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PubMed1981

Ecotropic and xenotropic type C retroviruses associated with reticulum cell neoplasms of SJL/J mice.

An ecotropic type C retrovirus (D1-MuLV) isolated from SJL/J mice was injected into neonatally thymectomized SJL/J mice. There was no acceleration of development of reticulum cell neoplasm (RCN) in these mice as compared with the control, uninoculated but similarly thymectomized group. The incidence of RCN at 10 and 11 months after injection was 14.6% and 12.5% respectively. Two female mice inoculated with D1-MuLV developed mammary adenocarcinoma. There was persistence of high titres of the ecotropic virus associated with RCN and mammary tumour of SJL/J mice. Xenotropic virus (X-MuLV) was detected in spleens of normal SJL/J mice at ages 6 and 12 months (60% and 80% respectively) but not at other ages. The X-MuLV isolated from SJL/J mouse embryo cell cultures treated with 5-iodo-2'-deoxyuridine (SJL-MEF-X-MuLV) and that isolated from a spontaneous RCN (SJL-RCN-X-MuLV) were compared with NZB-X-MuLV (NZB mouse origin) and AT124-X-MuLV (NIH Swiss mouse origin) in regard to their host range, ion and primer-template preference by reverse transcriptase, virus interference and neutralization characteristics. Cross-neutralization and gp70 competitive radio-immunoassays showed that D1-MuLV is more closely related to AKR-MuLV than to Rauscher-MuLV and appears to share some virus envelope antigens with SJL-X-MuLVs. The type-specific gag gene product (p12) from Balb:virus-2 and NZB-X-MuLV was used in competitive radioimmunoassay, and SJL-RCN-X-MuLV was found to be more closely related to Balb:virus-2 (MuLV-X alpha) than to NZB-X-MuLV (MuLV-X beta).

Animals↗
PubMed2002

Defective segment 1 RNAs that interfere with production of infectious influenza A virus require at least 150 nucleotides of 5' sequence: evidence from a plasmid-driven system.

The presence of at least 80-90 and more typically around 200 nucleotides (nt) at the 5' end of the virion-sense RNA in all naturally occurring defective influenza A virus RNAs suggests that this is essential sequence, whereas the 3'-end sequence may be as short as 25 nt. The stability of defective RNA on serial passage with infectious helper virus also depends on the length of 5'-end sequence. Here, we have studied the influence of 5'-end sequences of a panel of six defective segment 1 RNAs from H3N8 and H7N7 viruses on their ability to interfere with the multiplication of plasmid-produced infectious A/WSN virus (H1N1). Four of the H3N8 defective RNAs are identical in overall length but vary in the length of 5' sequence. Transfected defective RNAs interfered with infectious virus production in a concentration-dependent manner. The extent of interference also depended on the length of 5'-end sequence in the defective genome. This required at least 150 nt and was maximal with 220 nt of 5' end sequence. The reduction in virus multiplication was highly significant and correlated with the presence of detectable intracellular defective RNA. Packaging of full-length segment 1 RNA by progeny virus was inversely proportional to the packaging of defective segment 1 RNA and may explain the reduction in infectivity. In summary, a critical length of 5'-end sequence is essential for the interfering properties of defective influenza virus RNAs, which indicates that this plays some vital role in the virus life cycle.

5' Untranslated Regions↗
PubMed2004

Spatial analysis for exclusive interactions between subgroups I and II of Cucumber mosaic virus in cowpea.

The dynamics of virus interference in Cucumber mosaic virus (CMV) infection in cowpea were investigated by tissue-blotting and in situ hybridization. Using co-inoculation assays, we discovered that spatial competition between CMV-LE (subgroup I) and CMV-m2 (subgroup II) occurred in the inoculated leaves. Interestingly, competitive interactions between the two viruses also could be observed in the non-inoculated upper leaf tissues of the plants. Furthermore, the pattern of exclusive distribution was observed between challenge and protecting viruses in the serially inoculated leaves. Taken together, it is suggested that the dynamics of competitive interactions between the two subgroups could be characterized by exclusive infection and multiplication of the individual viruses in cowpea plants.

Cucumovirus↗
PubMed1984

Properties of defective interfering particles of Sindbis virus generated in vertebrate and mosquito cells.

