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PubMed1992

Spleen necrosis virus, an avian immunosuppressive retrovirus, shares a receptor with the type D simian retroviruses.

The reticuloendotheliosis viruses (REV) are a family of highly related retroviruses isolated from gallinaceous birds. On the basis of sequence comparison and overall genome organization, these viruses are more similar to the mammalian type C retroviruses than to the avian sarcoma/leukemia viruses. The envelope of a member of the REV family, spleen necrosis virus (SNV), is about 50% identical in amino acid sequence to the envelope of the type D simian retroviruses. Although SNV does not productively infect primate or murine cells, the receptor for SNV is present on a variety of human and murine cells. Moreover, interference assays show that the receptor for SNV is the same as the receptor for the type D simian retroviruses. We propose that adaptation of a mammalian type C virus to an avian host provided the REV progenitor.

Amino Acid Sequence↗
PubMed2004

High-resolution structure of a retroviral capsid hexameric amino-terminal domain.

Retroviruses are the aetiological agents of a range of human diseases including AIDS and T-cell leukaemias. They follow complex life cycles, which are still only partly understood at the molecular level. Maturation of newly formed retroviral particles is an essential step in production of infectious virions, and requires proteolytic cleavage of Gag polyproteins in the immature particle to form the matrix, capsid and nucleocapsid proteins present in the mature virion. Capsid proteins associate to form a dense viral core that may be spherical, cylindrical or conical depending on the genus of the virus. Nonetheless, these assemblies all appear to be composed of a lattice formed from hexagonal rings, each containing six capsid monomers. Here, we describe the X-ray structure of an individual hexagonal assembly from N-tropic murine leukaemia virus (N-MLV). The interface between capsid monomers is generally polar, consistent with weak interactions within the hexamer. Similar architectures are probably crucial for the regulation of capsid assembly and disassembly in all retroviruses. Together, these observations provide new insights into retroviral uncoating and how cellular restriction factors may interfere with viral replication.

Amino Acid Sequence↗
PubMed1992

Herpesviruses--immune escape artists?

Viral persistence depends on the successful avoidance of the host's immunologic surveillance system. This review, which focuses specifically on the herpesviruses, delineates several possible strategies for evading or delaying the immune response. One strategy common to all herpesviruses is the establishment of latency, a state in which the virus may be partially or even completely hidden from the immune system. Other proposed mechanisms of immune evasion include interaction of the virus with components of the humoral immune system, virus-induced modulation of cell-surface recognition structures, and virally mediated interference in antigen processing. Additional strategies include molecular mimicry and the ability of one particular herpesvirus to encode an immunosuppressive cytokine. Although a detailed understanding of the molecular mechanisms of herpesvirus-mediated immune evasion is currently lacking, future studies should identify those critical interactions between host and virus that may prove amenable to therapeutic intervention.

Animals↗
PubMed1977

The role of defective interfering particles in persistent infection of Vero cells by measles virus.

Persistent infections by measles virus were rapidly established in the majority of Vero cells when monolayers were infected with virus stocks that had been passed three to five times from an undiluted inoculum. These virus stocks had low infectivity titres but normal haemagglutinin titres and were able to cause interference. The ability of such virus stocks to establish persistent infections seems to be due to the presence of defective interfering particles rather than of virus mutants. Measles virus released from a persistently infected Vero cell line at the 93rd passage had properties similar to the undiluted passage virus that generated persistent infections.

Animals↗
PubMed1998

A defective interference-like phenomenon of human hepatitis B virus in chronic carriers.

Defective interfering (DI) particles have been found in many RNA and DNA viruses of bacteria, plants, and animals since their first discovery in influenza virus. However, this fundamental phenomenon has not been demonstrated in human natural infections. Using a new approach, here we provide the first experimental evidence for the existence of DI-like viruses in human chronic carriers of hepatitis B virus (HBV). Functional characterization of naturally occurring core internal deletion (CID) variants of HBV revealed all of the features of DI particles. When equal amounts of wild-type and CID variant DNAs were cotransfected into a human hepatoma cell line, Huh7, a three- to fivefold enrichment of CID variants was most often observed. The fluctuations of the virus populations between CID variants and helper HBV in three chronic carriers are reminiscent of the cycling phenomenon in other DI viral systems. This finding has important implications for chronic viral hepatitis and other chronic progressive viral diseases.

