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PubMed1980

Inhibition of AKR leukemogenesis by SMX-1, a dualtropic murine leukemia virus.

Intrathymic injection of SMX-1, a dualtropic murine leukemia virus (MuLV) originally derived from Moloney murine leukemia virus stocks, protects AKR mice from developing MuLV-accelerated leukemia and spontaneous leukemia. Thymuses of SMX-1-injected mice show no change in weight, morphology, or thymocyte size, and quantitative expression of Thy-1 and Lyt-2 differentiation antigens is identical to control mice. The amplified thymic expression of MuLV-related antigens that occurs spontaneously in 6-month-old preleukemic AKR mice or that can be induced in young AKR mice by leukemogenic AKR dualtropic MuLV is prevented by SMX-1. It appears unlikely that the protective effect of SMX-1 is explicable in terms of cross-immunogenicity with transforming MuLV or transformed cells. As SMX-1 persists for long periods after intrathymic injection and does not alter levels of thymic ecotropic MuLV, SMX-1 may interfere with the generation, spread, or leukemogenicity of dualtropic MuLV that form de novo in AKR thymus during the late preleukemic phase. SMX-1 provides a way to probe the events leading to cell transformation in AKR mice.

AKR murine leukemia virus↗
PubMed1980

Interferon induction by viruses. Sindbis virus: defective-interfering particles temperature-sensitive for interferon induction.

A defective-interfering (DI) particle of Sindbis virus was generated from a ts mutant of RNA-complementation group A by serially undiluted passages at 30 degrees C. This mutant induced interferon at a permissive temperature (30 degrees C), but not at a non-permissive temperature (40.5 degrees C); it also expressed homotypic interference throughout the range 30 to 40.5 degrees C. This demonstrates for the first time in a DI particle a ts function, namely, the ability to induce interferon. In addition, our data provide further evidence that the RNA genome of a Sindbis DI particle can be translated within the cell. We postulate that the products of translation function to produce the putative inducer of interferon, namely a molecule of dsRNA.

Defective Viruses↗
PubMed1974

Baboon virus isolate M-7 with properties similar to feline virus RD-114.

A virus (M-7) isolated from baboon placental tissue demonstrates many similarities to endogenous feline virus RD-114. Immunodiffusion analysis shows a group-specific antigen (gs-1) line of identity between M-7 and RD-114. Anti-RD-114 DNA polymerase IgG inhibits M-7 polymerase by 57% compared to 97% for RD-114. M-7 virus has helper activity as demonstrated by rescue of murine sarcoma virus (MSV) from sarcoma-positive leukemia-negative human amnion cells. The host range of the rescued M-7 pseudotype of MSV, MSV (M-7), is similar to that of RD-114 virus. MSV (M-7) is also able to transform baboon cells and causes no detectable transformation of feline cells without addition of helper feline leukemia virus. Interference properties of M-7 and RD-114 virus are identical. Virus-specific neutralizing antisera, although partially cross-reacting, can distinguish MSV (M-7) from MSV (RD-114). These similarities and differences between RD-114 and M-7 viruses are best explained as type-specific differences between two viruses within the same strain.

Amnion↗
PubMed1999

[Virus interaction in HBV and HCV super infection].

OBJECTIVE: To investigate virus interaction in HBV and HCV superinfection. METHODS: The changes of serum markers of 30 patients with HBV and HCV superinfetion were observed. Meanwhile, mutation of HBV precore region at nt 1,896 and the amount of TNF alpha and IL-6 in sera were also investigated. RESULTS: Compared with HBV or HCV single infection, positive rates of HBeAg, HBV DNA and HCV RNA in superinfectim were lower, positive rates of anti-HBe was higher, the average titers of HBsAg, anti-HBcIgG and anti-HCV were significantly lower, too. In some patients, HBsAg were seronegatively convested. Occurrence rate of HBV precore region mutation at nt1896 and levels of TNF alpha and IL-6 in sera were higher in super infection than those in single infection. CONCLUSION: Interference existed between HBV and HCV superinfection, conversion from HBeAg to anti-HBe was not only due to the suppression by HCV but also to the mutation of HBV precore region, and HCV may be a reason causing HBV precore region mutation through increasing the pressure of the body's immunosystem.

Adult↗
PubMedDate not supplied

Human polymicrobial infections.