Defective interfering (DI) particles of Sindbis virus were generated during serial, undiluted passage of a cloned virus stock in both chick embryo fibroblast (CEF) cells and Aedes albopictus mosquito cells. DI particle-containing stocks were identified by their ability to interfere with standard virus replication and to synthesize small DI RNA species in the cell type in which they were generated. DI RNA species generated during serial passage in CEF cells were able to replicate in both vertebrate and A. albopictus cells. Some of the DI RNA species generated during serial passage in A. albopictus cells replicated efficiently in both cell types while others, sometimes present in the same DI particle stock, failed to replicate in cells of vertebrate origin. These results suggest that evolution of DI RNA species during serial passage of Sindbis virus in mosquito cells may result in the loss or alteration of nucleotide sequences required for RNA synthesis in vertebrate cells.

Aedes↗
PubMed2003

Inhibition of HIV-1 replication in primary human T cells transduced with an intracellular anti-HIV-1 p17 antibody gene.

BACKGROUND: Previously we reported that human CD4(+) T cell lines stably expressing anti-HIV-1 gag p17 scFv/Ckappa in the cytosol or nucleus were resistant to HIV-1 challenge. Inhibition of HIV-1 by anti-HIV-1 gag p17 scFv/Ckappa occurred at both the pre- and post-integration steps of the viral cycle. To simulate more closely the in vivo infection process, in this study we tested anti-HIV-1 activity of anti-HIV-1 gag p17 scFv/Ckappa in primary human T cells. METHODS: Anti-HIV-1 gag p17 scFv/Ckappa gene that is targeted into cytoplasm was inserted into a MMLV vector and transfected into packaging cell line PT67. The recombinant virus was used to transduce primary human T cells and human CD4(+) T cell line Jurkat. Following transduction, transduction efficiency, transgene expression, and cell phenotypes were studied. Transduced cells were then challenged with 100 TCID(50) of HIV-1 IIIB and primary isolate 5AO12. Following challenge, HIV-1 replication was monitored by p24 production. RESULTS: Both transduced Jurkat and primary human T cells expressed the transgene. The expression of the transgene did not alter cell growth and CD4 or CD8 expression. However, HIV-1 replication in scFv/Ckappa-transduced Jurkat cells was inhibited by nearly 90% as compared with vector controls. More importantly, HIV-1 replication in primary human T cells from multiple donors transduced with the anti-HIV-1 gag p17 scFv/Ckappa gene was inhibited by as much as 99% as compared with primary T cells transduced with the vector control. The inhibition of replication was not due to interference in viral entry or reverse transcription. The less that HIV-1 replicated in different donor cells, the higher the degree of protection. CONCLUSIONS: The expression of the anti-HIV-1 gag p17 scFv/Ckappa gene construct in primary human T cells renders these cells resistant to HIV-1 and points to the potential clinical usefulness of this gene construct for anti-HIV-1 gene therapy.

Animals↗
PubMed1982

Demonstration of interference between dengue virus types in cultured mosquito cells using monoclonal antibody probes.

Cultured Aedes albopictus cells (clone C6/36), persistently infected (PI) with dengue virus type 1 (dengue-1) were found resistant to superinfection with dengue virus type 3 (dengue-3). This was determined by indirect immunofluorescent (IF) staining of cultures using monoclonal antibody against a dengue-3 type-specific antigen. Dengue-1 PI cultures stained with this antibody 3 days after superinfection with dengue-3 virus (m.o.i of 2) had dengue-3 antigen in 0.1 to 1.0% of the cells. Control cultures infected with dengue-3 at the same multiplicity contained dengue-3 antigen in greater than 90% of the cells. The resistance to superinfection was not interferon-mediated, and occurred within 20 h after primary infection. In cultures simultaneously infected with two dengue virus types, one virus type was excluded from replication in most cells. A small population of cells was also found (about 1%) that contained type-specific antigen of both dengue virus types.

Adsorption↗
PubMed1994

CD4 is a critical component of the receptor for human herpesvirus 7: interference with human immunodeficiency virus.

In this study, we demonstrate that the glycoprotein CD4, a member of the immunoglobulin superfamily, is a critical component of the receptor for human herpesvirus 7 (HHV-7), a recently discovered T-lymphotropic human herpesvirus. A selective and progressive downregulation of the surface membrane expression of CD4 was observed in human CD4+ T cells in the course of HHV-7 infection. Various murine monoclonal antibodies to CD4 and the recombinant soluble form of human CD4 caused a dose-dependent inhibition of HHV-7 infection in primary CD4+ T lymphocytes. Moreover, radiolabeled HHV-7 specifically bound to cervical carcinoma cells (HeLa) expressing human CD4. A marked carcinoma cells (HeLa) expressing human CD4. A marked reciprocal interference was observed between HHV-7 and human immunodeficiency virus (HIV), the retrovirus that causes the acquired immunodeficiency syndrome and also uses CD4 as a receptor. Previous exposure of CD4+ T cells to HHV-7 dramatically interfered with infection by both primary and in vitro-passaged HIV-1 isolates. Reciprocally, persistent infection with HIV-1 or treatment with the soluble form of gp120, the CD4-binding envelope glycoprotein of HIV-1, rendered CD4+ T cells resistant to HHV-7 infection. These data indicate that CD4 is critically involved in the receptor mechanism for HHV-7. The antagonistic effect between HHV-7 and HIV could be exploited to devise therapeutic approaches to AIDS.

