagglutinin. In contrast, the use of relatively dilute virus preparations (less than 10 particles per cell) permits partial responsiveness to lectin as well as the synthesis of moderate levels of TCGF. These finding suggest that viral inhibition of lymphocyte mitogenesis is mediated directly or indirectly by interference with the synthesis of functionally active TCGF activity.

Animals↗
PubMed1990

Non-immunological facets of poliovirus vaccines.

Failures of oral poliovirus vaccine lots in developing countries are explained by interference during their 'take' by other enteroviruses colonizing the host intestinal system. Oral poliovirus vaccines, on their part, have also exerted an interfering effect on multiplication of other enteroviruses. Apart from the intrafamilial enterovirus interference, oral poliovirus vaccine has not spared rotaviruses.

Child↗
PubMed1998

Mechanisms of CD95 (APO-1/Fas)-mediated apoptosis.

This review covers recent advances of CD95 signaling. It focuses on CD95-interacting molecules, formation of the death inducing signaling complex and the role of caspases, particularly caspase-8, and their death substrates. We also discuss the relevance of mitochondria in the CD95-mediated apoptotic process and how viral proteins interfere with crucial steps of this signaling pathway.

Animals↗
PubMed1980

Complementation analysis of measles virus mutants isolated from persistently infected lymphoblastoid cell lines.

Human lymphoblastoid cell lines persistently infected with measles virus release a heterogeneous population of virions. At least 80% of the infectious particles were temperature sensitive for plaque formation at 39 degrees C. Plaque-purified temperature-sensitive mutants from four persistently infected human lymphoblastoid cell lines were shown to be heterogeneous with respect to efficiency of plating at 31 and 39 degrees C, as well as to antigen and RNA production at 39 degrees C. The heterogeneity was confirmed by complementation analysis in which 21 temperature-sensitive isolates were found to represent at least four of the five previously described complementation groups of measles virus. Two isolates complemented four reference temperature-sensitive mutants. These isolates either represent new complementation groups or are members of the fifth complementation group, group E. The majority of isolates were found to have multiple mutations, and group B mutants (RNA-) predominated. Two temperature-sensitive isolates were able to interfere with production of parental measles virus at both permissive and nonpermissive temperatures.

Antigens, Viral↗