The mechanism of interference between an avian leukosis virus and Rous sarcoma virus. II. Early steps of infection by RSV of cells under conditions of interference.
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By electron microscopy, particles of defective interfering Semliki Forest virus (DI SFV) had a mean diameter of 46.8 nm compared with 55.9 nm for standard virus particles, a decrease of 16%. The difference was confirmed by measurements of the two-dimensional projected areas of DI and standard virus particles. We examined nine different DI virus preparations produced by four to 13 undiluted passages in BHK cells and all were found to contain a majority of the smaller type of particle. Calculation of the absolute number of small particles showed that there were 130 particles per interfering unit measured by the inhibition of virus RNA synthesis. However, a more sensitive assay based on interference with virus protein synthesis gave a particle: interference ratio of 6.5.
Two modes of exclusion of T1 by lambda are distinguished. "Early" exclusion depends on gene N, but not on gene Q. It is at least partially ineffective against T1am23. "Late" exclusion depends on gene Q and effects T1am23 as well as T1+. Early exclusion is a direct effect of N gene product, rather than N gene being required for the expression of some other lambda gene. Three host mutations, groN, nusA, and nusB, known to interfere with lambda replication by affecting N gene expression, also interfere with the ability of lambda to exclude T1.
Aedes triseriatus orally infected with a temperature-sensitive mutant of La Crosse virus were, at predetermined times post-infection, orally challenged with wild type La Crosse or Tahyna virus. Most mosquitoes challenged with wild type La Crosse virus within 24 hr of ingestion of the temperature-sensitive virus became superinfected. In contrast, the majority of mosquitoes challenged at 72 hr were resistant to superinfection. Mosquitoes challenged at 7 days or thereafter were refractory to superinfection with La Crosse or Tahyna virus. The onset of interference was correlated with virus titer and antigen expression in midgut cells.
OBJECTIVE: To observe the effect of attenuated varicella-zoster virus (VZV) on replication of HBV in vitro and vivo. METHODS: The attenuated VZV were inoculated into the ducks infected with DHBV and into the cultural HepG(2) 2.2.15 cells, respectively. DHBV DNA, HBsAg and HBeAg were detected from the duck serum and cell cultural fluid by dot-blot hybridization and EIA. RESULTS: The decline of DHBV DNA in duck serum was found in two dosage groups. Compared with pre-treatment, the level of AD value in 200 pfu/kg group was significantly decreased from 1.17+/-0.29 to 0.59+/-0.45 (10 day after VZV treatment) and 0.21+/-0.21 (5 day after withdrawal of VZV)(t =3.51, 7.54, P<0.001). The level in 400 pfu/kg group was from 0.70+/-0.25 to 0.32+/-0.17 on the 5th day of withdrawal of VZV (t =3.58, P<0.01), respectively after treatment. The inhibitory rates of HBeAg and HBsAg were 61% and 33%, respectively. The effect on HBeAg seems to be more obvious than on HBsAg. CONCLUSIONS: Attenuated VZV could significantly decrease serum DHBV DNA in DHBV-infected ducks and directly inhibit the HBeAg and HBsAg secreted by 2.2.15 cells, suggesting that VZV seems to interfere or inhibit the replication of DHBV.
Newcastle disease virus (NDV) strains interfere in different degree with the growth of the velogenic NDV strain Texas GB (homologous interference) and Sindbis virus (heterologous interference) in chick embryo fibroblast cells. Homologous interference was elicited by interferon-producing live or UV-inactivated strains and non-interferon-producing live or beta-propiolactone-inactivated strains and it was not influenced by actinomycin D. Thus, interferon had apparently no role in homologous interference of NDV. The growth of Sindbis virus was, however, much more inhibited by interferon-producing live or UV-inactivated NDV strains than with non-inducing ones and the interference was reversible by actinomycin D. Thus heterologous interference is apparently mediated by interferon. In chicken cells infected with the mesogenic NDV strain H, virus yields were 50 to 100 times lower at multiplicities of infection above 0.1 p.f.u./cell than below it. The interferon formed during infection played no role in auto-interference, but may well be held responsible for the mild cytopathic effect observed.
We have previously shown that mice simultaneously infected with the murine mammary tumor virus (MuMTV) and with certain slow murine leukemia viruses (MLV) have an increased resistance to the pathological effects of both agents. Here we report that milk-transmitted MuMTV also delays the development of the acute erythroleukemia induced by Friend leukemia virus (FLV), and retards, or prevents in some cases, the development of long-term lymphomas caused by its helper component. This is confirmed by the observation that the average life span of MuMTV-carrying mice infected with FLV or its helper component is prolonged by over 30% as compared to that of MuMTV-free animals infected with the same agents and by the finding that the replication of Friend viruses is reduced in mice neonatally exposed to MuMTV. Since the antibody responses of mice to MuMTV and to FLV were not cross-reactive, we searched for antiviral activity in the tissues of mice exposed to MuMTV, FLV, or the helper component of FLV. Low levels of interferon-alpha/beta were consistently detected in spleen extracts from mice infected with all these agents but could not be demonstrated in the spleens of uninfected BALB/c mice; thus, the chronic production of endogenous interferon is likely to play a major role in the reciprocal interference in vivo between retroviruses belonging to different genera.
Injection of a dual tropic virus (DTV) isolated from a T cell lymphoma AKR/J mice into the thymus of 14 day old AKR/J puppies accelerates lymphoma development; 90-100% of the injected mice develop the disease within 120 days. In contrast a cell free centrifuge CFC-666 prepared B cell lymphoma of AKR/J origin injected into the thymus of 14 day old AKR/J mice failed to accelerate T cell lymphomagenesis and actually prevented the spontaneous T cell lymphoma development. However, 50% of the treated mice developed B cell lymphoma with a latency of 417 + 18 days. DTV injection induces amplification of thymic expression of MuLV related antigens, besides changes in thymus subpopulation. Such changes emerge spontaneously in 5-6 month preleukemic AKR/J mice (at the time of spontaneous DTV formation in the thymus). These changes in the thymus were not observed following CFC-666 injection. We assume therefore that CFC-666 interferes with spontaneous DTV formation that contributes to T cell lymphomagenesis.
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