Detection of complement-dependent lytic antibodies in sera from bovine leukemia virus-infected animals by the 51Cr-release assay [proceedings].
5
Citation
0
Reference
10
Related Paper
Citation Trend
Keywords:
Lytic cycle
Bovine leukemia virus
Complement
Cite
A-type and B-type Epstein-Barr virus differ in their ability to spontaneously enter the lytic cycle.
In this study replication of A-type and B-type Epstein-Barr virus (EBV) strains has been assessed. A-type and B-type type lymphoblastoid cell lines (LCLs) were established by infecting B lymphocytes, isolated from five EBV-seropositive donors, with different A-type and B-type virus isolates. The presence of viral capsid antigens (VCA) in these LCLs was determined by immunofluoresence assay and by immunoblotting. All of the B-type EBV strains were capable of spontaneously generating virus regardless of the origin of the donor cells. In contrast the A-type strains, other than strain IARC-BL36, did not readily produce VCA in any of the different donor lymphocytes used. This study demonstrates another biological difference between the two virus types: their ability to spontaneously enter the lytic cycle.
Lytic cycle
Strain (injury)
Cite
Citations (32)
A monoclonal competitive radioimmunoassay (CompRIAm) which detects antibody to herpesvirus simiae (B virus) in monkey and human sera and antibody to SA8 virus in monkey sera but not antibody to herpes simplex virus in human sera is described. Of 232 serum samples from wild-caught cynomolgus monkeys, 117 serum samples were positive when tested by CompRIAm. The results were in close agreement (97.5%) with B virus neutralizing antibody results on the same sera. Sera from 97 wild-caught rhesus monkeys and 92 wild-caught baboons were also tested. The CompRIAm was able to differentiate between sera that had neutralizing antibody to B virus and SA8 virus and those that did not, although the discrimination was not as clear as that in the tests on cynomolgus monkey sera. Sequential sera from two humans with confirmed cases of B virus infection were tested by CompRIAm. B virus antibody was detected in sera from both humans. None of 237 other serum samples from blood donors and patients attending sexually transmitted disease clinics reacted in the CompRIAm.
Cite
Citations (22)
Viruses are obligate intracellular parasites, relying to a major extent on the host cell for replication. An active replication of the viral genome results in a lytic infection characterized by the release of new progeny virus particles, often upon the lysis of the host cell. Another mode of virus infection is the latent phase, where the virus is 'quiescent' (a state in which the virus is not replicating). A combination of these stages, where virus replication involves stages of both silent and productive infection without rapidly killing or even producing excessive damage to the host cells, falls under the umbrella of a persistent infection. Reactivation is the process by which a latent virus switches to a lytic phase of replication. Reactivation may be provoked by a combination of external and/or internal cellular stimuli. Understanding this mechanism is essential in developing future therapeutic agents against viral infection and subsequent disease. This article examines the published literature and current knowledge regarding the viral and cellular proteins that may play a role in viral reactivation. The focus of the article is on those viruses known to cause latent infections, which include herpes simplex virus, varicella zoster virus, Epstein-Barr virus, human cytomegalovirus, human herpesvirus 6, human herpesvirus 7, Kaposi's sarcoma-associated herpesvirus, JC virus, BK virus, parvovirus and adenovirus.
Cite
Citations (125)
A new strain of simian haemorrhagic fever (SHF) virus was isolated from chronically infected patas monkey no. 248 (P-248) in USU-104 cells. The P-248 isolate had the same size, morphology and cytoplasmic site of replication as the prototype LVR strain. However, the P-248 isolate caused a persistent infection without noticeable cytopathology in USU-104 cells rather than the strongly lytic infection produced by prototype LVR virus. The capacity of P-248 virus to produce a persistent, non-lytic infection of USU-104 cells was a very stable characteristic of the isolate. Extensive serial passage of this isolate through USU-104 cells (over 50 passages) and rhesus monkeys (six passages) failed to unmask virus with lytic properties for USU-104 cells. Culture medium from persistently infected cultures assayed in rhesus monkey peritoneal mononuclear phagocytes, where measurable cytopathology occurs, was found to contain about 10(5) to 10(6) TCID50/ml of cell-free P-248 virus. Immunolabelling techniques showed only a low percentage of infected cells in persistently infected cultures. The mechanism of persistence of the P-248 isolate in USU-104 cells has not been determined but evidence suggests it does not involve interferon or defective interfering particles.