Binding, Competitive↗
PubMed1985

The repeated regions of Semliki Forest virus defective-inferfering RNA interferes with the encapsidation process of the standard virus.

Two different defective interfering RNAs of Semliki Forest virus have been cloned and sequenced previously. These molecules have repeated sequence blocks between unique terminal regions. The late gene region of SV40 virus has been replaced with the repeating unit detected in both defective-inferfering (DI) RNAs, and by complementation with a tsA mutant of SV40 a mixed stock of recombinant and helper virus was obtained. Upon infection of monkey kidney cells the recombinant expressed the repeated part of the DI RNA (svDI301 RNA). Superinfection of these cells with standard Semliki Forest virus showed that (i) the synthesis of SFV genomic RNA is marginally if at all affected by the svDI301 RNA, (ii) the svDI301 RNA is not replicated by SFV-RNA-dependent RNA polymerase, and (iii) packaging efficiency of the standard SFV genome RNA into virions is clearly decreased in the presence of svDI301 RNA. These results suggest that the terminal regions of the DI RNA molecule are required for efficient replication while the central repeated elements are involved in encapsidation.

Animals↗
PubMed2004

Endogenous betaretroviruses of sheep: teaching new lessons in retroviral interference and adaptation.

The endogenous betaretroviruses of small ruminants offer an excellent model to investigate the biological relevance of endogenous retroviruses (ERVs). Approximately twenty copies of endogenous betaretroviruses (enJSRVs) are present in the genome of sheep and goats. enJSRVs are highly related to Jaagsiekte sheep retrovirus (JSRV) and the Enzootic nasal tumour virus (ENTV), the causative agents of naturally occurring carcinomas of the respiratory tract of sheep. enJSRVs interact/interfere at different levels both with the host and with their exogenous and pathogenic counterparts. enJSRVs blocks the exogenous JSRV replication by a novel two-step interference mechanism acting both early and late during the virus replication cycle. enJSRVs are highly active, they are abundantly and specifically expressed in the epithelium of most of the ovine female reproductive tract. The specific spatial and temporal expression of enJSRVs supports a role in trophoblast development and differentiation as well as conceptus implantation. In addition, enJSRVs are expressed during fetal ontogeny leading to the apparent tolerance of sheep towards the pathogenic JSRV. Thus, the sheep/enJSRVs system is a model that can be utilized to study many different aspects of ERVs and retrovirus biology. The impressive technologies developed to study the sheep reproductive biology, in conjunction with the knowledge gained on the molecular biology of enJSRVs, makes the ovine system an ideal model to design experiments that can functionally address the role of ERVs in mammalian physiology.

Adaptation, Physiological↗
PubMed1976

Long-term persistent vesicular stomatitis virus and rabies virus infection of cells in vitro.

BHK 21 carrier cells persistently infected with VSV Indiana for over 2 years have been shedding generally very low levels of mature infectious virus or mature T particles (averaging less than one-hundredth p.f.u./cell/day) yet most cells are producing virus antigens and are resistant to homologous superinfection. However, large amounts of biologically active T particle RNP can be recovered from cytoplasmic extracts of these carrier cells even at times when they are shedding no detectable infectious virus. This recovered cytoplasmic RNP replicates (with helper B virions) to produce mature T particles, interferes strongly after DEAE dextran-facilitated uptake and, together with B virions, allows the establishment of a persistent carrier state in exposed cells. No 'provirus' DNA copies of the VSV RNA genome are detectable (less than 1/40 copy/cell or I copy per 40 cells) in carrier cells after more than 2 years of persistent infection, and all transfection attempts have failed using DNA from these VSV carriers or DNA from carrier cells persistently infected with some other negative strand RNA viruses (measles, mumps, LCM, influenza, rabies). Infectious viruses shed after more than I year from carrier cells originally infected with wild-type B virions are small plaque mutants showing a slight temperature sensitivity. Cured cell populations can be obtained from the long term VSV carrier culture by cloning in the presence or absence of antiviral antibody.

Animals↗
PubMed1977

Investigations of reasons for the avirulence of the A7 strain of Semliki Forest virus in adult mice.

