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PubMed2004

Granzymes in cytolytic lymphocytes--to kill a killer?

Granzymes (gzm) are major components of the granules of cytolytic lymphocytes, natural killer and cytotoxic T cells. Their generally accepted mode of action consists of their directed secretion towards a virus-infected or neoplastic target cell and perforin-dependent delivery to the target cell cytosol, where they engage in various actions resulting in target cell apoptosis. Here, based on observations of infection of gzmAxB(-/-) mice with ectromelia virus, mousepox, we propose an additional--and distinct--function for gzmA and B. In this model, gzm constitute one of the first lines of defence of immune cells against virus infection of immune cells themselves. Accordingly, endogenous gzm interfere with viral replication in cytolytic lymphocytes either directly, as a result of their proteolytic activity, leading to destruction of viral proteins, or indirectly, via: (i) processes akin to the caspase cascade when acting as effector molecules in the induction of target cell apoptosis; or (ii) their capacity to induce early inflammatory mediators. We discuss the predictions of the model in the light of available data.

Animals↗
PubMed1999

Occult hepatitis B virus infection in patients with chronic hepatitis C liver disease.

BACKGROUND: Hepatitis B virus (HBV) infections in patients who lack detectable hepatitis B surface antigen (HBsAg) are called occult infections. Although such infections have been identified in patients with chronic hepatitis C liver disease, their prevalence and clinical significance are not known. METHODS: With the polymerase chain reaction, we searched for HBV DNA in liver and serum samples from 200 HBsAg-negative patients with hepatitis C virus (HCV)-related liver disease (147 with chronic hepatitis, 48 with cirrhosis, and 5 with minimal histologic changes). One hundred of the patients had detectable antibodies to the HBV core antigen (anti-HBc); 100 were negative for all HBV markers. Eighty-three were treated with interferon alfa. We also studied 50 patients with liver disease who were negative both for HBsAg and for HCV markers. In six patients found to have occult HBV infection, we evaluated possible genomic rearrangements through cloning or direct sequencing procedures. RESULTS: Sixty-six of the 200 patients with chronic hepatitis C liver disease (33 percent) had HBV sequences, as did 7 of the 50 patients with liver disease unrelated to hepatitis C (14 percent, P=0.01). Among the 66 patients, 46 were anti-HBc-positive and 20 were negative for all HBV markers (P<0.001). Twenty-two of these 66 patients (33 percent) had cirrhosis, as compared with 26 of the 134 patients with hepatitis C infection but no HBV sequences (19 percent, P=0.04). HBV sequences were detected in 26 of the 55 patients in whom interferon therapy was ineffective and 7 of the 28 patients in whom interferon therapy was effective (P=0.06). None of the sequenced HBV genomes had changes known to interfere with viral activity and gene expression. CONCLUSIONS: Occult hepatitis B infection occurs frequently in patients with chronic hepatitis C liver disease and may have clinical significance.

Adult↗
PubMed2004

CRE recombinase-inducible RNA interference mediated by lentiviral vectors.

Recently, several systems designed to trigger RNA interference by using small hairpin RNA driven by polymerase III promoters have been described. Here, we report a lentiviral-mediated small interfering RNA delivery system that can be induced by CRE recombinase. The system consists of a lentiviral vector carrying a mouse U6 promoter that is separated from a small hairpin RNA by a random DNA stuffer sequence flanked by modified loxP sites. The silencing cassette is not expressed until activated by addition of CRE recombinase delivered by a lentiviral vector. We have used this system to show specific down-regulation of GFP and two endogenous genes (the tumor suppressor p53 and the NF-kappaB transcription factor subunit p65) in vitro. Furthermore, down-regulation of both p53 and p65 resulted in the expected effect on downstream genes and cellular phenotype. We foresee multiple applications of this system both in vitro and in vivo to down-regulate specific targets in a tissue-specific and localized manner.

Base Sequence↗
PubMed1969

Transformation and chromosome changes induced by Epstein-Barr virus in normal human leukocyte cultures.

