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PubMed1980

Regeneration of DI particles of virulent and attenuated rabies virus: genome characterization and lack of correlation with virulence phenotype.

Two strains of fixed rabies virus were examined for their ability to regenerate defective interfering (DI) particles and for possible correlation of DI particle production with the expression of virulence. A plaque-purified stock of the attenuated ERA strain (ERApp), which characteristically caused an auto-interfering death response in adult mice inoculated i.c., was serially passed at a high m.o.i. inBHK-21 cells. By the sixth passage, DI particles were regenerated that corresponded in sedimentation velocity and DI/RNA size to the smallest of three sizes of DI particles produced by the parental stock virus. The regeneration of ERA DI particles in vivo was not detected during 15 serial high or low m.o.i. passages of infected newborn mouse brain, though the passaged virus consistently elicited an auto-interfering-type death response when assayed in adult mice. The attenuated Flury HEPpp strain regenerated up to three unique size classes of DI particles during serial passage in BHK-21 or murine neuroblastoma C1300 clone NA cells compared with the one band of DI particles produced by the parental Flury HEP stock virus. The BHK-21 cell-adapted Flury HEPpp virus failed to kill adult mice when inoculated at high concentrations after two serial passages in NA cells. However, the virus became fully virulent and a single band of regenerated DI particles was visible. Additional bands of defective particles were visible following the third serial passage in NA cells. Single-stranded RNA with a mol. wt. of 0.62 x 10(6) was extracted from the first DI particle population to be regenerated. This corresponded in mol. wt. to the DI/ssRNA characteristic of the parental attenuated Flury HEP virus. However, in the parental type DI/RNA, partially dsRNA could be isolated in addition to ssRNA. Double-stranded RNA could not be detected in the regenerated DI particles derived from the virulent NA cell-propagated Flura HEPpp virus. These results suggest that the virulence phenotype of fixed rabies viruses does not depend on the presence or absence of DI particles.

Animals↗
PubMed1980

An effect of interferon on the uncoating of murine leukaemia virus not related to the antiviral state.

Adsorption of murine leukaemia virus (MLV) to NIH/3T3 cells, as determined by analysing its reverse transcriptase activity in the cell membrane, was found to be unaffected by interferon (IFN). Virus penetration and uncoating were followed by quantifying intracellular virions in terms of sedimentable reverse transcriptase activity in the cytoplasmic fraction. The penetrating virions were found to accumulate to a higher level in IFN-treated cells than in untreated controls. Intracellular virions were uncoated in untreated cells shortly after their penetration, whereas their uncoating was delayed in the IFN-treated cells for 2 to 3 h. Neither virus uncoating nor the effect of IFN on this process appeared to require new protein synthesis, since both were unaffected by cycloheximide (CH).

Animals↗
PubMed1980

Effect of human fibroblast interferon on uncoating and release of murine leukaemia virus in NIH/3T3 mouse cells.

The effect of human fibroblast interferon (IFN), a heterologous IFN, on the uncoating of murine leukaemia virus (MLV) was investigated in exogenously infected NIH/3T3 mouse cells. Virus uncoating was determined by following the disappearance of the penetrating virus particles from the cytoplasm of the infected cells. Intracellular virus particles were estimated by sedimenting them at high speed from the cytoplasmic fraction of the infected cells and assaying their reverse transcriptase activity. In untreated control cells, uncoating started immediately after penetration, but in cells treated with human IFN, uncoating was delayed for 2 to 3 h. This delay led to prolongation of the infectious cycle, with delayed release of progeny virus. The delay in release did not result from inhibition by IFN of the process of release, since in NIH/3T3 cells chronically infected with MLV, treatment with IFN had no effect on virus release.

Animals↗
PubMed1981

Herpes simplex virus infection in human monocyte cultures: dose-dependent inhibition of monocyte differentiation resulting in abortive infection.

