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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↗
PubMed1967

Intrinsic interference: a new type of viral interference.

The hemadsorption-negative plaque test has revealed a new type of viral interference, termed intrinsic interference. Several unrelated types of noncytopathic viruses were shown to induce in infected host cells a state of interference unique in being directed solely against superinfection by Newcastle disease virus (NDV). The NDV-refractory state arises only in those individual cells of a population actually infected by the inducing virus, and presumably results from the action of a protein(s) coded for by the viral genome. Thus, intrinsic interference differs fundamentally from that mediated by an extrinsic protein detectable under conditions favoring resistance to a broad spectrum of viruses and characteristic of interference induced by interferon, the latter being coded for by the cell genome. Intrinsic interference is defined as a viral genome-induced cellular state of resistance to challenge by high multiplicities of NDV, coexistent with a state of susceptibility to a broad spectrum of other viruses, similarly tested at high multiplicities. The capacity to induce intrinsic interference was demonstrated with rubella virus, Sindbis virus (arbovirus, group A), West Nile virus (arbovirus, group B), poliovirus (MEF, type 2), the lactic dehydrogenase virus (Riley's agent), and an unidentified nonhemadsorbing, noncytopathic adventitious virus. A state of intrinsic interference was also observed in the V5 line of mouse cells carrying a murine leukemia virus, probably resulting from some heretofore unsuspected contaminating virus. The molecular basis for intrinsic interference is not known, but it appears to involve a step in the NDV growth cycle beyond that of viral attachment, entry, and eclipse.

Animals↗
PubMed1990

Simulation of mechanisms of viral interference in influenza.

Biological interference among viral agents might have significant implications for disease prevention and therapy. Field data for influenza yield conflicting evidence concerning the independence of infection rates, or disease severity, for two co-circulating viruses. To examine the effects of several assumed modes of interference for influenza, simulations of a Monte Carlo micropopulation model of influenza epidemics have been performed. Model parameters were selected so that the simulated attack rates for each of two different viral strains matched actual field data. Rates of infection were compared for single agents and for two viruses with only behavioural interference. Other simulations included temporary immunity to the other virus for the duration of the infection, and/or reduced shedding of viral particles for dual infections. Simulated viral competition had little impact on epidemic severity, duration, or size distribution. Under the conditions studied, viral interference in natural populations would be difficult to infer from field observations of attack rates. Other simulations extended a partial immunity and/or reduced viral shedding during an infection with a second virus. These indicated that interference might be suggested by field data, but it could not be demonstrated conclusively. Still other simulations showed that for epidemics with much higher attack rates for both viruses, it would be relatively easy to demonstrate interference. However, in order to observe interference between influenza strains, it would be necessary to monitor on an almost daily basis, using a method of viral detection which would have to be both highly specific and also very sensitive.

Adolescent↗
PubMed1989

Viral interference in the tick, Rhipicephalus appendiculatus. II. Absence of interference with Thogoto virus when the tick gut is by-passed by parenteral inoculation.

Genetic reassortment of Thogoto (THO) virus has been demonstrated in dually infected Rhipicephalus appendiculatus ticks. However previous results showed that oral superinfection is inhibited by interference. To ascertain the site of THO viral interference, ticks were infected parenterally or orally with a temperature-sensitive (ts) mutant of THO virus. Infected ticks were then challenged with wild-type (wt) THO virus via parenteral inoculation. Intra-stadial superinfection was carried out by parenteral inoculation of newly infected engorged ticks whereas inter-stadial superinfection involved inoculation of engorged ticks infected at the previous stage. In both instances viral interference was not observed, i.e. the challenge virus replicated and was delivered by bite to susceptible hosts. Therefore when the gut is bypassed, R. appendiculatus ticks are apparently permissive to dual infection even when there is a delay in the presentation of the superinfecting virus. These results demonstrate that interference following superinfection per os does not occur in the salivary glands, but may occur in the gut and possibly in a secondary site of viral replication such as the synganglion.

Animals↗
PubMed1973

Induction of viral interference: effects of poly rI-rC and diethylaminoethyl-dextran on the activity of the antiviral protein.

The activity of the antiviral protein induced by various ratios of poly rI.rC and diethylaminoethyl (DEAE)-dextran was studied. It was found that, when large doses of poly rI.rC were used, very little viral interference was observed. This effect was initially attributed to the cells being refractory for production of antiviral protein. Subsequent experiments offered alternative explanations suggesting that, at any given dosage of poly rI.rC, an excess of DEAE-dextran is necessary for the production of viral interference. It is suggested that DEAE-dextran acts by exposing a cell receptor site for poly rI.rC.

Animals↗
PubMed1985

Mutagenesis of a herpes simplex virus origin of DNA replication and its effect on viral interference.

Supercoiled plasmid molecules containing cloned copies of a DNA fragment which includes a functional herpes simplex virus type 1 origin of DNA replication were cleaved preferentially at two positions within the viral insert by nuclease S1. Plasmids with molecular linker insertions at these sites were constructed, and analysis of two representative plasmids demonstrated the presence of palindromic DNA sequences at the preferred cleavage positions. One of these palindromic sequences occurred within a 90 bp region in which the cis-acting sequences essential for viral origin function had previously been located. Insertion of a linker at this position abolished origin activity, demonstrating an essential role for sequences within the palindrome in the initiation of DNA synthesis. In transfection assays, plasmids containing a functional viral origin of DNA replication markedly interfered with the infectivity of non-defective viral DNA even in the absence of viral encapsidation signals. Inactivation of the origin greatly reduced this effect on DNA infectivity, suggesting that viral interference may be mediated by a mechanism involving the replicative machinery.

Base Sequence↗
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↗
PubMed1989

The L protein of a VSV mutant isolated from a persistent infection is responsible for viral interference and dominance over the wild-type.

The dominance of a mutant isolated from a persistent infection (VSV-Pi) over wild-type vesicular stomatitis virus (wt-VSV) in mixed infections was described previously (J. A. Jordan and J. S. Youngner, 1987, Virology, 158, 407-413). In an attempt to identify the VSV-Pi gene product responsible for transcriptional interference, various combinations of purified VSV-Pi and wt-VSV transcribing core proteins were analyzed in an in vitro transcription assay and compared to homologous wild-type controls. The reconstitution studies revealed that the VSV-Pi RNA dependent-RNA polymerase (L protein) has a dominant activity which works in trans to inhibit wt-VSV transcription.

Animals↗