Simian
Cite
Citations (15)
Bovine leukemia virus
Cite
Citations (22)
SUMMARY Monoclonal antibodies prepared against Tacaribe and Junin viruses have been used to define further the serological relationships between arenaviruses of the Tacaribe complex. A close relationship was found between these two viruses and the heterologous Amapari and Machupo viruses, with Pichinde virus and Parana virus being more distantly related. Among the antibodies specific for Tacaribe virus, five were found to react with viral antigens at the surface of infected cells and to neutralize virus infectivity in vitro. These five antibodies could be differentiated by competitive immunoassay as recognizing at least two antigenically distinct epitopes. The kinetics of reaction between antibody and virus were examined for all five neutralizing antibodies. One antibody (2.25.4) effectively neutralized all infectious virus. The remaining four directed against a second epitope gave significant persistent fractions which could be reduced by addition of complement, anti-mouse immunoglobulin, or antibody 2.25.4. Variants of Tacaribe virus resistant to neutralization by antibody 2.25.4 were obtained by growth in the presence of this antibody and neutralization kinetics were reexamined using the heterologous monoclonal neutralizing antibodies. Several different neutralization profiles were obtained, suggesting that point mutations resulted in conformational changes at topographically selected distinct epitopes recognized by the remaining antibodies.
Cite
Citations (34)
More than 200 cells were cloned from populations of mammalian cells persistently infected with Japanese encephalitis virus. Only four cloned cultures contained cells that had viral antigen measurable by immunofluorescence and that released infectious virus, yet all clones harbored virus-specific RNA. Superinfection of cloned cells with wild-type Japanese encephalitis virus did not produce cytopathic effects, but resulted in production of viral antigen and infectious virus in formerly nonproducing clones. Cocultivation of nonproducer clone cells with normally permissive cells did not induce virus production, nor did treatment of nonproducer clones with various inhibitors of DNA, RNA, or protein synthesis. It is suggested that the cloning procedure may have selected for a particular subpopulation of cells and that defective virus is also involved in establishment and maintenance of persistent infection.
clone (Java method)
Viral transformation
Superinfection
Viral Interference
Helper virus
Permissiveness
Cite
Citations (17)
Four cynomolgus monkeys (Macaca fascicularis) were inoculated in the lips and tongues with B virus. Virus shedding and antibody responses were monitored for up to 50 days postinfection. Virus was isolated from the oral cavities of all monkeys at 6 days postinfection despite the absence of observable lesions. Virus was not isolated from genital swabs or serum. Antibodies to both B virus and herpes simplex virus were detected by neutralization between days 8 and 12. Virus-specific IgM and IgG antibodies were measured by antibody capture radioimmunoassay. IgM was first detected on day 6; by contrast, IgG did not appear until day 12. Antibodies reactive in a competitive radioimmunoassay appeared by day 12 and peaked at 30 to 40 days postinfection. This study provides data on which to base the diagnosis of primary B virus infection in cynomolgus monkeys.
Viral Shedding
Cite
Citations (25)
A search was made in LCM virus-immune mice for virus-specific antibodies. With the help of an L-cell plaque assay, neutralizing antibody was readily detected. There were no essential differences between mouse strains, but marked differences existed between virus strains. Whereas the inoculation of either large or small doses of WE strain virus led to the early production of considerable concentrations of neutralizing antibody, in the case of E-350 strain virus, high doses were required and a much longer time interval had to elapse before the threshold of detection was attained. In addition to neutralizing antibody, LCM virus-infected mice produced sensitizing antibody (detected by the enhancing effect of an anti-mouse Ig antiserum on the ability of a serum to reduce virus infectivity) and complement-fixing antibody. Previous failures to detect neutralizing antibody in LCM virus-immune mice might have been caused by properties of the chosen virus, but in many instances lack of a suitable assay host is a more likely explanation.
Arenavirus
Cite
Citations (22)