Monocyte-enriched cultures of human blood leukocytes were exposed to herpes simplex virus (HSV) at different multiplicities of infection (m.o.i., from about 10 to 0.001 p.f.u./cell). Highest maximum progeny virus titres were invariably obtained with low initial m.o.i., i.e. those between 0.01 and 0.0001 p.f.u./cell, while little if any infectious progeny was produced in cultures inoculated with the highest virus concentrations. By the time of maximum virus production, i.e. 5 to 7 days after inoculation, monocytes in the uninfected cultures had mostly differentiated to macrophages. This differentiation was partially inhibited in cultures initially exposed to the higher concentrations of HSV. Synthesis of HSV antigens was detected by indirect immunofluorescence both in the high m.o.i. cultures and in the productively infected cultures. By this criterion, a maximum of 10 to 15% of all adherent cells became infected in both culture types. It is suggested that the higher doses of HSV, by inhibiting cellular maturation, also prevent the subsequent completion of its own infectious cycle.

Cell Differentiation↗
PubMed1981

Influence of the host cell on the genomic and subgenomic RNA content of defective-interfering influenza virus.

Clonally derived stocks of defective-interfering (DI) influenza virus prepared by chick embryo fibroblast (CEF) cells were all deficient in genomic RNAs 1, 2 and 3 but had different patterns of subgenomic RNAs. A single passage at high multiplicity in L cells altered the pattern of genomic RNAs independently of the subgenomic species, while in BHK cells the opposite situation prevailed. Therefore, there is no simple relationship in DI influenza virus between the loss of genomic RNA segments and the presence of subgenomic RNAs.

Animals↗
PubMed1981

Assay of defective-interfering semliki forest virus by the inhibition of synthesis of virus-specified RNAs.

We describe a simple, rapid and reproducible assay for defective-interfering Semliki Forest virus (DI SFV) which is based on the inhibition of synthesis of virus-specified RNAs in SFV-infected cells. Using the assay, we have been able to show that DI virus is generated by a single passage in baby hamster kidney (BHK) cells in an inoculum which contained no detectable DI virus and we have calculated the u.v. target size of the interfering activity.

Animals↗
PubMed1981

The characteristics required for a Sendai virus preparation to induce high levels of interferon in human lymphoblastoid cells.

The capacity of an egg-grown Sendai virus preparation to induce interferon in the human lymphoblastoid cell Namalwa is dependent on its passage history. Virus which has been serially passaged at high dilution is a poor inducer, whereas virus serially passaged undiluted is a good inducer. Such a good induce preparation has a low infectivity to haemagglutination ratio as the result of a high content of defective-interfering (DI) particles. Using DI particles purified on glycerol gradients, it is shown that for the induction of maximum interferon titres both infectious and DI particles are required. DI particles alone induce little or no interferon. Addition of DI particles to fully infectious Sendai virus preparations increased the interferon yield obtained from Namalwa cells some 60- to 100-fold.

Cell Line↗
PubMed1983

Cell surface receptor-mediated internalization of interferon: its relation to the antiviral activity of interferon.

The binding of [3H]leucine-labelled pure human interferon alpha from Namalwa cells to human FL and Daudi cells was studied, and evidence obtained to indicate receptor-mediated internalization of interferon. Cell surface-bound and internalized interferons were quantified separately as trypsin-released and unreleased radioactivities, respectively. At 37 degrees C, surface-bound interferon reached a maximum after 1 h and then decreased, while internalized interferon reached a maximum after 2 h. At 21 degrees C, in contrast, surface-bound interferon reached a maximum after 2 h and did not decrease thereafter; no internalization was observed. The same was true at 37 degrees C in the presence of NaF, indicating dependence of internalization on temperature and energy. In control cultures at 37 degrees C, internalized interferon, after reaching a maximum, decreased after prolonged incubation, and concomitantly acid-soluble radioactivity appeared in the culture medium. The decrease in internalized interferon and the emergence of degraded interferon were inhibited by the lysosomotropic agents, ammonium chloride and chloroquine. The fate of labelled interferon, bound to the cell surface of FL cells at 21 degrees C was studied at 37 degrees C, and the results indicated that trypsin-unreleased interferon was derived from the surface-bound interferon, and was secreted in part into the culture fluid in a degraded form upon prolonged incubation. The relation of internalization of interferon to its biological activity was studied in three ways. In FL cells, the antiviral activity was not induced when internalization of interferon was entirely blocked (at 21 degrees C or in the presence of NaF at 37 degrees C). In Daudi cells, both 2'-5'-oligoadenylate (2-5A) synthetase induction by interferon and internalization of interferon were inhibited completely by diethyldithiocarbamate (DDC), whereas in the case of FL cells, DDC inhibited neither 2-5A synthetase induction nor internalization of interferon. Raji cells, which have an interferon-specific binding site on the cell surface but are insensitive to interferon, were found not to internalize interferon, whereas other Burkitt's lymphoma cells, Daudi and Namalwa, which are sensitive to interferon, did internalize it. These findings suggest (but do not prove) that internalization is required for the establishment of interferon activity.

