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PubMed1977

Role of carbohydrate in biological functions of Friend murine leukemia virus gp71.

Purified gp71 of Friend murine leukemia virus (FLV) can interfere with virus infection, absorb neutralizing antibody, and in the presence of group-specific anti-gp71 antibody, hemagglutinate sheep erythrocytes. Interference by FLV gp71 with several murine leukemia viruses (MuLV) was tested in the XC and S + L- assay systems. Treatment of gp71 with trypsin or Pronase eliminated its interfering capacity. However, treatment with neuraminidase or a mixture of glycosidase enzymes, which left the major serological properties of gp71 intact, did not reduce the interference potential of gp71 for FLV or AKR MuLV. The capacity of gp71 to absorb type- or group-specific virus-neutralizing antibodies was similarly affected by the various enzyme treatments. In contrast, indirect hemagglutination by gp71 was abolished not only by proteases but also by treatment with glycosidase enzymes, although neuraminidase had no effect. Preliminary data indicate that infectivity of FLV or xenotropic MuLV was not affected by short treatment with glycosidase enzymes.

AKR murine leukemia virus↗
PubMed1977

[Interaction of the Sindbis virus and Rauscher and Friend leukoviruses in primary cultures and subcultures of mouse fibroblasts in the early stages of persistence].

The interaction between Friend and Raucher leukoviruses and Sindbis togavirus was studied in primary cultures of mouse fibroblasts and subcultures passaged for 77 days. In primary cultures, two types of virus interactions were observed: neutralism and interference. In interference, the release of the infectious Sindbis virus from the cells is blocked. According to electron microscopic observations, its reproduction terminates by formation of virus nucleocapsid. The blocking of the togavirus maturation is stable in primary cultures but reversible upon subcultivation of the cells infected with oncorna- and togavirus. Rauscher and Sindbis viruses are capable of joint persistence in subcultures with a gradual decrease of the infectivity of togavirus and the leukemogenic activity of oncornavirus.

Animals↗
PubMed1980

Viruses isolated from cells persistently infected with vesicular stomatitis virus show altered interactions with defective interfering particles.

Virus mutants isolated from persistent infections of vesicular stomatitis virus in BHK-21 cells were much less susceptible to interference mediated by the defective interfering particle used to establish the persistent infection. This mutational change occurred as early as 34 days in the persistent infection and continued for over 5 years. The earliest variants showed no oligonucleotide map changes and no difference in the temperature-sensitive phenotype from the original virus, but the later variants exhibited extensive map changes. These results suggest a possible role for defective interfering particles in the selection of the mutants.

Animals↗
PubMed1985

Beneficial role of a nonpathogenic orbi-like virus: studies on the interfering effect of M14 virus in mice and mosquitoes infected with Japanese encephalitis virus.

M14 virus, isolated from Culex tritaeniorhynchus mosquitoes collected in a Beijing suburb, was identified as a noncytopathogenic orbi-like virus. It was found to interfere with the growth of Japanese encephalitis (JE) virus, a mosquito-borne virus which infects humans, pigs, and horses in much of Asia, including China. JE virus is transmitted by C. tritaeniorhynchus mosquitoes and causes encephalitis in humans and horses and abortion in pigs. Because it had potential as an interfering agent for the biological control of JE, the M14 virus was characterized and its interfering effect was studied in mice and in C. tritaeniorhynchus mosquitoes.

Animals↗
PubMed1987

The membrane glycoprotein of Friend spleen focus-forming virus: evidence that the cell surface component is required for pathogenesis and that it binds to a receptor.