CONTEXT: Polymicrobial diseases, caused by combinations of viruses, bacteria, fungi, and parasites, are being recognised with increasing frequency. In these infections, the presence of one micro-organism generates a niche for other pathogenic micro-organisms to colonise, one micro-organism predisposes the host to colonisation by other micro-organisms, or two or more non-pathogenic micro-organisms together cause disease. STARTING POINT: Recently, Gili Regev-Yochay (JAMA 2004; 292: 716-20) and Debby Bogaert (Lancet 2004; 363: 1871-72), and their colleagues, suggested another interaction: microbial interference-the ability of Streptococcus pneumoniae carriage to protect against Staphylococcus aureus carriage, and the inverse effect of pneumococcal conjugate vaccination on the increased carriage of Staph aureus and Staph-aureus-related disease. Strep pneumoniae carriage protected against Staph aureus carriage, and the bacterial interference could be disrupted by vaccinating children with pneumococcal conjugate vaccines that reduced nasopharyngeal carriage of vaccine-type Strep pneumoniae. WHERE NEXT: The medical community is recognising the significance of polymicrobial diseases and the major types of microbial community interactions associated with human health and disease. Many traditional therapies are just starting to take into account the polymicrobial cause of diseases and the repercussions of treatment and prevention.

Antibiosis↗
PubMed1983

The process of virus assembly in insect virus mixed infections.

Interference occurred upon infection of the cabbage moth caterpillars (Mamestra brassicae L.) with a mixture of nuclear polyhedrosis virus (NPV) and cytoplasmic polyhedrosis virus (CPV), resulting in the impairment of virus assembly, and formation of abnormal nucleocapsids. At the same time protein supercapsids were produced normally, but contained no infectious virions. When insects were infected with related viruses, the virions developed as usual, but the protein supercapsids revealed abnormal forms.

Animals↗
PubMed1982

Chronic production of defective-interfering particles by hamster embryo cultures of herpesvirus persistently infected and oncogenically transformed cells.

Highly passaged defective-interfering (DI) particle preparations of equine herpesvirus type 1 (EHV-1) were found to mediate the co-establishment of persistent infection and oncogenic transformation of permissive hamster embryo cells. Four cell lines, designated DI-1 to DI-4, were shown to possess biological properties typical of transformed cells and to induce the rapid formation of metastatic fibrosarcomas when injected into syngeneic LSH hamsters. Corresponding DI tumour cell lines, designated DI-1T to DI-4T, were found to be virus non-producing, to be transplantable in the hamster, and, like the four parent DI cell lines, to express EHV-1-coded antigens and to be resistant to superinfection with EHV-1 but not with a heterologous virus, vesicular stomatitis virus. All transformed cell lines, but not the tumour cell lines, contained a population of cells (2.6 to 9%) that continued to release infectious virus after 100 passages in culture. The production of interferon and selection of temperature-sensitive mutants did not appear to play a role in the maintenance of persistent infection. However, it was demonstrated that these persistently infected cells continued to release not only infectious virus but also DI particles after more than 2 years in culture. DI particles were shown to be present in released virus by: (i) detection of the defective virus DNA species (density 1.724 g/ml; standard EHV-1, density 1.716 g/ml) by CsCl analytical ultracentrifugation techniques; (ii) measurement of interference activity of virus released from DI-1 to DI-4 cells against standard EHV-1 replication; (iii) the presence of the 35 megadalton Bg/II fragment unique to the DI particle genome in DNA of released virus. These studies indicate that herpesvirus DI particles may function both in the initiation and maintenance of persistent infection and alter the cytocidal effects of infection to allow the establishment of oncogenic transformation and persistent infection.

Animals↗
PubMed1971

Production of hemadsorption-negative areas by serums containing Australia antigen.

Exposure of human Wi-38 cells to human serums containing Australia antigen, and presumably serum hepatitis virus, renders the cells refractory to infection by Newcastle disease virus as detected by the hemadsorption-negative plaque test for intrinsic interference. Induction of the Newcastle disease virus refractory state could be passed in cell culture with up to a 1 : 100,000 dilution of material obtained from cells "infected" with serums containing Australia antigen after filtration (0.45-microm pores) and heating to 60 degrees C for 1 hour. Human antiserums to the Australia antigen prevented induction of the Newcastle disease virus refractory state.