Biological Transport↗
PubMed1984

Persistent infection of human fibroblasts by hepatitis A virus.

Infection of human embryo fibroblasts with hepatitis A virus (HAV), a picornavirus, leads to an inapparent, persistent infection; cultures can be passed serially with consistent recovery of the virus in the supernatant. All of the cells of a HAV carrier culture are infected and proliferate. Subcultivation under HAV-immune serum cannot achieve a cure or even a reduction in the number of infected cells in HAV carrier cultures. No interferon activity can be detected during HAV infection and persistence. Addition of exogenous interferon eliminates HAV infection in vitro. Persistence of HAV in vitro appears to contradict the clinical course of HAV infection in vivo. The system presented offers the possibility of evaluating the role of immunological injury of HAV-infected cells, an injury which may lead to damage of these cells and to elimination of HAV during an HAV infection in vivo.

Carrier State↗
PubMed1984

Isolation and characterization of subspecies of murine interferon alpha.

Interferon produced by mouse L-929 cells by incubation with poly(rI).poly(rC) is known to be composed of a mixture of MuIFN-alpha and MuIFN-beta. The alpha component was separated from the bete species by affinity chromatography over a monoclonal anti-MuIFN-beta agarose column and partially purified by gel filtration. MuIFN-alpha, prepared by this method was separated into at least five subspecies by chromatofocusing. The approximate pI values of these components are greater than or equal to 7.5, 6.5, 6.2, 5.9 and 5.6, respectively. Component 3 (pI 6.2) was the most prominent subspecies present in our MuIFN-alpha preparations, representing 40 to 50% of the total antiviral activity. Component 1 (pI greater than or equal to 7.5) which accounted for about 5% of the antiviral activity on mouse cells, differed in some properties from the other interferon subspecies. It showed a relatively high antiviral activity on heterologous cells and it was eluted from a Sephadex column after the other alpha subspecies. Furthermore, it showed a diminished binding to heparin as compared to the other MuIFN-alpha subspecies, indicating a lower affinity for polynucleotides.

Animals↗
PubMed1985

Preliminary characterization of a persistent infection of HeLa cells with human rhinovirus type 2.

We were able to initiate a persistent infection (PI) in HeLa cells with a temperature-sensitive (ts-) mutant of rhinovirus type 2 (TS-1), but not with the corresponding wildtype (wt) virus. The ability to initiate a PI may be related to the multiplicity of infection. Persistence was established at 37 degrees C but not at 32 degrees C and the virus isolated from the PI was no longer temperature-sensitive. Infectious virus was continually produced at low levels throughout the course of the PI and cell cultures underwent multiple episodes of partial destruction (crisis) and subsequent recovery. PI virus and the initiating virus were neutralized to the same extent by hyperimmune polyclonal TS-1 antiserum indicating that no significant change had occurred with respect to serological type. The presence of either interferon or virus-related interfering activity could not be demonstrated in the PI cultures. Superinfection experiments in cells that were 'cured' of PI virus indicated the selection of a cell population during persistence that could no longer support the growth of homologous-type virus. This effect became less pronounced upon further passage of the cured cells. When compared with the wt and ts viruses, the PI virus yielded comparable amounts of infectious virus in HeLa cells but with decreased synthesis of RNA.

HeLa Cells↗
PubMed1985

Evidence that IFN-alph/beta induces two antiviral states active against different viruses.

IFN-alpha/beta has been suggested to require only one round of mRNA and protein synthesis to induce an antiviral state. We have examined the mechanism of induction of the antiviral states shown against three types of viruses: mengovirus (plus strand, sense RNA), vesicular stomatitis virus (VSV, minus strand RNA), and vaccinia virus (DNA). Mouse L cells were treated with IFN-alpha/beta and cycloheximide and then with actinomycin D on a schedule which allowed only one round of mRNA and protein synthesis. The cells were challenged with virus under single cycle growth conditions to determine the amount of antiviral activity against the particular challenge virus employed. These studies confirmed that most of the antiviral effect directed against VSV is achieved with one round of macromolecular synthesis. However, most of the antiviral effect directed against mengovirus and vaccinia virus seemed to require more than one round. These results suggest that IFN-alpha/beta induces two different antiviral states: one requiring one round of synthesis which is primarily responsible for the inhibition observed for VSV; and another requiring more than one round of synthesis which is primarily responsible for the inhibition observed for mengovirus and vaccinia virus.