The leukemogenic membrane glycoprotein of Friend spleen focus-forming virus (SFFV) has an apparent Mr of 55,000 (gp55), is encoded by a recombinant env gene, and occurs on cell surfaces and in intracellular organelles. There is evidence that the amino-terminal region of gp55 forms a dualtropic-specific domain that is connected to the remainder of the glycoprotein by a proline-rich linker (C. Machida, R. Bestwick, B. Boswell, and D. Kabat, Virology 144:158-172, 1985). Using the colinear form of a cloned polycythemic strain of SFFV proviral DNA, we constructed seven in-phase env mutants by insertion of linkers and by a deletion. The mutagenized SFFVs were transfected into fibroblasts and were rescued by superinfection with a helper murine leukemia virus. Four of the mutants cause erythroblastosis. These include one with a 6-base-pair (bp) insert in the ecotropic-related sequence near the 3' end of the gene, two with a 12- or 18-bp insert in the region that encodes the proline-rich linker, and one with a 6-bp insert in the dualtropic-specific region. The other mutants (RI, Sm1, and Sm2) are nonpathogenic and contain lesions in dualtropic-specific region. The other mutants (RI, Sm1, and Sm2) are nonpathogenic and contain lesions in dualtropic-specific sequences that are highly conserved among strains of SFFV. A pathogenic revertant (RI-rev) was isolated from one mouse that developed erythroblastosis 3 weeks after infection with RI. RI-rev contains a second-site env mutation that affects the same domain as the primary mutation does and that increases the size of the encoded glycoprotein. All pathogenic SFFVs encode glycoproteins that are expressed on cell surfaces, whereas the nonpathogenic glycoproteins are exclusively intracellular. The pathogenic SFFVs also specifically cause a weak interference to superinfection by dualtropic MuLVs. These results are compatible with the multidomain model for the structure of gp55 and suggest that processing of gp55 to plasma membranes is required for pathogenesis. The amino-terminal region of gp55 binds to dualtropic murine leukemia virus receptors, and this interaction is preserved in the SFFV mutants that cause erythroblastosis.

Animals↗
PubMed2002

Interference between enterovirus and reovirus as a limiting factor in environmental virus detection.

AIMS: Faecal material from raw sewage or other sources lacking effective treatment sometimes contaminates water for human consumption. The relevant Italian regulations therefore call for testing drinking and recreational water for the presence of enterovirus. METHODS AND RESULTS: Traditional methods of analysis are based on revealing the typical cytopathic effects of enterovirus on cell cultures. However, the presence in environmental samples of different types of virus may cause interference phenomena that mask such cytopathic effects. The paper reports on an experimental test of this interference hypothesis. Buffalo Green Monkey cell cultures were co-infected via mixed suspensions of the polio type 3 virus and reovirus type 1. Cytopathic effects were then sought and the presence of enterovirus tested for via RT-PCR. CONCLUSIONS, SIGNIFICANCE AND IMPACT OF THE STUDY: The results obtained indicate that the normally high sensitivity of tests for the detection of enterovirus in samples is considerably decreased by the simultaneous presence of reovirus.

Animals↗
PubMed1978

Defective interfering particles of parvovirus H-1.

Defective interfering particles of the parvovirus H-1 were produced by serial propagation at high multiplicities of infection. Such particles interfere with the synthesis of capsid proteins and infectious virus of standard H-1. The interference is sensitive to UV irradiation, dependent on the multiplicity of the challenge virus, and is active in heterotypic infections against parvovirus H-3 or LuIII. Defective interfering particle genomes have alterations characterized by integral numbers (1 to 10 or more) of a 60-base-pair addition in the neighborhood of the origin of replicative-form DNA replication and deletions that are located primarily within two regions, 32 to 44 or 80 to 90 on the genome map. Some of the implications of these findings are discussed.

Capsid↗
PubMed1993

Gibbon ape leukemia virus and the amphotropic murine leukemia virus 4070A exhibit an unusual interference pattern on E36 Chinese hamster cells.

The gibbon ape leukemia virus (GaLV), the amphotropic mouse leukemia virus (A-MLV) 4070A, and the xenotropic mouse leukemia virus (X-MLV) exhibit wide but not identical species host ranges. However, most Chinese hamster cells resist infection by all three viruses. We have now determined that the Chinese hamster cell line E36 differs from other Chinese hamster cell lines in that it is susceptible to infection by wild-type GaLV, A-MLV, and X-MLV. Surprisingly, analysis of the interference pattern of GaLV and A-MLV in E36 cells indicated that GaLV and A-MLV interfere in a nonreciprocal fashion. E36 cells productively infected with GaLV were resistant to superinfection by both GaLV and amphotropically packaged recombinant retroviral vectors. In contrast, E36 cells infected with A-MLV were resistant to superinfection with an amphotropic vector but could still be infected by a GaLV vector. These results imply the existence of a receptor on E36 cells that interacts with both GaLV and A-MLV.

3T3 Cells↗
PubMed1993

Alterations of the stalk of the influenza virus neuraminidase: deletions and insertions.

