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Viral interference and interferon.

Viral interference is a phenomenon for which a cell infected by a virus becomes resistant toward a second outcoming infection by a superinfectant virus. Even though other mechanisms are known, it can be assumed that most cases of viral interference occurring in natural conditions are mediated by interferon, a low molecular weight protein produced by the infected cell in response to a stimulus provided by viral nucleic acid(s). The interferon produced by a cell can migrate to other cells not yet involved by the spreading infection, transmitting to them the antiviral-resistant state. Available evidence indicates that interferon acts by inducing the production of a second cellular protein, called antiviral protein, which is directly responsible for the antiviral state through some alterations of the cellular, virus-directed, proteosynthetic system. In addition to the antiviral activity, the interferon system can affect the growth of several nonviral organisms and that of tumour cells; rather controversial effects have been shown also on the immune responses; the mechanisms underlying these effects are still nuclear. However a relationship to the specific immune system is suggested also by the finding that interferon can be liberated by sensitized T-lymphocytes following antigenic stimulus. Activation of the interferon system can be operated in vitro and in vivo also by several non-viral substances of various nature, such as nucleic acids, polysaccharides, aromatic amines, etc. This fact, considering that interferon has been shown to play a critical role on the mechanisms of recovery from viral infections, may open new perspectives for their possible prophylactic and/or therapeutic use in viral diseases. This problem can be approached also by administering exogenous interferon. Encouraging preliminary results have so far been obtained either with interferon or its inducers. However, several problems of various nature have to be resolved before considering the actual use of interferon system as a wide range antiviral drug in natural viral diseases of man.

Animals↗
PubMed1976

Diffusible viral interference during arbovirus plaque formation.

A radially diffusing zone of nonspecific interference was observed surrounding plaques of Western equine encephalitis virus. The increase in diameters of the zones of interference were linear and more rapid than increases in plaque diameters. These observations raise the possibility that viral-induced interference could account for the diminished growth of Western equine encephalitis virus plaques with time or even the initial formation of plaques. In addition, this system could be used as a model to study localized host defenses during early infection of solid tissues in vivo.

Encephalitis Virus, Western Equine↗
PubMed1977

[Potentiating effect of cycloheximide on viral interference].

The degradation of the antiviral state can be delayed in vitro by antimetabolites, when added between 5-7 hours after interferon. We explore in this chronological order whether antiviral resistance induced by Newcastle disease virus (N.D.V.) in vivo could be modified by an antimetabolite. Cycloheximide was selected for this study because of its reversible biological effect and lack of toxicity in our experimental conditions. The model system employed was Syrian Hamsters, using N.D.V. as an interferon inducer and encephalomyocarditis virus (E.M.C.) as a challenge virus. A constant and significant increase in survival of animals treated with N.D.V.+cycloheximide is probably related to a delay in the degradation of the antiviral state and not to interferon superinduction.

Animals↗
PubMed1979

Cytomegalovirus infection in guinea pigs. III. Persistent viruria, blood transmission, and viral interference.

Chronic persistent infection with cytomegalovirus (CMV) was studied in random-bred Hartley and inbred strain 2 guinea pigs. Infectious virus was isolated from the urine, kidney, spleen, pancreas, salivary gland, and cervix, but not from buffy coat of persistently infected guinea pigs. Strain 2 animals developed a high rate of chronic viruria, which was not related to isolation of CMV from renal tissue. In female strain 2 guinea pigs viruria was more than twice as prevalent as in males (56% vs. 24%). Transfusion of buffy coat from persistently infected strain 2 animals resulted in CMV infection in both isogenic and allogenic blood recipients, but buffy coat from uninfected donors did not activate CMV in persistently infected isogenic and allogenic blood recipients. Experimental CMV infection of young strain 2 guinea pigs interfered with the expression of guinea pig herpes-like virus, a common endogenous virus in strain 2 animals.

Animals↗
PubMed1979

Viral interference phenomena induced by foot-and-mouth disease temperature-sensitive mutants in bovine kidney cells.