Amino Acid Sequence↗
PubMed1970

Focus formation by a murine sarcoma leukemia virus complex. II. Quantitative aspects of the interaction between radiation leukemia virus and its murine sarcoma virus pseudotype in strain C57BL mouse embryo cells.

A quantitative study has been made of the interactions between radiation leukemia virus (RadLV), its murine sarcoma virus pseudotype, and their C57BL host cells. The elimination of interference phenomena by delayed infection of cells with RadLV made possible the quantitative determination of the pseudotype in terms of defective sarcoma and endogenous RadLV particles. This in turn permitted the quantitative assessment of RadLV helper activity and of the various factors which influence the accuracy and sensitivity of the helper assay.

Animals↗
PubMed1998

Interaction of virulent and attenuated tick-borne encephalitis virus strains in ticks and a tick cell line.

An interference between a thermosensitive (ts) mutant and the wild-type (wt) of tick-borne encephalitis (TBE) virus in Ixodes ricinus L. and Rhipicephalus appendiculatus (Neumann) ticks is reported. I. ricinus females were dually infected by a parenteral inoculation of ts and wt strains at 10-day interval. Interference was demonstrated by the lowered ability of wt virus to replicate in ticks previously infected by ts virus. The wt virus was demonstrated in only 30% of the ticks; the average virus titre was lowered by 2.1 log10 compared with the control group, which was infected with the wt virus only. The oral infection of R. appendiculatus ticks with the same viruses also revealed an interference with the growth of the superinfecting wt virus. While in the control group all the ticks became infected, in the dually infected group the wt virus was found in only 50% of the ticks. However, when the ticks were infected orally with ts virus and superinfected parenterally with the wt virus, no interference was observed. In a R. appendiculatus-derived cell line persistently infected with the ts virus (100% of the cells), a partial inhibition of the growth of the superinfecting wt virus was observed. The ts virus retained its thermosensitive phenotype throughout the persistent infection of both the ticks and the tick cell line.

Animals↗
PubMed1996

Inhibition of viral replication by genetically engineered mutants of the duck hepatitis B virus core protein.

The hepatitis B virus (HBV) nucleocapsid consists of 240 viral core proteins that are arranged in a highly symmetrical structure, HBV replication can only take place inside intact nucleocapsids. In the present study, we investigated whether genetically engineered core mutants can inhibit viral replication by interfering with the formation of intact nucleocapsids. Using the duck hepatitis B virus (DHBV) model, a series of core protein mutants was generated. Polymerase chain reaction-amplified fragments from the bacterial lacZ gene expressing up to 282 amino acids were added either to the amino- or carboxy-terminus of the DHBV core protein. In addition, carboxy-terminal extensions were generated by fusing the DHBV core protein with the DHBV small surface protein or various fragments of the viral polymerase. Finally, the green fluorescent protein (GFP) was fused in-frame to the carboxy-terminus of the DHBV core protein. In this chimeric protein, GFP is still functional and can act as a reporter molecule. The various core protein mutants were tested for their potential antiviral activity by cotransfection with a replication-competent DHBV construct into the avian hepatoma cell line LMH. Carboxy-terminal, but not amino-terminal, DHBV core mutants inhibited DHBV replication by up to 90% at an effector-to-target ratio of 1:10, thus displaying a dominant negative phenotype. Antiviral activity was species-specific and caused by posttranslational interference with viral replication. The DHBV core-GFP fusion protein should be an ideal tool to assess the antiviral potential of dominant negative core proteins in vivo.

Amino Acid Sequence↗
PubMed2005

Retroviral superinfection resistance.