The neuraminidase (NA) of influenza viruses cleaves sialic acids from receptors, prevents self-aggregation and facilitates release of virus during budding from host cells. Although the structure and function of the globular head of the influenza virus NA has been well studied, much less is known about the stalk of the NA, the region between the viral membrane and the globular head. Applying a reverse genetics system, we altered the stalk of the influenza A/WSN/33 virus NA by making deletions, insertions and mutations in this region of the gene. Our data show that the length of the NA stalk can be variable. Deletions of up to 28 amino acids and insertions of up to 41 amino acids in the stalk region did not abolish formation of infectious progeny virus. The data also indicate that the cysteine at position 76 is essential for formation of infectious virus, and that deletions beyond the cysteine did not result in infectious virus. Interestingly, shortening of the length of the stalk region by 28 amino acids resulted in a virus with a markedly reduced growth rate in MDCK cells as compared to that in MDBK cells. An insertion of 41 extra amino acids into the stalk did not significantly interfere with viral growth in MDCK or MDBK cells, which suggests that the stalk region would tolerate the introduction of long foreign sequences.

Amino Acid Sequence↗
PubMed1985

Characterization of virulent and avirulent A/chicken/Pennsylvania/83 influenza A viruses: potential role of defective interfering RNAs in nature.

In April 1983, an influenza virus of low virulence appeared in chickens in Pennsylvania. Subsequently, in October 1983, the virus became virulent and caused high mortality in poultry. The causative agent has been identified as an influenza virus of the H5N2 serotype. The hemagglutinin is antigenically closely related to tern/South Africa/61 (H5N3) and the neuraminidase is similar to that from human H2N2 strains (e.g., A/Japan/305/57) and from some avian influenza virus strains (e.g., A/turkey/Mass/66 [H6N2]). Comparison of the genome RNAs of chicken/Penn with other influenza virus isolates by RNA-RNA hybridization indicated that all of the genes of this virus were closely related to those of various other influenza virus isolates from wild birds. Chickens infected with the virulent strain shed high concentrations of virus in their feces (10(7) 50% egg infective dose per g), and the virus was isolated from the albumin and yolk of eggs layed just before death. Virus was also isolated from house flies in chicken houses. Serological and virological studies showed that humans are not susceptible to infection with the virus, but can serve as short-term mechanical carriers. Analysis of the RNA of the viruses isolated in April and October by gel migration and RNA-RNA hybridization suggested that these strains were very closely related. Oligonucleotide mapping of the individual genes of virulent and avirulent strains showed a limited number of changes in the genome RNAs, but no consistent differences between the virulent and avirulent strains that could be correlated with pathogenicity were found. Polyacrylamide gel analysis of the early (avirulent) isolates demonstrated the presence of low-molecular-weight RNA bands which is indicative of defective-interfering particles. These RNAs were not present in the virulent isolates. Experimental infection of chickens with mixtures of the avirulent and virulent strains demonstrated that the avirulent virus interferes with the pathogenicity of the virulent virus. The results suggest that the original avirulent virus was probably derived from influenza viruses from wild birds and that the virulent strain was derived from the avirulent strain by selective adaptation rather than by recombination or the introduction of a new virus into the population. This adaptation may have involved the loss of defective RNAs, as well as mutations, and thus provides a possible model for a role of defective-interfering particles in nature.

Animals↗
PubMed2003

Tacaribe virus Z protein interacts with the L polymerase protein to inhibit viral RNA synthesis.

Tacaribe virus (TV) is the prototype of the New World group of arenaviruses. The TV genome encodes four proteins, the nucleoprotein (N), the glycoprotein precursor, the polymerase (L), and a small RING finger protein (Z). Using a reverse genetic system, we recently demonstrated that TV N and L are sufficient to drive transcription and full-cycle RNA replication mediated by TV-like RNAs and that Z is a powerful inhibitor of these processes (N. López, R. Jácamo, and M. T. Franze-Fernández, J. Virol. 65:12241-12251, 2001). In the present study we investigated whether Z might interact with either of the proteins, N and L, required for RNA synthesis. To that end, we used coimmunoprecipitation with monospecific antibodies against the viral proteins and coimmunoprecipitation with serum against glutathione S-transferase (GST) and binding to glutathione-Sepharose beads when Z was expressed as a fusion protein with GST. We demonstrated that Z interacted with L but not with N and that Z inhibitory activity was dependent on its ability to bind to L. We also evaluated the contribution of different Z regions to its binding ability and functional activity. We found that integrity of the RING structure is essential for Z binding to L and for Z inhibitory activity. Mutants with deletions at the N and C termini of Z showed that amino acids within the C-terminal region and immediately adjacent to the RING domain N terminus contribute to efficient Z-L interaction and are required for inhibitory activity. The data presented here provide the first evidence of an interaction between Z and L, suggesting that Z interferes with viral RNA synthesis by direct interaction with L. In addition, coimmunoprecipitation studies revealed a previously unreported interaction between N and L.

