Host Restriction of Friend Leukemia Virus. Role of the Viral Outer Coat (mice/fv-1 locus/vesicular stomatitis virus)
|
|
- Arthur Gaines
- 5 years ago
- Views:
Transcription
1 Proc. Nat. Acad. Sci. USA Vol. 70, No. 9, pp , September 1973 Host Restriction of Friend Leukemia Virus. Role of the Viral Outer Coat (mice/fv-1 locus/vesicular stomatitis virus) THEODORE G. KRONTIRIS, RUY SOEIRO, AND BERNARD N. FIELDS Albert Einstein College of Medicine, Departments of Cell Biology and Medicine, Bronx, New York Communicated by Harry Eagle, June 8, 1973 ABSTRACT Host restriction of oncogenesis of RNA tumor viruses in vivo is associated with several gene loci. One of these genes, the Fv-1 locus in mice, is expressed in vitro and may be studied in mouse-embryo cultures that are restrictive or permissive for replication of Friend leukemia virus. Two strains of Friend leukemia virus, N- or B-tropic, show reciprocal ability to replicate successfully in either NIH Swiss (N-type) or BALB/c (B-type) cells that differ at the Fv-1 locus. These two strains of virus and two cell lines form a system to measure host restriction in Vitro. Measurement of adsorption of Friend leukemia virus to permissive or restrictive cells reveals no difference in rate or total amount of virus bound. Furthermore, studies with virions of vesicular stomatitis virus phenotypically mixed within an envelope containing Friend leukemia virus protein show no differences in penetration or replication of vesicular stomatitis virus. These results strongly suggest that host restriction of Friend leukemia virus is due to an intracellular event in the viral replication cycle. The complexity of virus-host interactions in the ultimate production of leukemic disease is well illustrated by the genetic aspects of the host response to murine RNA tumor viruses. Although host response is a multigenic effect, one gene in particular, the Fv-1 locus in mice, determines susceptibility or resistance to exogenous Friend or other murine leukemia virus infections (1-4). In vivo, this gene determines the susceptibility of mice to Friend disease and, in vitro, controls the ability of Friend leukemia virus (FLV) to replicate successfully (2, 3, 5). This gene influences the cell-tocell spread of endogenous virus produced in response to chemical induction in mouse-embryo cells in culture (6, 7) and the spontaneous appearance of endogenous virus in mice (7, 8). An understanding, therefore, of the molecular basis for host restriction of this gene would be of major importance in the overall study of the relationship of host cell and viral genes in viral oncogenesis. Strains of murine leukemia virus exist, termed N- or B- tropic, defined by their ability to replicate successfully in either NIH Swiss (N-type) or BALB/c (B-type) strains of mice that differ at the Fv-1 locus (2-5). Certain strains (e.g., Rauscher and Moloney leukemia virus) replicate equally well in either cell type and are termed NB-tropic. Both N- and B-tropic strains of Friend virus exist as defined in vivo by Lilly and Steeves (10). In vitro, the reciprocal inability of the N-strain of FLV (N-FLV) to grow in BALB/c cells or of Abbreviations: N-FLV, N-tropic Friend leukemia virus; B-FLV, B-tropic FLV; MLV, murine leukemia virus; VSV, vesicular stomatitis virus; MOI, multiplicity of infection; S +L- sarcomapositive, leukemia-negative, PFU, plaque-forming units the B virus (B-FLV) to grow in NIH cells has been demonstrated (Krontiris et al., unpublished results), and forms the basis of a system in which host restriction may be studied in vitro. Studies of the antigenicity of these two virus strains suggest that they cannot be distinguished by immunological techniques (10). This finding has suggested that host restriction by nonpermissive cells is a