The retroviral phenomenon of superinfection resistance (SIR) defines an interference mechanism that is established after primary infection, preventing the infected cell from being superinfected by a similar type of virus. This review describes our present understanding of the underlying mechanisms of SIR established by three characteristic retroviruses: Murine Leukaemia Virus (MuLV), Foamy Virus (FV), and Human Immunodeficiency Virus (HIV). In addition, SIR is discussed with respect to HIV superinfection of humans. MuLV resistant mice exhibit two genetic resistance traits related to SIR. The cellular Fv4 gene expresses an Env related protein that establishes resistance against MuLV infection. Another mouse gene (Fv1) mediates MuLV resistance by expression of a sequence that is distantly related to Gag and that blocks the viral infection after the reverse transcription step. FVs induce two distinct mechanisms of superinfection resistance. First, expression of the Env protein results in SIR, probably by occupancy of the cellular receptors for FV entry. Second, an increase in the concentration of the viral Bet (Between-env-and-LTR-1-and-2) protein reduces proviral FV gene expression by inhibition of the transcriptional activator protein Tas (Transactivator of spumaviruses). In contrast to SIR in FV and MuLV infection, the underlying mechanism of SIR in HIV-infected cells is poorly understood. CD4 receptor down-modulation, a major characteristic of HIV-infected cells, has been proposed to be the main mechanism of SIR against HIV, but data have been contradictory. Several recent studies report the occurrence of HIV superinfection in humans; an event associated with the generation of recombinant HIV strains and possibly with increased disease progression. The role of SIR in protecting patients from HIV superinfection has not been studied so far. The phenomenon of SIR may also be important in the protection of primates that are vaccinated with live attenuated simian immunodeficiency virus (SIV) against pathogenic SIV variants. As primate models of SIV infection closely resemble HIV infection, a better knowledge of SIR-induced mechanisms could contribute to the development of an HIV vaccine or other antiviral strategies.

Animals↗
PubMed2005

PEG conjugation moderately protects adeno-associated viral vectors against antibody neutralization.

AAV gene therapy vectors have significant clinical promise, but serum neutralization poses a challenge that must be overcome. We have examined the potential of conjugating the AAV surface with activated polyethylene glycol chains to protect the vector from neutralizing antibodies. Two key parameters were investigated: the polymer chain size and the PEG:lysine conjugation ratio. Transduction data revealed that the vector is fully infectious until a critical PEG conjugation reaction ratio was exceeded, and this critical level was found to vary with polymer chain size. At this key conjugation ratio, however, particles were moderately protected from serum neutralization, 2.3-fold over unmodified vector, demonstrating that there is a small window of PEGylation for which particles are still fully infective and benefit from antibody protection. TEM results and structural analysis indicate that the drop of infectivity as the PEG concentration is increased beyond the critical conjugation ratio may be due to a combination of steric interference with viral regions necessary for infection as well as reaction at important lysine residues. However, this first study analyzing the potential of PEG to protect AAV from serum neutralization shows that the approach has promise, which can be further enhanced if the locations of PEG attachment can be more finely controlled.

Antibodies↗
PubMed1990

Improvement in potency assay of measles-mumps-rubella trivalent vaccine: interference between components and measures for its elimination.

In the potency assay of trivalent measles-mumps-rubella (MMR) vaccine by the immunocytochemical focus assay reported previously (Fukuda et al., 1987), development of rubella foci in RK13 cells was inhibited in the presence of a large excess of mumps component, resulting in an underestimation of the titre of the rubella component. When RK13 cells are infected with the mixture of mumps and rubella viruses, mumps virus interfered with the growth of rubella virus. Interference was mediated most likely by interferon induced by mumps virus. The interference was eliminated by a partial neutralization of mumps component by the addition of anti-mumps serum to the inoculum to RK13 cells. Improved method of potency assay of MMR vaccine incorporating the above measures and other modifications are described.

Animals↗
PubMed1988

Deoxycytidine kinase is constitutively expressed in human lymphocytes: consequences for compartmentation effects, unscheduled DNA synthesis, and viral replication in resting cells.