Arenaviruses, New World↗
PubMed1993

Selective interference with class I major histocompatibility complex presentation of the major immediate-early protein following infection with human cytomegalovirus.

Responses of cytotoxic T-cells (Tc) to human cytomegalovirus (CMV) represent the predominant mechanism by which hosts resist CMV infection. The CMV major immediate-early protein (IE) is present throughout the virus replicative cycle. Studies were performed to determine whether Tc specific for IE effectively lyse CMV-infected targets and are thus capable of providing protective immunity against infection. After in vitro stimulation of peripheral blood mononuclear cells with CMV-infected autologous fibroblasts, Tc specific for IE were not readily detectable in CMV-reactive polyclonal Tc lines. However, after stimulation of peripheral blood mononuclear cells with cells selectively expressing IE, weak but detectable IE-specific Tc responses were observed. The frequency of IE-specific Tc clones derived from cultures stimulated with IE-expressing cells was 50 to 100 times lower than the frequency of Tc clones specific for other CMV proteins isolated from cultures stimulated with CMV-infected cells. All of the IE-specific Tc clones, which efficiently lysed targets selectively expressing IE, demonstrated minimal lysis of CMV-infected fibroblasts, despite abundant IE expression in these target cells. In contrast to these results with IE, other viral proteins were efficiently presented during all phases of CMV infection. These data suggest that CMV has evolved a unique mechanism for selectively limiting the presentation of the potentially immunogenic IE protein, which may preclude IE-specific Tc from providing protective immunity to CMV infection.

Antigen-Presenting Cells↗
PubMed2003

The hepatitis C virus persistence: how to evade the immune system?

Hepatitis C virus (HCV) is an emerging virus of medical importance. A majority of HCV infections become chronic and lead to chronic hepatitis, liver cirrhosis and hepatocellular carcinoma. HCV usually induces robust immune responses, but it frequently escapes the immune defense to establish persistent infection. The fact that HCV exists as an evolving quasispecies plays an important role in the selection of escape mutants. Furthermore, several viral proteins interfere with cellular functions, in particular, those involved in the immune response of the host. Several HCV proteins also modulate cell signalling through interaction with different effectors involved in cell proliferation and apoptosis, or in the interferon-signalling pathway. In addition, HCV infects immune cells such as B and T cells, and thus affects their normal functions. These various strategies used by HCV to counter the immune response of the host are reviewed here. A better understanding of these mechanisms would help design new therapeutic targets.

Epitopes↗
PubMed1980

Rabies serogroup viruses in neuroblastoma cells: propagation, "autointerference," and apparently random back-mutation of attenuated viruses to the virulent state.

Each of several strains of fixed rabies virus was found to replicate to high titers in C1300 mouse neuroblastoma (clone NA) cells, without adaptation. Rabies serogroup Lagos bat, Mokola, and Duvenhage viruses also replicated efficiently in NA cells. Kotonkan and Obodhiang viruses replicated efficiently after adaptation, to titers not previously obtained in vitro. Infection in NA cells was frequently more cytopathic than in BHK-21 cells, allowing titration of Kotonkan and Obodhiang viruses by plaque assay. Duvenhage virus caused syncytium formation. Serial propagation of rabies viruses at a high multiplicity of infection in NA cells led to a rapid decline in virus yields; similar "autointerference" has not previously been demonstrated with rabies virus in other cell systems. Rabies virus infection in NA cells exhibited extreme sensitivity to interference by experimentally added defective interfering virions. Although several strains of attenuated rabies virus consistently reverted rapidly to virulence after propagation in NA cells, other strains of attenuated rabies and rabies serogroup viruses acquired increased virulence at a more gradual rate or not at all, suggesting that diverse characters may control virulence. When attenuated Flury HEP rabies virus was serially propagated at a low multiplicity of infection in either NA cells or suckling mouse brain, virulence appeared at a very variable rate, indicating that these systems may selectively enhance replication of randomly occurring virulent virus mutants.