Culture Techniques↗
PubMed1995

HIV-1 down-regulates CD4 costimulation of TCR/CD3-directed tyrosine phosphorylation through CD4/p56lck dissociation.

One consequence of HIV type 1 (HIV-1) infection is the gradual loss of responsiveness of T lymphocytes to Ags both in vitro and in vivo. It has been suggested that the underlying mechanism that contributes to this T cell dysfunction before CD4+ cell decline involves down-regulation of surface receptors, alterations in intracellular redox status, interference by viral Ags, and later in infection, the absence or alteration of specific cytokine production. In this report, we demonstrate that infection of the T-lymphocytic cell line H9 with the LAI isolate of HIV-1 results in profoundly altered regulation of CD4-induced costimulation of TCR/CD3-directed signaling. TCR/CD3-induced tyrosine phosphorylation of the intracellular enzyme phospholipase-C gamma 1 and the surface receptor/substrates CD5 and CD6 was unaffected by virus infection, whereas augmented responses normally observed after the co-ligation of CD4 with TCR/CD3 on T lymphocytes were absent in HIV-1-infected H9 cells. Costimulation of TCR/CD3-induced signaling via MHC class II molecules was also down-regulated in virally infected cells. TCR/CD3 and HLA-DR receptor expression remained intact in infected cultures for at least 3 wk, whereas CD4 surface expression was gradually lost but maintained for up to 1 wk, suggesting that the absence of costimulation early in infection was not surface receptor density-dependent. In HIV-1-infected cells, CD4 was not physically linked with its associated tyrosine kinase p56lck, whereas normal levels of p56lck were readily recovered from the cellular cytoplasm. Similar observations were noted in cultures of H9 cells infected with a field isolate of HIV-1 obtained from cultured PBMC from an infected donor. HIV-1 infection of T lymphocytes thus down-regulates potentially critical early signal transduction events by a mechanism that appears to involve interference of CD4 receptor association with p56lck. A potential outcome of these biochemical effects may include the limited responsiveness of infected T cells to antigenic stimulation observed during HIV-1 infection.

CD4 Antigens↗
PubMed1993

The E1 replication protein of bovine papillomavirus type 1 contains an extended nuclear localization signal that includes a p34cdc2 phosphorylation site.

Bovine papillomavirus (BPV) DNA replication occurs in the nucleus of infected cells. Most enzymatic activities are carried out by host cell proteins, with the viral E1 and E2 proteins required for the assembly of an initiation complex at the replication origin. In latently infected cells, viral DNA replication occurs in synchrony with the host cell chromosomes, maintaining a constant average copy number of BPV genomes per infected cell. By analyzing a series of mutants of the amino-terminal region of the E1 protein, we have identified the signal for transport of this protein to the cell nucleus. The E1 nuclear transport motif is highly conserved in the animal and human papillomaviruses and is encoded in a similar region in the related E1 genes. The signal is extended relative to the simple nuclear localization signals and contains two short amino acid sequences which contribute to nuclear transport, located between amino acids 85 and 108 of the BPV-1 E1 protein. Mutations in either basic region reduce nuclear transport of E1 protein and interfere with viral DNA replication. Mutations in both sequences simultaneously prevent any observable accumulation of the protein and reduce replication in transient assays to barely detectable levels. Surprisingly, these mutations had no effect on the ability of viral genomes to morphologically transform cells, although the plasmid DNA in the transformed cells was maintained at a very low copy number. Between these two basic amino acid blocks in the nuclear transport signal, at threonine 102, is a putative site for phosphorylation by the cell cycle regulated kinase p34cdc2. Utilizing an E1 protein purified from either a baculovirus vector system or Escherichia coli, we have shown that the E1 protein is a substrate for this kinase. An E1 gene mutant at threonine 102 encodes for a protein which is no longer a substrate for the p34cdc2 kinase. Mutation of this threonine to isoleucine had no observable effect on either nuclear localization of E1 or DNA replication of the intact viral genome.

Amino Acid Sequence↗
PubMed1973

Infectivity and RNA patterns as functions of high- and low-dilution passage of murine sarcoma-leukemia virus: evidence for autointerference within an oncornavirus population.