Deoxycytidine kinase specific activity was high in human peripheral lymphocytes and increased less than 2-fold when the lymphocytes were stimulated by phytohemagglutinin A. Ion-exchange chromatography showed the same profile of deoxycytidine kinase activity in resting and proliferating cells. This enzyme could also efficiently phosphorylate deoxyadenosine and deoxyguanosine. In contrast, the thymidine kinase activity was very low in resting peripheral lymphocytes and increased more than 40-fold upon stimulation. Similar relative changes in the activities of the two enzymes were observed in human T-lymphoblast cells (CCRF-CEM) separated by centrifugal elutriation into cells of different cell cycle phases. The ratio of deoxycytidine to thymidine kinase activities is 20:1 in extracts from resting human lymphocytes and 1:2 in PHA-stimulated cells. This drastic change in deoxyribonucleoside phosphorylating activities during the cell cycle in human lymphocytes is of importance for studies on unscheduled DNA synthesis, for the design of therapies to interfere with viral DNA metabolism, and for a correct interpretation of the compartmentation effects observed in DNA precursor metabolism.

Cell Compartmentation↗
PubMed1984

Three different serotypes of human rotavirus determined using an interference test with coxsackievirus B 1.

MA104 cells were used to titrate human rotavirus, and its capacity to render the cells resistant to coxsackievirus B 1 infection enabled us to determine easily the infectious titer of three prototype human rotaviruses. When rabbit antisera prepared against these prototype viruses were used for the neutralization test, the viruses could be discriminated from each other by a specific neutralization test.

Enterovirus B, Human↗
PubMedDate not supplied

[Interference associated with cell cultures chronical by infected with the Junin virus].

Supernatants from Vero cells persistently infected with Junin virus interfered with cytolitic and lethal activities of standard virus. Two Vero cell sublines, chronically infected with Junin virus named VRJ1 and VRJ3, were obtained after prolonged cultivation of cells which survived primary infection. VFJ1 was maintained over a period of 48 days, by biweekly serial transfers while VRJ3, similarly treated, was cultivated for 385 days. One of the characteristics of these cell lines was resistance against superinfection with homologous virus that ordinaily produced CPE and plaques in normal Vero cells; the cells were then considered chronically infected. Supernatants taken at different cell passage level were tested for its interference activity after centrifugation to eliminate floating cells and debris. The degree of CPE intensity caused by inoculation of Vero cells with 10(4), 10(5) or 10(6) TCID 50 of standard virus was markdely deppressed (Figure 1) by coinfection with supernatant from passage 3 of VRJ3 (VRJ1p1), VRJ1p1 supernatant also had interference activity as shown by coinfection with standard virus and expressed by plaque forming inhibition(Table 1). The plaque production of standard virus was inhibited by coinfection with VRJ1p1 supernatant which did not originate plaques when inoculated alone. The interference capacity of VRJ1p6 supernatant was reduced (Table 1) coincidentally with the formation of 55 PFU/ml. Interference activity was neutralized by Junin specific antiserum and inhibited by chloroform treatment. When Vero cells infected with VRJ1p6 supernatant were challenged with standard virus 72 hs later, an inhibition of 98% was achieved (Table 2) in contrast with value of 35% showed in Table 1.

Animals↗
PubMed1976

Naturally occurring murine leukemia viruses in wild mice: characterization of a new "amphotropic" class.

A new class of murine leukemia viruses, isolated from wild Mus musculus trapped in California, is described. These viruses, designated "amphotropic," replicate in mouse, rabbit, mink, human, guinea pig, and rat cells, but not in hamster, quail, or duck cells. They show N-tropism for mouse cells, and do not trigger the XC cell response. They are distinct by interference and virus neutralization testing from the previously recognized mouse-tropic and xenotropic MuLV classes. Mouse-tropic viruses occuring along with three of the four amphotropic isolates were found to be distinguishable by virus neutralization from other mouse-tropic murine leukemia virus strains of laboratory mouse origin.

Animals↗
PubMed1977

Persistent infection of BHK21/WI-2 cells with rubella virus and characterization of rubella variants.