Three separate attempts to establish long-term leukocyte cultures from the peripheral blood of a healthy adult who had no evidence of previous infection with Epstein-Barr virus were consistently unsuccessful. On the other hand, in vitro infection of buffy-coat cells of this donor with Epstein-Barr virus resulted in blastoid transformation of the lymphocytes and long-term growth potential. The transformation was accompanied by major chromosome changes. The significance of these findings in relation to lymphoproliferative diseases in man remains to be determined.

Cell Transformation, Neoplastic↗
PubMed1969

Induction of interferon by preparations of synthetic single-stranded RNA.

A study was undertaken to help determine whether synthetic nonbase-paired, single-stranded RNA as well as synthetic base-paired, double-stranded RNA could induce interferon. Synthetic polyriboinosinic acid and polyribocytidylic acid induced interferon and interferon-like resistance in several different cell culture systems. However, in the intact rabbit only the most active preparations of single-stranded RNA induced circulating interferon when injected intravenously. The induced interferon and antiviral effect in tissue culture and animals was shown to have characteristics of the interferon system. Contamination of the single-stranded synthetic RNA materials by small amounts of base-paired, double-stranded RNA was ruled out by failure to find sufficient heterologous nucleic acid bases by differential activities of single-stranded and double-stranded RNA's in different cell systems and by failure to detect double-stranded RNA in poly-rI upon chromatography on benzoylated DEAE-cellulose.

Animals↗
PubMed1969

Foot-and-mouth disease virus inhibition induced in mice by synthetic double-stranded RNA (polyriboinosinic and polyribocytidylic acids).

Synthetic 2-stranded RNA-a helical complex formed by duplexing homopolymers of polyriboinosinic and polyribocytidylic acids (poly I:C)-induced host resistance to foot-and-mouth disease virus when microgram quantities were injected into mice. There was a graded response as shown by titrations of polynucleotide complex or virus. Protection was effective for >48 hours after a single injection of polynucleotide complex. Survival and serum interferon titers were directly related.

Animals↗
PubMed1970

Recovery of a new virus from apparently normal chick cells by infection with avian tumor viruses.

Cells derived from the majority of chick embryos, although free of presently known avian tumor virus particles, appear to contain genetic materials similar to those found in this virus group. After infection of these cells with avian leukosis or Rous sarcoma virus, the genetic factor was recovered by incorporation into mature infectious virus. The newly isolated virus (RAV-60) did not require the assistance of another virus for its replication. The virus had most of the attributes of an RNA-containing avian leukosis virus, and its outer structure resembled the Rous sarcoma virus known as RSV(0).

Alpharetrovirus↗
PubMed1975

A novel murine oncornavirus with dual eco- and xenotropic properties.

Infection of Swiss mouse 3T3FL cells with a clonal isolate of Moloney leukemia virus (MLV-IC) resulted in virus progeny composed of at least three different murine helper oncornaviruses. Each entity was purified in appropriate cells by several sequential terminal dilution isolations and was grouwn to high titers. Besides ecotropic MLV-IC there was a pure xenotropic virus and a third novel virus with properties of both eco- and xenotropic viruses. The purified xenotropic virus had a wide host range, was restricted in mouse cells, and was inactivated by normal mouse sera like other xenotropic isolates. The purified virus with hybrid properties (HIX) could infect a wide range of mammalian cells, which included both N and B mouse cells. HIX gave single-hit titrations with equal titers on both mouse and cat indicator cells. Envelope properties of HIX were examined by virus preinfection interference, by interference involving viral glycoprotein, and by neutralization with specific antisera. Both xenotropic and MLV-IC type ecotropic determinants were found on the virus coat. The origins of HIX and the xenotropic virus were investigated in detail. The original MLV-IC stock had HIX type virus in low titer but no detectable pure xenotropic virus. Infection of mouse cells with a single infectious unit of the ecotropic virus from the MLV-IC virus stocks could at times give rise to HIX type virus. HIX type virus, passed once through heterologous rat cells, was subjected to long-term passage either in infected mouse or cat cells. After several months HIX type virus disappeared from some mouse and cat cell systems. The possible hybrid nature of HIX and the origins of newly appearing xenotropic viruses are discussed.