Heterogeneity of buoyant density and RNA content of virions of Moloney murine leukemia-sarcoma complex [MSV (MLV)] was the result of passage at low dilution. Heterogeneous stocks revealed two major RNA components in the population, with the smaller component, apparent mol wt 4 x 10(6) to 5 x 10(6), becoming predominant upon serial passage at low dilution. Concomitantly, infectivity titers of both MLV and MSV decreased upon serial passage at low dilution. MSV (MLV) passaged at high dilution retained high titers and a rather homogeneous high-molecular-weight RNA population characteristic of high-buoyant-density virions. Interference of both MLV and MSV replication was demonstrated by employing mixed inocula containing both low- and high-dilution passage stocks of MSV (MLV). In contrast to results with MSV (MLV), MLV freed of MSV by limit dilution did not show heterogeneity of buoyant density or of RNA when propagated at low dilution.

Animals↗
PubMed2005

Use of different but overlapping determinants in a retrovirus receptor accounts for non-reciprocal interference between xenotropic and polytropic murine leukemia viruses.

BACKGROUND: Retrovirus infection depends on binding of the retroviral envelope (Env) protein to specific cell-surface protein receptors. Interference, or superinfection resistance, is a frequent consequence of retroviral infection, and occurs when newly-synthesized Env binds to receptor proteins resulting in a block to entry by retroviruses that use the same receptors. Three groups of viruses demonstrate a non-reciprocal pattern of interference (NRI), which requires the existence of both a common receptor utilized by all viruses within the group, and a specific receptor that is used by a subset of viruses. In the case of amphotropic and 10A1 murine leukemia viruses (MLV), the common and specific receptors are the products of two related genes. In the case of avian sarcoma and leukosis virus types B, D, and E, the two receptors are distinct protein products of a single gene. NRI also occurs between xenotropic and polytropic MLV. The common receptor, Xpr1, has been identified, but a specific receptor has yet to be described. RESULTS: Using chimeric receptor proteins and interference studies, we have identified a region of Xpr1 that is uniquely utilized by xenotropic MLV and show that this receptor domain is required for non-reciprocal interference. CONCLUSION: We propose a novel pattern of receptor usage by xenotropic and polytropic MLV to explain the NRI observed between these viruses. We propose that the specific and common receptor determinants for xenotropic and polytropic viruses are simultaneously present in discreet domains of a single Xpr1 protein.

Animals↗
PubMed1976

Infection of resistant avian cells by subgroup B Rous sarcoma virus.

Chicken fibroblasts derived from the H & N flock, which have been characterized as resistant to subgroup B avian oncornaviruses in focus assays, can be infected in suspension shortly after trypsinization by subgroup B sarcoma and leukosis viruses. Once cells are plated, resistance to infection reappears rapidly. C/BE cell suspensions obtained by treatment with EDTA instead of trypsin are not as sensitive to infection. Late interference established by preinfection with subgroup B leukosis viruses is not overcome by trypsinization. In addition to C/BE H & N chicken cells, C/ABE RPRL line 7 cells can also be infected by subgroup B viruses shortly after trypsinization; however, none of the cell types can be made sensitive to subgroup E infection. These results are discussed in relation to current information on the genetic control of resistance to avian oncornaviruses.

Animals↗
PubMedDate not supplied

[Heterogeneity of an influenza virus population in the manifestation of biological functions (author's transl)].

In a population of influenza virus, virions have different degree of the functional capacities to produce infectious virus, to induce neuraminidase production and to interfere with infectious virus. Fractions of virus were found which had a poor capacity for production of infectious progeny and a relatively high induction of neuraminidase synthesis as well as induction of heterogenous light fractions of RNA in cells. In the population of defective virus a fraction of particles possessing marked interfering activity in the absence of infectivity was found.

Animals↗
PubMed1995

[Gene therapy for hereditary and acquired human diseases].