consequence of an intracellular event. However, no direct evidence is available which would define the step in FLV replication at which restriction occurs. Experiments to be presented here attempt to define whether differences in adsorption and penetration of virus, steps of replication usually associated with the virus envelope, are involved in restriction of FLV by nonpermissive cells. Since the ratio of virus particle to plaque-forming units (PFU) for FLV is not known, a study of the binding of radiolabeled virus to host cell might measure mainly biologically inert material. Therefore, absorption of virus was studied by means of infectivity titer rather than binding of radiolabeled virions. Furthermore, in order to isolate effects of the virus coat in the study of penetration, we used vesicular stomatitis virus (VSV) virions phenotypically mixed within an envelope containing FLV protein. The results of these studies suggest strongly that host restriction of FLV is due to a limiting intracellular step in viral replication. MATERIALS AND METHODS Cells. Primary Swiss (N-type) and BALB/c (B-type) mouse-embryo cells were obtained from Microbiological Associates, Rockville, Md. The cells were used at the second or third passage for all experiments and maintained the in vitro characteristics of restriction described by Pincus et al. (7, 8). S+L- (sarcoma-positive, leukemia-negative) cells, kindly provided by Dr. Robert Bases, are Swiss 3T3 cells transformed with the Moloney strain of murine sarcoma virus as described by Bassin (11). All cell lines were maintained in Eagle's minimal essential medium supplemented with 10% fetal-calf serum (Grand Island Biologicals), iglutamine, and penicillin-streptomycin. Viruses. Friend leukemia virus strains F-S (N-tropic) and F-T (B-tropic) (10) were obtained as spleen extracts of infected mice from Dr. Frank Lilly. Each strain was passaged in susceptible mouse-embryo cell cultures. Infected cell supernatants were harvested and frozen at -85 to provide tissue-culture passage stocks of "N" and "B" virus which were then used for all subsequent experiments. VSV, Indiana serotype, was
2 2550 Microbiology: Krontiris et al. TABLE 1. Titration of FLV infectivity in S+L- cells Dilution Virus type N-FLV No. of plaques 37, 45 18, 6 4, 4 PFU per ml (X 1Q-6) 1.3 ± ±0 B-FLV No. of plaques 59, 51 17, 20 7, 6 PFU per ml (X 10-6) 1. 8 ± ± ±0. 1 Serial dilutions of N-FLV and B-FLV stocks were assayed in S+L- cells. Numbers of plaques from duplicate plates and the resultant calculated titers (PFU/ml) are presented for each dilution. Dilution is in logarithmic units. obtained from Dr. Donald Summers. A temperature-sensitive mutant of VSV (ts 45) was kindly supplied by Dr. C. R. Pringle (12, 13). Plaque Assays. Infectivity of FLV was titered both by the S+L- plaque assay (14) and the XC assay (15), with the appropriate N- or B-type mouse-embryo cells. Preliminary studies demonstrated that titers of N-FLV and B-FLV, as determined by the S+L- assay, were comparable to those obtained with the XC assay. This S+L- cell line originated from a Swiss 3T3 cell transformed by murine sarcoma virus. Although this line was originally B-tropic (Bassin, personal commaunication), our studies indicated no loss of infectivity titer of N-tropic FLV when assayed in this cell. Furthermore, the multiple-hit curve normally demonstrated by N-FLV when titered in BALB/c cultures (Hartley, J. W., Pincus, T. & Rowe, W. P., personal communication) was not seen in the S+L- assay. That is, the number of plaques of FLV decreases appropriately by 10-fold per 10-fold dilution of virus (Table 1). Moreover, titers of N- or B-FLV calculated from dilutions over a 10-fold range are constant. If host restriction occurred in these cells, the plaque number would decrease to