A strain of Semliki Forest virus (A7) which is avirulent in adult mice killed baby mice in a similar manner to strain V13 which was also virulent for adult mice. In the muscle and brains of baby mice A7 and V13 replicated and produced haemagglutinating activity similarly. Our previous suggestion that defective interfering particles were present in the brains of A7-infected adult mice appears not to be so. The interference formerly detected was due to an inhibitor present in brain tissue of adult and baby mice both normal and infected. Homogenates of A7-infected adult brain produced normal RNA species in BHK cells and not those characteristic of defective interfering particles. Organ culture experiments indicated that avirulence of A7 was not due to lack of release of virus from infected adult brain cells. Also, A7 as well as V13 was detected and was probably replicating in all parts of the brain and spinal cord that were sectioned and examined. Evidence is presented that suggests that the reason for the avirulence of A7 for adult mice compared with its virulence for baby mice may relate to a lower ability to replicate in brain tissue per se rather than to interaction with host defence mechanisms.

Age Factors↗
PubMed1993

trans-dominant interference with virus infection at two different stages by a mutant envelope protein of Friend murine leukemia virus.

A dominant negative mutant Friend murine leukemia virus (FMLV) env gene was cloned from an immunoselected Friend erythroleukemia cell. The mutant env had a point mutation which resulted in a Cys-to-Arg substitution at the 361st amino acid in the FMLV envelope protein (Env). The mutant Env was retained in the endoplasmic reticulum (ER) and accumulated because of its slow degradation. The NIH 3T3 cells expressing the mutant env were resistant to ecotropic Moloney MLV (MoMLV) penetration, suggesting that the mutant Env traps the ecotropic MLV receptors in the ER. When the mutant env gene was transfected into and expressed in the cells persistently infected with MoMLV, the wild-type Env was trapped in the ER, and the MoMLV production was suppressed. Thus, the mutant Env accumulating in the ER trans-dominantly and efficiently interfered with the ecotropic MLV infection at both the early and the late stages.

3T3 Cells↗
PubMed1978

OK 10 virus, an avian retrovirus resembling the acute leukaemia viruses.

The OK 10 virus complex was isolated from a liver tumour of a chicken which, as an embryo, had been inoculated intravenously with a field isolate of an avian leukosis virus. The OK 10 virus complex contains at least two viruses: the interference assay and serum neutralization test indicate that the helper virus belongs to subgroup A. One of the viruses, OK 10 V, induces distinct foci in chick embryo cells under agar overlay and cells from the foci form colonies in soft agar. These properties allow in vitro assay of the virus. Injection of virus or infected cells into chicks induces acute leukaemia but no local tumours. Another virus, OK 10 AV (associated virus), comprises about 99% of the OK 10 complex. The virus does not induce foci in chick embryo cells. In chickens it causes leukosis 17 months after injection. Electron micrographs of OK 10 virus stocks show typical C type virus particles. These particles have a density of 1.16 g/ml and contain 70S RNA which, after heat denaturation, releases type b RNA subunits. The OK 10 virus complex apparently represents a strain of acute leukaemia viruses.

Alpharetrovirus↗
PubMed1998

Interference with Physalis mottle tymovirus replication and coat protein synthesis by transcripts corresponding to the 3'-terminal region of the genomic RNA--role of the pseudoknot structure.

The role of the 3' noncoding (NC) region of Physalis mottle tymovirus genomic RNA in the multiplication of the virus was examined using an in vivo protoplast assay system. Coat protein (CP) synthesis was specifically inhibited by sense 3' NC region transcripts. To establish the role of the pseudoknot structure present in the NC region in virus multiplication, four site-specific mutants, two of which disrupted the pseudoknot structure while the other two restored the structure, were constructed. Interestingly, none of the four sense mutant transcripts inhibited CP synthesis, suggesting that the specific sequence representing the 3' terminal pseudoknot structure may play an important role in virus multiplication. However, the wild-type antisense 3' NC transcript as well as the four antisense mutant transcripts inhibited CP synthesis, suggesting that the inhibitions by antisense transcripts could be due to the formation of RNA-RNA hybrids at the 3' end of the genomic RNA.

Capsid↗
PubMed1976

Temperature-sensitive mutants of vesicular stomatitis virus are conditionally defective particles that interfere with and are rescued by wild-type virus.