Animals↗
PubMed1983

Interference between non-A, non-B and hepatitis B virus infection in chimpanzees.

Pre-existing chronic or concurrent acute non-A, non-B (NANB) virus infection has been found to interfere with hepatitis B virus (HBV) replication and to delay and moderate markedly the appearance of disease related to HBV infection in chimpanzees. The mechanism for this phenomenon remains unclear. These findings are of practical significance for vaccine safety testing and evaluation of methods for virus inactivation in chimpanzees. The possible occurrence of dual NANB and HBV infection requires that prolonged follow-up be carried out. Attempts to carry out inactivation studies on materials containing both types of virus may also provide misleading observations.

Alanine Transaminase↗
PubMed1984

Modulation of Semliki Forest virus-induced infection of mice by defective-interfering virus.

Preparations of defective-interfering (DI) Semliki Forest virus (SFV) differed qualitatively in their ability to protect mice against lethal SFV-induced encephalitis. The preparations fell into three categories: (1) DI virus p13a protected the majority of mice and left them immune to subsequent challenge with 100 50% lethal doses of SFV; (2) DI virus p4 protected mice to a similar extent, but the susceptibility of all surviving mice to challenge suggested that the protection was mediated without the intervention of the adaptive immune response; and (3) DI virus p5 did not protect mice even though its interference titer was similar to that of the protective preparations. How DI viruses p4 and p13a modulate this lethal infection is not clear; the failure of p4 to stimulate protective immunity suggests that nonadaptive host responses are important, but neither p4 nor p13a altered the course of infection with a heterologous neurotropic virus. Compared with avirulent SFV infection, both DI virus-modulated infections were poorly immunogenic with regard to the humoral immune response, although a minority of mice did have high levels of neutralizing antibody. Other, unknown factors are evidently at work and remain to be elucidated.

Animals↗
PubMed1981

Genetic analysis of prophage effects on heteroimmune superinfection in Serratia marcescens.

Plaque formation of phage kappa on Serratia marcescens strain HY normally depends on the presence of either a psi or y prophage in the indicator bacteria. Bacterial ink mutants allowing kappa growth in the absence of either prophage were isolated from the doubly cured strain HY (psi, y)--. By means of a kappa mutant, named gdy, an active participation of kappa in antagonizing inhibition of its own growth on HY (psi, y)-- was demonstrated. The gdy mutation is closely linked to gene cIII coding for the kappa repressor. The prophages psi and y enable kappa to grow undisturbed probably by modifying the kappa DNA during replication in such a way that it is not susceptible to the ink+ effect. Whereas kappa grown on HY (psi, y)--ink-- gave only rare productive infections of HY (kappa, y)--, psi and y grown on the same strain were fully infective. The interference exerted by a kappa prophage on vegetative propagation of y is based upon a multi-component mechanism, the interference being removed, or diminished by mutations residing either inside or outside of the kappa prophage. The responsive phage gene iny+ is dominant over its mutant allele iny--; hence it codes for a diffusible product. Both on the vegetative and the prophage genome iny is located near gene lI responsible for lysogenic conversion of bacteria to non-adsorption of kappa. The restriction-modification system of HY is not involved in the growth inhibition of kappa by HY (psi, y)--. Contrary to the other phages used in this work y is refractory to restriction.

Bacteriophages↗
PubMed1981

An interference phenomenon associated with a measles virus SSPE isolate (Halle).

A measles virus (Halle SSPE isolate) induced ring plaque phenomenon (concentric rings of living and dead cells) has been shown to be associated with the temperature-dependent production of interfering particles. The interfering particles have been purified by potassium tartrate linear gradient centrifugation and have buoyant densities of 1.15 g/ml (M particle) and 1.06 g/ml (L particle) respectively. Both interfering particle population have been shown to decrease the yield of wild-type measles virus from infected cells by 50% when co-infection experiments were performed. Neither the M or L particle population interfered with the growth of VSV in the same host-cell system.

Animals↗