Persistently infected cell lines of BHK21/WI-2 cells have been established by infection with the wild type rubella virus strain M-33. These cell lines, BHK-MP1 and BHK-MP2, showed immunity-like resistance to superinfection with M-33 virus at both 34 degrees and 39.5 degrees C. They also showed intrinsic interference with the replication of Newcastle Disease Virus at 34 degrees C but not at 39.5 degrees C. They released a small number of infectious virus particles which were temperature sensitive variants, being able to form plaques at 34 degrees C, but not at 39.5 degrees C on BHK21/WI-2 and on its derivative, BSR. When BHK-MP1 cells were cultured at 34 degrees C in growth medium containing 10--20 microgram/ml of 5-bromodeoxyuridine (BudR) there was a 5- to 10-fold increase in infectious virus in the medium as compared with the untreated controls. Mitomycin C (0.5 microgram/ml) treatment for 7 hours likewise stimulated the release of virus from these cells. The enhancement of viral release by BudR was completely blocked by pretreatment with actinomycin D (5 microgram/ml) for 3 hours prior to BudR treatment. Since the variant can be induced by these prophage inducers and inhibited by actinomycin D it is suggested that the viral genome is converted to a DNA provirus which is analogous to the lysogenic state of bacteriophage.

Animals↗
PubMed2002

Retroviral interference on STAT activation in individuals coinfected with human T cell leukemia virus type 2 and HIV-1.

Human T cell leukemia virus (HTLV) type-2 is a human retrovirus whose infection has not been tightly linked to human diseases. However, the fairly high prevalence of this infection among HIV-1-positive individuals indicates the importance of better understanding the potential interference of HTLV-2 infection on HIV-1 infection and AIDS. We previously demonstrated that one signature of PBMC freshly derived from HIV-1-infected individuals is the constitutive activation of a C-terminal truncated STAT5 (STAT5Delta). Therefore, we analyzed the potential activation of STATs in HTLV-2 monoinfected and HTLV-2/HIV-1 dually infected individuals. We observed that PBMC of HTLV-2-infected individuals do not show STAT activation unless they are cultivated ex vivo, in the absence of any mitogenic stimuli, for at least 8 h. The emergence of STAT activation, namely of STAT1, in culture was mostly related to the secretion of IFN-gamma. Of note, this phenomenon is not only a characteristic feature of HTLV-2-infected individuals but also occurred with PBMC of HIV-1(+) individuals. Surprisingly, HTLV-2/HIV-1 coinfection resulted in low/absent STAT activation in vivo that paralleled a diminished secretion of IFN-gamma after ex vivo cultivation. Our findings indicate that both HTLV-2 and HIV-1 infection prime T lymphocytes for STAT1 activation, but they also highlight an interference exerted by HTLV-2 on HIV-1-induced STAT1 activation. Although the nature of such a phenomenon is unclear at the present, these findings support the hypothesis that HTLV-2 may interfere with HIV-1 infection at multiple levels.

CD4-Positive T-Lymphocytes↗
PubMed1991

African cassava mosaic virus DI DNA interferes with the replication of both genomic components.

Natural infections of the geminivirus African cassava mosaic virus (ACMV) are known to be associated with low levels of defective interfering (DI) DNAs. Recently it has been demonstrated that extrachromosomal copies of the DI DNA, mobilized and amplified from an integrated DI DNA dimer, can ameliorate ACMV symptoms in transformed Nicotiana benthamiana, providing a possible means for the control of cassava mosaic disease. To further understand the molecular basis of the interference phenomenon, we have compared the ability of ACMV and tomato golden mosaic virus (TGMV) genomic components to replicate in leaf discs derived from DI DNA-transformed and control plants. Results indicate that the ACMV DI DNA interferes with the replication of both genomic components of ACMV to a similar extent. TGMV DNA A replicates to normal levels in transformed leaf discs and plants because it is unable to mobilize and amplify ACMV DI DNA. Differences in the relative levels of ACMV genomic components in transformed leaf discs and plants are discussed in terms of DNA replication and the availability of the genomic components for spread throughout the plant.

Blotting, Southern↗