Cystic Fibrosis (CF) and AIDS are primary candidate disorders to be treated by gene therapy, owing to their lethality and the absence of efficient clinical treatments. Treatment of CF by gene therapy will require the transfer of the functional CFTR cDNA into the diseased human airway epithelia since mutations within the CFTR gene are responsible for CF. We have therefore cloned the human CFTR cDNA and developed a recombinant E1-deleted adenoviral vector carrying a CFTR expression cassette. We demonstrated in vitro the ability of this vector to efficiently transduce human lung cells isolated from CF patients and to correct their phenotype. Efficient in, vivo delivery of the CFTR cDNA to the airways of cotton rats and rhesus monkeys was also obtained and no dissemination of the recombinant viral vector in other tissues than the airways was observed. We have therefore designed a phase I clinical trial involving CF patients. In contrast to the monogenic CF disease, the mechanisms of AIDS pathogenesis still remain poorly understood. Such limited knowledge of the disease constitutes a serious restriction to the development of a rational gene therapy strategy for AIDS. Since HIV, the causative agent of AIDS, predominantly infects cells of the hematopoietic system, pluri- or multipotent stem cells may constitute potential targets for the introduction of a foreign anti-HIV gene that will inhibit HIV replication and/or spread. Reimplantation of the genetically modified stem cells into asymptomatic HIV-infected patients should theoretically allow the repopulation of the host's immune system with mature CD4+ cells expressing novel molecules that interfere with viral replication, thus slowing the progression of AIDS. We identified several new transdominant inhibitors derived from the viral TAT and REV proteins and showed their ability to confer to human CD4 lymphocytes resistance against HIV1 infection. Retroviral vectors carrying these potential therapeutic genes have been developed and are currently being tested in vivo in newly developed transgenic animal models, in humanized SCID mice and in macaques.

Acquired Immunodeficiency Syndrome↗
PubMed1997

Inhibition of MHC class I antigen presentation by viral proteins.

An essential part of the immune response to viral infections is the recognition and elimination of infected cells by cytotoxic T lymphocytes. For this purpose a display mechanism has evolved which is present in almost all nucleated cells: the major histocompatibility complex class I antigen processing pathway. Both self and foreign antigens are degraded in the cytosol to peptides which are translocated into the endoplasmic reticulum where they are loaded onto MHC class I molecules. Pathogens living inside the cell are evolving under the constant selection pressure of such immune surveillance. As a result such infectious organisms have developed a variety of strategies to prevent their antigens from being presented. Since our understanding of the cell biology of antigen presentation has greatly advanced in recent years, it has now become possible to unravel several of the molecular mechanisms by which viruses interfere with MHC class I antigen presentation. Examples for the interference of viral molecules with components of the MHC class I pathway are presented in this review.

Animals↗
PubMed1992

Reticuloendotheliosis type C and primate type D oncoretroviruses are members of the same receptor interference group.

The reticuloendotheliosis viruses (REVs), originally isolated from avian species, constitute a group of retroviruses which are more closely related to mammalian retroviruses than to other avian retroviruses. The envelope glycoproteins of members of the REV group display a striking amino acid sequence identity with a group of primate oncoretroviruses which belong to a single receptor interference group and include all of the type D and some type C primate oncoretroviruses. Members of the REV group also have a broad host range which covers most avian cells and some mammalian cells, including those of simian and human origin. In view of this broad host range and the envelope sequence similarities, we investigated the cross-interference pattern between REV and primate virus groups to determine whether they utilized the same receptor. Superinfection experiments using a vector virus containing an Escherichia coli lacZ gene showed that reticuloendotheliosis and simian oncoretroviruses constitute a single receptor interference group on both human and canine cells and indicate that the viruses bind to the same receptor to initiate infection. These results suggest that this receptor binding specificity has been maintained over a wide range of retroviruses and may be responsible for the broad spread of these retroviruses between different orders of vertebrates.

Amino Acid Sequence↗
PubMed1974

Studies on live rubella vaccine. V. Quantitative aspects of interference between rubella, measles and mumps viruses in their trivalent vaccine.

Rubella vaccine combined with measles and mumps vaccines was administered in a single injection to children of 1 to 5 years of age. All three vaccines were serologically effective, and the clinical reactions caused by measles vaccine were considerably alleviated, when 6 x 10(3) PFU of rubella and 10(4) TCD50 per dose of mumps vaccines were combined with 5 x 10(4) TCD50 of measles vaccine. When a larger amount of mumps vaccine (3 x 10(5) TCD50/dose) was used, it caused interference with the rubella and measles viruses, i.e., the antibody response to rubella virus became poor and the incidence of clinical reactions to measles virus decreased. On the other hand, when 5 x 10(5) TCD50/dose of measles vaccine was combined with 10(4) TCD50/dose of mumps vaccine, the clinical reactions to measles virus were decreased but were almost the same as those induced by this vaccine alone.

Child, Preschool↗