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PubMed1996

Characterization of an envelope mutant of HIV-1 that interferes with viral infectivity.

A mutant human immunodeficiency virus (HIV-1) provirus encoding an envelope (Env) protein with a truncated transmembrane protein cytoplasmic domain was defective for replication. Coexpression of the mutant with a wild-type (wt) HIV-1 provirus potently inhibited the production of infectious virus. The maximum inhibitory effect was reached when the ratio of mutant to wt proviral DNA was 2:1. This transdominant defect in infectivity conferred by the mutant Env did not appear to involve the late steps of virus replication, since the synthesis, precursor processing, and intracellular transport of the Env proteins were not blocked; nor did it prevent the incorporation of the envelope proteins into virions or the subsequent release of the virus. Although the mutant Env protein still retained syncytia-forming ability, the truncated protein was unable to mediate cell-to-cell transmission of the virus. Moreover, coexpression with the mutant effectively inhibited the ability of the wt Env to mediate cell-to-cell transmission. The mutant Env protein formed a complex with the wt protein when they were coexpressed, producing heterooligomeric structures which appeared to be severely defective in an early, post-CD4 binding step of the virus life cycle despite the inclusion of wt Env in the complexes.

Animals↗
PubMed1966

Specific cell-surface alteration by enteroviruses as reflected by viral-attachment interference.

Crowell, Richard L. (Hahnemann Medical College, Philadelphia, Pa.). Specific cell-surface alteration by enteroviruses as reflected by viral-attachment interference. J. Bacteriol. 91:198-204. 1966.-Exposure of HeLa cells to high levels of coxsackievirus B3 produced cells which were refractory to attachment of coxsackievirus B1, whereas poliovirus T2 attached normally. Under similar conditions, poliovirus T2 was found to interfere with the attachment of poliovirus T1 to HeLa cells without affecting the attachment rate of coxsackievirus B3. The data confirm earlier findings that the receptor sites on HeLa cells, which bind members of group B coxsackieviruses, are distinct from those for polioviruses. Quantitatively, coxsackieviruses B1 and B3 were found to be mutually exclusive in the attachment interference assay to suggest that they compete for the same receptors on the HeLa cell surface. The finding that input multiplicities of B3 virus which exceeded 500 saturated the homologous viral receptors of HeLa cells was unexpected, but was consistent with the results of interference assays. Excessive amounts of input virus did not, however, inhibit eclipse of homologous cell-associated virus. Attachment interference between enteroviruses occurred even though the interfering virus was eclipsed prior to addition of challenge virus. The finding that enterovirus attachment interference was reversible with acid pH suggested that attachment and eclipse of enterovirus does not result in a permanent alteration of the cell membrane and that these events occur at the cell surface.

Culture Techniques↗
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↗
PubMed2000

Mechanism of interference mediated by human parainfluenza virus type 3 infection.

Viral interference is characterized by the resistance of infected cells to infection by a challenge virus. Mechanisms of viral interference have not been characterized for human parainfluenza virus type 3 (HPF3), and the possible role of the neuraminidase (receptor-destroying) enzyme of the hemagglutinin-neuraminidase (HN) glycoprotein has not been assessed. To determine whether continual HN expression results in depletion of the viral receptors and thus prevents entry and cell fusion, we tested whether cells expressing wild-type HPF3 HN are resistant to viral infection. Stable expression of wild-type HN-green fluorescent protein (GFP) on cell membranes in different amounts allowed us to establish a correlation between the level of HN expression, the level of neuraminidase activity, and the level of protection from HPF3 infection. Cells with the highest levels of HN expression and neuraminidase activity on the cell surface were most resistant to infection by HPF3. To determine whether this resistance is attributable to the viral neuraminidase, we used a cloned variant HPF3 HN that has two amino acid alterations in HN leading to the loss of detectable neuraminidase activity. Cells expressing the neuraminidase-deficient variant HN-GFP were not protected from infection, despite expressing HN on their surface at levels even higher than the wild-type cell clones. Our results demonstrate that the HPF3 HN-mediated interference effect can be attributed to the presence of an active neuraminidase enzyme activity and provide the first definitive evidence that the mechanism for attachment interference by a paramyxovirus is attributable to the viral neuraminidase.

Cell Line↗
PubMed1989

In vivo interference by Newcastle disease virus in chickens, the natural host of the virus.