Cultures of bovine kidney (BK) cells infected with temperature-sensitive (ts) mutants of foot-and-mouth disease virus (FMDV) were incubated at 38.5 degrees C, a temperature nonpermissive for mutant virus growth and RNA synthesis. The cells were subsequently resistant to viral growth and RNA synthesis when superinfected with wild-type FMDV and with heterologous fowl plague virus. The extent of interference was proportional to the multiplicity of infection of the ts mutant. It increased with time elapsed between infection with mutant and challenge infection, becoming greater than 99 percent after 24 hours. Interference was not proportional to decreased levels of cellular protein synthesis. The interference could be produced in the presence of actinomycin D, and thus was apparently mostly caused by the ts mutant itself rather than by interferon. The interference could not be produced in other less susceptible cell lines. Supernatant fluids from the BK cells infected with ts mutant virus interfered with wild-type FMD viral growth and RNA synthesis in fresh BK cells, and also showed low levels of activity in a vesicular stomatitis virus-plaque reduction assay. The properties of the supernatant fluid-interfering agent resembled to some extent those of an interferon. The ts mutant-mediated interference factor was apparently not able to diffuse into the supernatant fluid.

Animals↗
PubMed1975

Interferon action II. Membrane-bound alkaline ribonuclease activity in chick embryo cells manifesting interferon-mediated interference.

Membrane fractions from chick embryo cells manifesting viral interference mediated by interferon or poly(I)-poly(C) contain high levels of an alkaline ribonuclease. Enhanced RNase activity is not observed when inhibitors of cell protein or RNA synthesis are present during interferon treatment, or when heterologous interferon is used. The RNase associated with comparable membrane fractions from cells treated with mock-interferon is about 1/10 as active, and shows qualitative differences. In principle, divergent views of interferon action may be reconciled to a common mode of action by postulating that viral interference results from a newly induced or activated RNase of cellular origin and proper specificity that acts to reduce the accumulation and functional capacity of newly synthesized viral RNAs, particularly mRNA. Previous data in support of interferon's acting to inhibit virion-derived transcription in vivo are now interpreted as demonstrating enhanced degradation of viral transcripts (mRNA).

Animals↗
PubMed1975

The mode of inhibition of herpes simplex and vesicular stomatitis ocular viral infections in the rabbit and hamster by an interferon inducer tilorone dihydrochloride.

Ocular viral infections are a major cause of loss of vision and their effective control by applications of chemical compounds has been extensively investigated. To achieve such a control, better understanding of virus-host-drug interactions become a necessity. Two models, hamster and rabbit cornea, were selected for assays of protection afforded by tilorone dihydrochloride against herpes simplex (HSV) and vesicular stomatitis viruses (VSV). To obtain basic biologic comparison between viral interference and interferon-induction by tilorone, the hamster cornea system was first studied to produce a mutual viral interference by double infection. Furthermore, its effect against ascending herpetic ocular infection into encephalitis was evaluated in the rabbit. This compound was reported to have promising results in improving manifestations such as corneal ulceration, uveitis and conjunctivitis.

Animals↗
PubMed1979

Phenotypic mixing between murine oncoviruses and murine cytomegalovirus.

In vitro interactions between murine cytomegalovirus (MCMV) and murine leukaemia viruses (MuLV), two groups of enveloped viruses capable of causing persistent or latent infections in vivo, were examined for evidence of phenotypic mixing. The growth of MCMV in murine cells productively infected with ecotropic MuLV was shown to result regularly in the production of phenotypically mixed particles having the envelope antigens of MuLV and the genome of MCMV [MCMV(MuLV) pseudotypes]. The identity of such pseudotype particles was confirmed by the use of specific anti-MuLV serum and by the demonstration of restriction due to viral interference of penetration of these particles on MuLV-infected murine cells. This restriction was independent of N- or B-tropism. The production of reverse pseudotypes could not be examined because of the lytic effects of MCMV on the requisite assay cells.

Animals↗
PubMed1975

Nonspecific enhancers of resistance in man.

Nonspecific enhancers of resistance may include (1) viral interference, (2) interferon, (3) interferon inducers, (4) bacterial interference, (5) bacterial products such as Coley's "toxins," endotoxins, or staphylococcal, BCG, and Corynebacterium parvum vaccines, (6) transfer factor, and (7) well-defined chemicals such as dinitrochlorbenzene, levamisole, and vitamin C. These are discussed only as they have been applied to man to learn whether or not they have enhanced his ability to resist infections and growth of tumors. Preliminary studies suggest that a variety of relatively safe and effective nonspecific enhancers may soon be available for clinical use.

Adjuvants, Immunologic↗
PubMed1979

Defective influenza viral ribonucleoproteins cause interference.