a greater degree than predicted by the given dilution, that is, the calculated titer for each dilution would not be constant, but would decrease with virrus dilution (multiple-hit kinetics). Our findings indicate that in S+L- Swiss 3T3 cells, host restriction of N-FLV no longer occurs. VSV plaque assays were done in 60 X 15-mm tissue culture dishes (Falcon Plastics) seeded with 2 X 106 mouse-embryq or 2.5 X 106 HeLa or L cells. After 24 hr, plates were inoculated and overlayed with 1% agarose (Sargeant-Welch). For plaque enumeration, the plates were subsequently overlayed with neutral red agarose (1%) at 36 hr (370 incubation) or at hr (310 incubation) and examined for plaques 24 hr later, after which time there was no significant increase in plaque number. Adsorption of FLV to Mouse-Embryo Cells. Confluent monolayers of N- and B-type mouse-embryo cells in 60 X 15-mm dishes were inoculated with 0.3 ml of N-FLV or B-FLV in Eagle's medium at a multiplicity of infection (MOI) of The plates were agitated by tilting periodically at 370 and, at stated times, the entire inoculum volume was withdrawn and titrated on S+L- cells. All experiments were done with duplicate plates. As a control for nonspecific surface adsorption and heat inactivation, empty dishes were inoculated and the medium was titered. Isolation of PhenotypicaUy Mixed Virions of VSV. Both Swiss and BALB/c mouse-embryo cultures were inoculated, respectively, with N-FLV and B-FLV (MOI 2.0). After 6 days, when maximum FLV yields occur, such cultures were superinfected with a temperature-sensitive mutant of VSV (ts 45) at a MOI of 5-10 PFU per cell. Control uninfected mouse-embryo cultures were infected with VSV as a source of stock VSV. The VSV-superinfected cultures were incubated at 310 for a further 20 hr; the cells were suspended mechanically into their medium, and sonicated. The sonicate was clarified by centrifugation at 2000 X g for 10 min, and aliquots were frozen at Phenotypically mixed virions of VSV were selected from the mixed progeny of such an infection by heating a 1:10 dilution of virus sample at 450 for 1 hr. This treatment removes the coat from the ts mutant, producing viral cores, and decreases the titer of stock VSV (ts 45) by 4-5 logarithmic units (16). The demonstration of residual phenotypically mixed virions [VSV(FLV) ] was determined as described (17). Surface specificity of the phenotypically mixed virions was examined by virus neutralization and host range, by formation of plaques on HeLa, L, or FLV-infected mouse-embryo cells. Neutralization was done by mixing one volume of virus sample with one volume of a 1: 5 dilution of antibody against VSV prepared in mouse (hyperimmune ascitic fluid) (18). Where indicated, an additional 1 volume of antiserum against FLV prepared in mouse was added. (This antiserum, produced by infection of BALB/c mice with both N- and NBtropic FLV, was kindly provided by Dr. Frank Lilly.) Virus appropriately diluted with medium was a neutralization control. These mixtures were incubated overnight at 40. Plates were inoculated with suitable dilutions of virus, incubated 1 hr at 25, washed several times with complete medium, and overlayed with agar. TABLE 2. Proc. Nat. Acad. Sci. USA 70 (1973) Adsorption of FLV to N- or B-type cells Mouse- % Re- Virus embryo Min- Titer main- (inoculum) cell type utes (X 10-5) ing Exp. I. N-FLV N (5 X 105PFU) B B-FLV B (5 x 105PFU) N Exp. II. N-FLV No cells (2 X 105 PFU) Confluent monolayers of either N-type or B-type mouseembryo cells were inoculated in duplicate with 0.3 ml of either N-FLV or B-FLV at an MOI of Inocula were withdrawn at the times indicated and titered for infectivity on S+L- cells. Unadsorbed virus is expressed as the percent remaining virus relative to the amount recovered at 0 min.