Homologous and heterologous viral interference is a common occurrence that has been well studied in vitro. In the present study, homologous viral interference between the LaSota and NYP strains of Newcastle disease virus (NDV) was studied in vivo in chickens, the natural host for NDV. The LaSota strain is avirulent and widely used as a vaccine in poultry industry, while the NYP strain is highly virulent and causes acute disease and death in chickens within four to six days after infection. Chickens generally became resistant to NYP strain challenge 12 hours after intranasal or intratracheal inoculation with LaSota strain virus. The resistance was manifested by reduction in chicken morbidity and mortality, decrease in virus replication in the chicken respiratory tract (p less than 0.05), and inhibition of NYP strain induced gross and microscopic lesions. Interferon was first detected in the chicken respiratory tract and blood at 3 to 6 hours; it peaked at 12 to 24 hours and was maintained for 48 hours after viral inoculation, indicating that interferon induction might be one possible mechanism of the interference between the two strains. This study suggests a role for viral interference in vaccination against virulent viruses.

Animals↗
PubMed1974

Cytomegalovirus interference in vitro.

Cytomegalovirus (CMV) was shown to induce a state of viral interference in human embryo fibroblast cultures (HEF). This interference was characterized by: (i) requirement for infectious virus; (ii) a latent period (48 to 96 h) for establishment of the interference; (iii) activity against a representative group of heterologous viruses; (iv) loss of interfering activity when challenged with a high multiplicity of infection; (v) lack of effect on adsorption of virus; (vi) mediation by a soluble product of CMV-cell interaction that it is not blocked by anti-CMV antibody; and (vii) absence of detectable interferon, although the soluble mediator shares a number of characteristics with interferon. This state of interference in HEF cultures could be simulated by extended exposure to subdetectable levels of human interferon. It is postulated that CMV induced the production of a soluble, interferon-like mediator of viral interference and that continuous exposure of the HEF culture to this mediator resulted in the development of resistance to a number of heterologous viruses.

Culture Techniques↗
PubMed1989

Natural anti-TNP antibodies from rainbow trout interfere with viral infection in vitro.

Normal and viral-infected rainbow trout (RT) were tested for serum antibody activity against self and nonself antigens. Particularly high titres of anti-trinitrophenyl (TNP) antibodies were noted, as in other fish species. To analyse this, the anti-TNP antibodies were isolated by affinity chromatography and their capacity to interfere with viral infection in vitro was studied. We selected RT fibroblasts as target cells, and two common pathogenic viruses in trout, a rhabdovirus, viral haemorrhagic septicaemia virus (VHS) and a birnavirus, the infectious pancreatic necrosis virus (IPN). Anti-TNP antibodies were examined for their capacity to neutralize VHS and IPN viruses. Data obtained show that the anti-TNP antibodies, even at high concentrations, only partially neutralized virus. In contrast, when anti-TNP antibodies were assayed for their protective activity using RT fibroblast cells infected with VHS or IPN viruses, results showed high protective activity, regardless of serum origin or of the virus used, when the antibodies were added to the cell culture after viral infection. Therefore, our experiments indicate that the protective activity does not seem to be due to a direct interaction of the antibodies with the viruses. It is suggested that virus-modified cell surface self structures exhibit new epitopes which interact with the anti-TNP antibodies. Such an interaction would allow anti-TNP antibodies to participate in a non-specific defence mechanism against viral infection.

Animals↗
PubMed1991

Non-replicating deletion mutants of brome mosaic virus RNA-2 interfere with viral replication.