Temperature-sensitive (ts) mutants of vesicular stomatitis virus belonging to complementation groups I, II and IV inhibited the replication of wild-type vesicular stomatitis virus when mixed infections were carried out in BHK21 cells at 32, 37, and 39.5 C. The group IV mutant (ts G 41) was most effective in this regard; wild-type virus yields were inhibited almost 1,000-fold in mixed infections with this mutant at 32 C. In the case of group I and II mutants, inhibition of wild-type virus replication at 37 and 39.5 C was accompanied by an enhancement (up to 15,000-fold) of the yields of the coinfecting ts mutant. The yields of the group IV mutant (ts G 41) were not enhanced by mixed infections with wild-type virus at any temperature, although this mutant inhibited wild-type virus replication at all temperatures. The dominance of the replication of ts mutants at 37 C provides a rationale for the selection and maintenance of ts virus in persistently infected cells.

Cell Line↗
PubMed2001

Identification of two sequences in the cytoplasmic tail of the human immunodeficiency virus type 1 envelope glycoprotein that inhibit cell surface expression.

During synthesis and export of protein, the majority of the human immunodeficiency virus type 1 (HIV-1) Env glycoprotein gp160 is retained in the endoplasmic reticulum (ER) and subsequently ubiquitinated and degraded by proteasomes. Only a small fraction of gp160 appears to be correctly folded and processed and is transported to the cell surface, which makes it difficult to identify negative sequence elements regulating steady-state surface expression of Env at the post-ER level. Moreover, poorly localized mRNA retention sequences inhibiting the nucleocytoplasmic transport of viral transcripts interfere with the identification of these sequence elements. Using two heterologous systems with CD4 or immunoglobulin extracellular/transmembrane domains in combination with the gp160 cytoplasmic domain, we were able to identify two membrane-distal, neighboring motifs, is1 (amino acids 750 to 763) and is2 (amino acids 764 to 785), which inhibited surface expression and induced Golgi localization of the chimeric proteins. To prove that these two elements act similarly in the homologous context of the Env glycoprotein, we generated a synthetic gp160 gene with synonymous codons, the transcripts of which are not retained within the nucleus. In accordance with the results in heterologous systems, an internal deletion of both elements considerably increased surface expression of gp160.

Amino Acid Sequence↗
PubMed1976

[New lambdoid phages of Escherichia coli. II. Comparison of several genetic characteristics with lambda phages].

Functions of some newly isolated lambdoid phages and phage lambda genes were compared by their ability to interact with unrelated phages and the product of the bacterial gene gro P. 19 of 23 lambdoid phages studied interfere with prophage P2, that points out the presence of functionally active genes, essential for spi+ phenotype in their genomes. The development of 4 lambdoid phages with spi- phenotype is independent on the prophage P2 presence. Most of lambdoid phages show the reduced growth ability on the C600 groP- bacterial lawn. This indicates that they have a function similar to the gene P of phage lambda. The development of phage phi M417 in bacterial mutants groP- is not disturbed, which indicates that the gene P of phage phi M417 is different from that of the phage lambda. Newly isolated phages, that are homoimmune to phage lambda, restrict the development of T4 rII phage. The rest lambdoid phages have no rex function. The growth efficiency of lampodid phages on E. coli C cells, carrying Eco R1 plasmid, varies from 10(-6) to 10(-8) that presumbaly indicates on different amounts of restionci strites in DNA of these phages.

Coliphages↗
PubMed1986

A new class of retrovirus present in many murine leukemia systems.

A new class of MuLV has been detected and isolated from normal and leukemic AKR, C58, SJL, and NFS.AKV mice as well as from NFS mice inoculated with Friend or Moloney ecotropic viruses. These new viruses are XC negative and serologically cross-react with MCF env antigens but are ecotropic in host range, being able to only infect mouse cells to varying degrees and unable to infect mink or other cells infectable by MCF or xenotropic viruses. Viruses of this type from AKR mice cross-interfere with Moloney ecotropic and MCF viruses in SC-1 cells and appear to have properties similar to those of the SL3-2, GPA-V2, and R-XC- isolates. Analysis of their genomes by restriction endonuclease mapping of proviral DNA indicates structures similar to class II MCFs with the 5' half of the genome being like ecotropic viruses and the env region exhibiting restriction sites characteristic of MCF viruses. In normal AKR mice, these ecotropic recombinant-like viruses are found in spleen and bone marrow as early as 1 week of age, but first appear in the thymus at 3-4 months of age. These viruses have not been detected in mice with no or low expression of ecotropic viruses (NFS, NZB, DBA/2, BALB/c, C57BL/6). Because of their apparent recombinant structure and ecotropic host range we have provisionally designated them ecotropic recombinant virus (ERV) to distinguish them from the MCF class of recombinant MuLV.

Animals↗