3 Proc. Nat. Acad. Sci. USA 70 (1973) RESULTS Adsorption of FLV. Initial experiments were designed to determine whether significant differences existed between susceptible and resistant cells as to their ability to adsorb a given virus type. In each case, both the kinetics and final amount of virus adsorbed were studied. At all times, the ability to perform the experiment with two virus and two cell types served as an internal control. A series of confluent plates of BALB/c or Swiss mouseembryo cells were inoculated with either N-FLV or B-FLV. At intervals, the entire volume of medium was withdrawn and the virus remaining unadsorbed was titrated by means of the S+L- cell assay. Although initiation of replication of RNA tumor viruses is optimal during exponential cell growth and appears to require cellular DNA synthesis (19, 20), preliminary studies indicated that the rate of uptake of virus from the medium was not significantly influenced by the degree of confluence of the monolayer. The absolute amount of virus adsorbed increased only slightly for a defined viral inoculum as cell density increased from about half-confluent (7 X 105 cells per dish) to a fully-confluent (2 X 106 cells per dish) monolayer. Results of these studies are shown in Table 2. Virus recovered immediately on inoculation was designated as 100% unadsorbed; each subsequent figure is represented as the percent virus remaining in medium after each adsorption period. These results indicate clearly that virus of either N or B tropism adsorbs equally well to either resistant or susceptible cells. Furthermore, no significant differences can be observed in the rate of uptake. The maximal amount of adsorption has occurred within the first 15 min after inoculation of viruses onto either cell type. In this experiment, uptake of N-FLV was nearly complete by 15 min and represented 75-80% of the input virus. We can conclude that host restriction is not associated with failure to bind to the restrictive cell type. Cell Penetration of Phenotypically Mixed Virions of VSV. Experiments were designed to test the penetration of FLV Host Restriction of Friend Leukemia Virus 2551 into restrictive or permissive cells. Since virus at the cell surface may be neutralized by antiserum, penetration may be measured by protection of adsorbed virus from neutralization. The results, although consistent with equal rates of penetration, were difficult to reproduce, and we turned to other means to demonstrate this point. It has recently been reported (17) that superinfection of cells infected with either avian myeloblastosis or murine leukemia virus with VSV yields a small proportion of progeny VSV that could not be neutralized with VSV antiserum. This fraction of VSV possessed antibody neutralization, host range, and interference properties of the leukemia virus. Furthermore, the phenomenon appeared to be due to phenotypic mixing, for after a single passage of uninfected cells, all the progeny reverted to wild-type VSV. The percentage of phenotypically mixed VSV in the mixture of virus types produced by such an infection can be increased by the use of a VSV temperature-sensitive mutant (ts 45) (16). This mutant is thermolabile; unlike the wildtype virus, its titer of infectivity can be reduced by 4-5 logarithmic units by heating at 450 for 1 hr. Thermolability in ts 45 is a property of an abnormal VSV coat protein, and the thermal loss of infectivity is due to production of noninfectious viral cores. Superinfection with ts 45 of cells infected with murine leukemia virus (MLV) at the permissive temperature (310) results in progeny virus, the bulk of which is thermolabile. Most of the heat-resistant progeny are VSV cores phenotypically mixed within a MLV coat [VSV(MLV) ]. Since such a preparation of VSV may be essentially freed of particles with VSV-specific coat proteins by heat treatment, we reasoned that the resultant, essentially pure, VSV(MLV) could be used to examine the role of the FLV coat in host restriction. Preliminary studies showed that VSV replicated equally well on either N or B mouse-embryo cultures; therefore we postulated that VSV(FLV), once virus penetration had occurred, should be able to replicate normally. However, if the FLV envelope proteins were involved in the host-restriction mechanism, then a VSV virion whose envelope was TABLE 3. Characterization of wild-type and ts 45 VSV Virus grown Antiserum Exp. Virus in treatment Heat NME BME HeLa L N/NME I VSV NME (wild type) Anti-VSV Anti-FLV anti-flv II VSV NME (wild type) VSV NME (ts 45) III VSV NME (ts 45) Anti-VSV Anti-FLV VSV (wild type or ts 45) grown in mouse-embryo cells, was titered for infectivity in the cell lines indicated. Before inoculation, virus was treated with antiserum or heat or both. NME and BME, N- and B-type mouse-embryo cells, respectively. NINME, N-type mouseembryo cells infected with N-FLV.