Ribonucleoproteins (RNPs) isolated from infectious and defective interfering (DI) influenza virus (WSN) contained three major RNP peaks when analyzed in a glycerol gradient. Peak I RNP was predominant in infectious virus but was greatly reduced in DI virus preparations. Conversely, peak III RNP was elevated in DI virus, suggesting a large increase in DI RNA in this fraction. Labeled [(32)P]RNA was isolated from each RNP region and analyzed by electrophoresis on polyacrylamide gels. Peak I RNP contained primarily the polymerase and some HA genes, peak II contained some HA gene but mostly the NP and NA genes, and peak III contained the M and NS genes. In addition, peak III RNP from DI virus also contained the characteristic DI RNA segments. Interference activity of RNP fractions isolated from infectious and DI virus was tested using infectious center reduction assay. RNP peaks (I, II, and III) from infectious virus did not show any interference activity, whereas the peak III DI RNP caused a reduction in the number of infectious centers as compared to controls. Similar interference was not demonstrable with peak I RNP of DI virus nor with any RNP fractions from infectious virus alone. The interference activity of RNP fractions was RNase sensitive, suggesting that the DI RNA contained in DI RNPs was the interfering agent, and dilution experiments supported the conclusion that a single DI RNP could cause interference. The interfering RNPs were heterogeneous, and the majority migrated slower than viral RNPs containing M and NS genes. These results suggest that DI RNP (or DI RNA) is also responsible for interference in segmented, negative-stranded viruses.

Defective Viruses↗
PubMed1978

A biological perspective of slow virus infection and chronic disease.

Sequential events characterize the interaction of viruses with parenchymal cells, and acute lytic infections of tissues and organs have broad biological attributes. A knowledge of these permits a keener understanding of persistent, intermittent herpesvirus infections and persistent, continuous respiratory virus infections. In addition to unique biochemical mechanisms which may permit the latter chronic infections to evolve, the roles of defective and mutant strains of virus, viral interference, and the genetic, developmental and immunological expressions of the host are of considerable and provocative importance. The traditional view of viral infections embraces a broad spectrum of acute pathological and inflammatory events. The relationship of measles virus to subacute sclerosing panencephalitis, the elucidation of the latency of herpes simplex virus, and the slow unmasking of the pathogenesis of multiple sclerosis have illustrated the subtle elements of persistent viral infections of the human being. These chronic neurological diseases have provided the opportunity and stimulus for sharp dissection of the biological and biochemical processes which embellish the logical link of viral infections to other forms of chronic human illness.

Antibody Formation↗
PubMed1979

Variable infection of Vero cells and homologous interference after co-cultivation with HeLa cells with persistent defective infection by Edmonston measles virus.

The HeLa subline K11A-HG-1 (line of HeLa cells persistently infected with Edomonston measles virus but containing little or no transmissible infectious virus) was co-cultivated with Vero cells. Focal syncytia were formed containing measles antigen and accumulations of nucleocapsid-like structures with no detectable production of transmissible infectious virus or positive hemadsorption. The infection aborted between 2 and 3 weeks after preparation of co-cultures. Upon subculture of co-cultures, occasionally complete infections (progressive syncytial degeneration, hemadsorption, and production of transmissible infectious virus) appeared. A linear dose response curve for nontransmissible infection was obtained along with evidence that measles antigen had to be present on the surface of K11A-HG-1 cells for their infectivity for Vero cells. The basis for initiation of Vero cell infection by living K11A-HG-1 cells, but not by nonviable intact K11A-HG-1 cells killed by a virus-preserving technique, nor by disrupted K11A-HG-1 cells, is, at present, a matter of speculation. However, several lines of evidence were obtained which suggested that subsequent development of delayed variable transmissible Vero cell infection occurred because of a type of viral interference, including the presence of an inhibitor in K11A-HG-1 cultures, the bulk of which was cell-associated.

Antigens, Surface↗
PubMed1976

Suppression of the avian sarcoma virus genome in 8-azaquanine-resistant, transformed, hamster cells.

The avian sarcoma virus genome (Schmidt-Ruppin strain) in transformed hamster cells resistant to 8-azaquanine [Ha(SR)AG-50] was strongly suppressed. The suppression was genetically stable and could not be overcome by attempts at induction with 5-iodo-2'-deoxyuridine. Fusion of hamster cells, which had suppressed virus genome, with chicken Rous-associated virus (RAV-1)-preinfected cells easily rescued the sarcoma virus. The rescued virus had envelope properties of RAV-1, as determined by viral interference, virus neutralization, and plating on genetically resistant chicken cells. By repeatedly cloning the rescued virus, we determined that virus recombined in the rescue experiment and that the recombinant virus had the envelope properties of helper virus used for its rescue. Cells with suppressed avian sarcoma virus genome were suitable for preparation of different recombinant viruses.

Animals↗