Animals↗
PubMed1986

Persistence of virulent Semliki Forest virus in mouse brain following co-inoculation with defective interfering particles.

Semliki Forest virus (SFV) normally causes an acute lethal encephalitis in mice following intranasal inoculation. However, animals co-administered with 10 LD50 SFV and defective interfering (DI) SFV survive the infection without clinical signs of disease. In this report we demonstrate the isolation of infectious virus from the brains of 12/169 protected mice up to 6.5 months post-infection. Although, with one exception, mice were clinically normal, five of 12 of the SFV isolates were identical to the original virus as judged by plaque morphology, maximum temperature for growth, virulence in mice and pathology. Others were less virulent (although not any were plaque or temperature-sensitive mutants) and on re-inoculation into fresh mice caused a demyelinating pathology which was not an attribute of the original inoculum. How the virulent virus can persist in brain, sometimes in amounts in excess of 100 LD50, without causing disease remains to be determined.

Animals↗
PubMed1986

Very rapid generation/amplification of defective interfering particles by vesicular stomatitis virus variants isolated from persistent infection.

Multiply cloned variants of vesicular stomatitis virus (VSV) were found to generate/amplify defective interfering (DI) particles at a rate greatly exceeding the rates normally observed for wild-type VSV (or for other mutants of VSV). A single undiluted passage of the first clonal pool of this variant virus produced concentrated visible bands of DI particles on sucrose gradients whereas wild-type and other mutant strains of VSV required from three to six or more serial undiluted passages. Since DI particle amplification by wild-type VSV at each undiluted passage can exceed 10,000-fold enrichment, these variant virus clones were generating/amplifying DI particles many millions of times more rapidly than were wild-type and other mutant strains of VSV. This rate of generation/amplification is so high that it was not feasible to obtain accurate estimates of the rates of generation (or amplification) of these DI particles.

Animals↗
PubMed1986

Subclinical infections in mice resulting from the modulation of a lethal dose of Semliki Forest virus with defective interfering viruses: neurochemical abnormalities in the central nervous system.

The lethal encephalitis caused in mice by Semliki Forest virus (SFV) is modulated to a subclinical infection by administration of defective interfering SFV, although virus still multiplies both in the central nervous system (CNS) and systemically. Here we report that such infections result in unique and selective changes in the normal levels of CNS neurotransmitters some of which persist after infectious virus can no longer be detected. This represents a previously undocumented category of infection which may have a bearing on the aetiology of those human neurological and neuropsychiatric diseases to which viruses are believed to contribute.

Animals↗
PubMed1987

Selection and characterization of interferon-sensitive cells derived from an interferon-resistant NIH 3T3 line.

We have developed a selection protocol to isolate interferon (IFN)-sensitive subclones directly from an IFN-resistant cell population. The protocol uses encephalomyocarditis virus (EMCV) as a selection agent in combination with pretreatment with low doses of IFN and subsequent growth in the presence of virus-neutralizing antiserum. We have applied this protocol to the partially IFN-resistant NIH 3T3 clone 1 line and have obtained a number of IFN-sensitive subclones. Sensitivity to IFN was restricted to protection against EMCV. Replication of vesicular stomatitis virus as well as cell growth were resistant to IFN treatment as in the original clone 1 line. We have compared levels of 2',5'-oligoadenylate (2-5A) synthetase, dsRNA-activated protein kinase and 2-5A-dependent RNase in some IFN-sensitive subclones and found no difference from the resistant clone 1 cells. Markedly decreased levels of 2-5A-dependent RNase and thus a defective 2-5A pathway have been implicated as a possible cause for the partial resistance of clone 1 cells to IFN. Since the selected IFN-sensitive subclones are of the same phenotype in this respect as the clone 1 line we suggest that inhibition of EMCV in these lines occurs through a mechanism independent of the 2-5A system.

2',5'-Oligoadenylate Synthetase↗