4 2552 Microbiology: Krontiris et al. Proc. Nat. Acad. Sci. USA 70 (1973) TABLE 4. Phenotypically mixed virions of VSV Virus Antiserum Log titer in Virus grown in treatment Heat NME BME HeLa L N/NME VSV NME (ts 45) N-FLV anti-flv <2.0 <2.0 VSV BME (ts 45) B-FLV anti-flv N- or B-type mouse-embryo cells, infected, respectively, with N-FLV or B-FLV were superinfected with ts 45 VSV. The progeny of this double infection were characterized as to thermal stability, neutralization by antiserum, and host range as in Table 3. Results are expressed as logarithm of infectivity titer remaining on each cell type with or without antiserum or heat treatment. specified either by N- or B-type FLV might demonstrate reduced titers when assayed on the nonpermissive cell. In order to isolate phenotypically mixed virions of VSV [VSV(FLV)1, N- and B-type mouse-embryo cells, infected with N-FLV and B-FLV, respectively, were superinfected with ts 45 VSV. Analysis of progeny VSV produced in uninfected mouse-embryo cells is seen in Table 3. Stock VSV, wild type or ts 45, grown in N-type mouse-embryo cells when assayed directly on either N- or B-type mouse-embryo cells shows the same titer (Exps. I and II). When assayed on HeLa or L cells, the titer of ts 45 VSV was consistently 0.5 logarithmic units greater (Exp. II). No interference with VSV titer was observed when assayed on mouse-embryo cells infected with N-FLV. Heat treatment reduces the titer 5 logs, and demonstrates clearly the effect of the ts mutation. The same extent of neutralization with antiserum made against Indiana serotype VSV was observed on treatment of ts 45 VSV (Exps. I and III). An additional control of our antiserum reagents showed no neutralization of either wildtype or ts 45 VSV with FLV antiserum. These data show that no immunological differences could be observed between the neutralization antigen of wild-type and ts 45 VSV by this antiserum, and that no VSV neutralizing antibodies could be detected in FLV antiserum. VSV(FLV) should possess the following characteristics: (i) because of the FLV envelope, they should be neutralized by antiserum directed against FLV, (ii) they should demonstrate the host range of FLV, that is, they should show reduced efficiency of plating on either HeLa or L cells, and (iii) their replication in mouse-embryo cells previously infected with FLV should be inhibited due to viral interference (16, 17). The progeny of virus produced by superinfection of mouseembryo cells infected with N-FLV were tested for these traits (Table 4). Unheated virus forms plaques equally on N- and B-type mouse-embryo cells, and, as above, demonstrates a slightly greater titer on HeLa and L cells. These titers mainly represent VSV encapsidated within a VSVspecific coat protein produced at 310. Heat treatment of this mixture reduces the titer on mouse-embryo cells about 3 logarithmic units, and now the heat-resistant virions have the host range of FLV, that is, they have a lower titer on HeLa or L cells, or on mouse-embryo cells infected with FLV. These facts are consistent with the results expected of a VSV(FLV) phenotypically mixed virion. As further evidence that FLV envelope protein is present, no neutralization of infectivity occurs on exposure of heated virions to antiserum against VSV; but a further drop of 2.5 logarithmic units of infectivity is seen when this heat-resistant fraction is also exposed to FLV neutralizing antiserum. These findings clearly demonstrate that VSV virions bearing FLV envelope protein are responsible for the major heat resistant infectivity titer found here on mouse-embryo cells. The point to be stressed, however, is that the titer of VSV(N- FLV) on either N- or B-type mouse-embryo cells is exactly the same. These results (Table 4) are verified when a similar analysis of VSV(B-FLV) is done. Again, no restriction of VSV phenotypically mixed virus is demonstrated by the two types of mouse-embryo cells. These results demonstrate that phenotypically mixed VSV(FLV) virions can be obtained which by neutralization, host range, and interference pattern possess the envelope specificities of FLV. Results of plaque assays on mouseembryo cells demonstrate that VSV(N-FLV) and VSV(B- FLV) are not restricted by either B- or N-type cells, respectively. This finding suggests strongly that the outer FLV envelope protein is not involved in host restriction. DISCUSSION Host restriction of RNA tumor viruses has been described clearly in avian cells with the Rous sarcoma complex (21) and in murine cells with the Friend complex. The biological and genetic characteristics of host restriction