Naturally occurring defective interfering RNAs (DI-RNAs) and satellite RNAs greatly reduce the accumulation of their helper virus in vivo, but often modulate symptom expression in an unpredictable manner. Deletion mutants Nc/S, Na/M and Sa/Nc + M/S, derived from brome mosaic virus (BMV) RNA-2, failed to replicate when co-inoculated with BMV RNAs-1 and -2 to barley protoplasts. However, the inoculum RNA corresponding to these deletion mutants was extremely stable and could have been mistaken for plus-strand progeny had minus-strand progeny analysis been omitted. These results accentuate the need for such tests in evaluating the ability of mutant viral sequences to replicate. One of the mutants, Nc/S, effectively interfered with the accumulation of BMV RNAs-1 and -2 in barley protoplasts. This non-replicating interfering RNA was termed NRI RNA-2 Nc/S. When present with RNAs-1 and -2 at low inoculum amounts (1 microgram), NRI RNA-2 Nc/S reduced replication of RNA-2, the parental RNA, by 63% and preferentially interfered with minus-strand RNA accumulation. At higher levels (4 micrograms), it completely displaced replication of both RNAs-1 and -2. Mutations eliminating translation of a truncated p2a protein from NRI RNA-2 Nc/S did not alleviate the interference effect, demonstrating that a defective replicase protein was not responsible for the decreased accumulation of genomic RNA. At an NRI RNA: genomic RNA inoculum molar ratio of 1:1, NRI RNA-2 Nc/S reduced the accumulation of all helper virus RNAs by 55%. Since this reduction was seen for both wild-type RNA-3 and delta SGP RNA-3, a deletion mutant of RNA-3 that lacks the subgenomic promoter necessary for coat protein expression, it was evident that the effective interference mediated by NRI RNA-2 Nc/S was not mitigated by encapsidation. The ability of the NRI RNAs to mimic satellite DI RNAs in depressing helper virus replication suggests that their expression in transgenic plants may provide a new and widely applicable approach for inducing resistance to viral infection.

Blotting, Northern↗
PubMed1974

Mechanism of Sindbis virus-induced intrinsic interference with vesicular stomatitis virus replication.

Heterologous viral interference is induced by Sindbis virus against vesicular stomatitis virus (VSV) in a manner analogous to intrinsic interference with Newcastle disease virus replication. Interference in both systems (i) depends upon early expression of the inducing virus genome, (ii) shows similar kinetics of induction, (iii) does not involve interferon action, and (iv) appears to be manifest as an all-or-none effect. VSV can be added to the list of viruses blocked by intrinsic interference. Sindbis virus-induced intrinsic interference with VSV replication is not mediated through homotypic interference by defective interfering particles; rather, T-particle and B-particle synthesis is inhibited. Significantly, intrinsic interference has no effect on primary transcription directed by the virion-associated transcriptase in VSV-challenged cells. However, Sindbis virus appears to induce interference with the VSV-RNA synthesized subsequent to primary transcription, namely, that which is dependent on protein synthesis. Thus, the target of intrinsic interference appears to be a reaction subsequent to primary transcription but prior to the appearance of protein synthesis-dependent VSV RNA, secondary transcription.

Animals↗
PubMed2004

Intracellular approach for blocking JC virus gene expression by using RNA interference during viral infection.

The human polyomavirus, JC virus (JCV), encodes two regulatory proteins at the early (T antigen) and the late (agnoprotein) phases of viral infection whose activities are important for the production of the viral capsid proteins and the dysregulation of several host factors and their functions. For this study, we designed and utilized an RNA interference strategy via small interfering RNAs (siRNAs) that targeted the expression of T antigen and agnoprotein in human astrocytic cells. The treatment of cells with specific siRNA oligonucleotides targeting a conserved region of T antigen, nucleotides (nt) 4256 to 4276 (Mad-1 strain), caused a >50% decline in the level of T antigen and in its transcriptional activity upon the viral capsid genes as well as a significant reduction in viral DNA replication in infected cells. Similarly, a single siRNA that aimed at nt 324 to 342 of agnoprotein noticeably reduced early and late viral protein production. A combined treatment of the infected cells with both T-antigen and agnoprotein siRNAs completely abolished viral capsid protein production, indicative of the ability of the siRNAs to effectively halt multiplication of the virus in infected cells. These observations provide a new avenue for possible treatments of patients with the JCV-induced demyelinating disease progressive multifocal leukoencephalopathy.

Antigens, Viral, Tumor↗
PubMed1967

Analysis of additional interference occurring after the removal of interferon.

Cultures of chick cells exposed to interferon continued to decrease in virus-producing ability during incubation after the interferon was removed. The rate of development of the additional interference and the degree of viral interference finally manifested were dependent on the concentration of interferon to which the cultures were exposed and the time of exposure. Additional interference occurred also in infected cells. Additional interference was inhibited by actinomycin D and puromycin. The best explanation of additional interference is that it results from interferon that is fixed to the cells during their initial period of contact.

Animals↗