Animals↗
PubMed1975

Chromosomal localization of human genes governing the interferon-induced antiviral state.

Interferon sensitivity of different normal and aneusomic human cells and of different mouse-human hybrids cells has been compared. G21 trisomic cells are more sensitive than diploid cells; whereas, on the contrary, triploid cells are normal in their human interferon sensitivity. Among other aneusomic cell lines tested, E16 trisomic cells are significantly less sensitive. These data are in favor of the hypotheses that the G21 chromosome carries genetic information for structural proteins involved in the receptor system for interferon, that there is a regulatory mechanism governing the antiviral state, and that the E16 chromosome is a possible candidate for carrying information for such a depressive regulatory mechanism. None of the chromosome abnormalities studies are involved with interferon synthesis.

Cell Line↗
PubMed1979

Internal genome deletions in two distinct classes of defective interfering particles of vesicular stomatitis virus.

We have characterized the genome sequences represented in two defective interfering particles derived from the heat-resistant strain of vesicular stomatitis virus by means of end-labeling and hybridization techniques. Both defective particle RNAs, which differ slightly in size, contain 5'-end sequences identical to each other and to that of the standard infectious virus genome, for at least the first approximately 55 bases. In contrast, the 3'-end sequences of these two RNAs are different. The 3'-end sequence of the smaller RNA is identical to that of the standard genome for at least the first 48 bases. The 3'-end sequence of the larger RNA is an inverted complement of its 5' end for approximately 65 bases. The bulk of the sequences in both RNAs is derived from the 3' half of the standard genome. We also show that the two defective particles differ in vitro transcription and in vivo replication properties. These results provide direct evidence for the presence of internal genome deletions in defective interfering particles of negative-stranded RNA animal viruses and demonstrate the existence of at least two distinct classes of these particles.

Chromosome Deletion↗
PubMed1979

Sequence relationships among defective interfering influenza viral RNAs.

Each clone of ts-52 and ts+ WSN influenza virus, when serially passaged at high multiplicity, gives rise to defective interfering (DI) virus with a unique set of new RNA species. The new RNAs (DI RNA) from several DI viruses were examined by the technique of RNase T1 oligonucleotide two-dimensional electrophoresis. It was found that each DI RNA arises from a specific segment of standard viral RNA. All DI RNA studied arose from the viral polymerase genes (P1, P2, and P3). DI RNAs originating from the same polymerase gene were interrelated. Certain of these DI RNAs appeared to contain completely overlapping nucleotide sequences. Others contained both overlapping and nonoverlapping nucleotide sequences. The latter DI RNAs may be formed from the progenitor viral RNA segment by a mechanism other than a common initiation (or termination) point and a simple deletion from one end.

Base Sequence↗
PubMed1980

Kinetics of decay in the expression of interferon-dependent mRNAs responsible for resistance to virus.

We used 5,6-dichloro-beta D-ribofuranosyl-benzimidazole (DRB), a selective and reversible inhibitor of mRNA production, to investigate the regulation of the pathway leading to resistance to viruses in cells treated with interferon (IF). DRB allows initiation of transcription but promotes premature termination of the nucleotide chains, so that it abolishes interferon-dependent protection against viruses. When the DRB is removed, synthesis of complete mRNAs can resume. Mouse L-929 cells were exposed to 100 microM DRB before and during a 1-hr pulse of IF followed by treatment with antibody to IF to prevent cell-to-cell spread of IF after that time. At different intervals thereafter the cells were washed and the DRB was replaced by medium; after further incubation, the cells were infected with vesicular stomatitis virus. Resistance to virus was inversely proportional to the duration of the block imposed by DRB. When the DRB was removed soon after the IF pulse, substantial protection from virus ensued, but none developed when removal of the DRB was deferred for 5-6 hr. Cells exposed to DRB for 5 hr, then pulsed with IF for 1 hr, still mounted a strong antiviral response. The data show that the ability of cells to resist viral infection decays within 5-6 hr after treatment with IF. Whether the decay is due to shutoff of transcription of mRNAs, or to their destruction or degradation, or whether regulation takes place at one or more subsequent steps in the antiviral pathway, remains to be determined.

Animals↗