in these two systems differ markedly. The allele for susceptibility (permissiveness) to Rous sarcoma virus in chick cells is dominant (22), whereas in mice the allele for resistance (nonpermissiveness) to FLV is dominant (1, 7, 8). Host range of avian viruses is strictly correlated with the serotype of the viral envelope. This is not the case for host restriction of FLV, since no serological differences between the envelope antigens of N-FLV and B-FLV have been demonstrated (9). Host restriction in chicks is virtually absolute (21, 23), whereas restriction of FLV is relative (7, 8, 24). The correlate of this latter fact is the phenomenon of a multiple-hit curve seen on titration of
5 Proc. Nat. Acad. Sci. USA 70 (1973) FLV in restrictive cells compared with the single-hit curve seen in permissive cells. Host restriction in avian cells appears to act at the step of viral penetration of host cells (23, 25, 26). As in chick cells with Rous sarcoma virus, the results presented in this paper demonstrate that FLV adsorbs equally well to permissive and restrictive cell types. We have further shown that VSV(FLV) mixed virions can be prepared as characterized by neutralization, host range, and interference specificity of FLV. The result that these mixed virions form plaques equally well on both N- and B-type mouse-embryo cells suggests strongly that host restriction of FLV is due to an intracellular step in virus replication and does not involve an interaction of FLV envelope and the cell surface. Zavada (16) has reported that only neutralization antigen of MLV is exchanged with VSV in formation of the mixed virion. However, McSharry et al. (27) have demonstrated that two glycoproteins are exchanged in formation of phenotypically mixed virions of VSV and simian virus-5. Since MLV appears to contain at least two envelope glycopeptides (28), it is possible that more than one of the surface proteins is necessary to demonstrate host restriction. Furthermore, it could be argued that VSV mixed virions therefore penetrate cells by a mechanism fundamentally different from that of FLV alone. This conclusion is not supported by our results showing the decreased titer of VSV(FLV) when assayed on mouse-embryo cells infected with FLV. Rather, the viral interference, which presumably reflects interference with penetration of the superinfecting virus, demonstrated by VSV(FLV), implies a similarity of adsorption and uptake with native FLV. These data suggest another interesting fact, that viral interference is associated with the neutralization antigen of the leukemia virus. The observation that both N-FLV and B-FLV form plaques with a one-hit curve on S+L- cells deserves some comment. Since S +L- cells represent B-tropic Swiss 3T3 cells transformed by Moloney sarcoma virus, one might expect that N-FLV would exhibit a reduced efficiency of plating on this cell line. It is possible that the presence of the Moloney sarcoma virus genome somehow alters the cell to permit normal replication. These data are consistent with two possibilities; either that Moloney sarcoma virus genome provides a direct helper effect for intracellular replication of otherwise restricted FLV, or that in these transformed cells expression of the Fv-1 gene is suppressed. These possibilities are testable, and may allow further exploration of the intracellular step that is limiting in the FLV restriction phenomenon. NOTE ADDED IN PROOF Corroborating the result that host restriction is not due to Host Restriction of Friend Leukemia Virus 2553 the virus envelope is the data of Yoshikura, H. (1973) J. Gen. Virol. 19, , with pseudotypes of murine sarcoma virus, and that of Huang, A. S., Besmer, P., Chu, L. & Baltimore, D. (1973) J. Virol., in press, who have independently performed similar experiments with VSV and N-FLV. We thank Drs. Frank Lilly and C. R. Pringle for donating the virus strains used in these experiments, and Dr. Donald Summers who suggested the use of phenotypically mixed virions. Special thanks to Mr. James Hsiang for technical assistance. This work was supported by Contract NIH NCI CP of the Special Virus Cancer Program. We were supported by grants as follows: T.K. is supported by a training grant to the M.D.- Ph.D. Program (5T5-GM ); R.S., National Institutes of Health, AI-TO1-Al , Health Research Council of the City of New York no. I-755, and an NIH Career Development Award, 1-K04-CA ; B.F., National Institutes of Health, AI-TO1-A , American Cancer Society Faculty Research Award No. PRA Lilly, F. (1970) J. Nat. Cancer Inst. 45, Pincus, T., Hartley, J. W. & Rowe, W. P. (1971) J. Exp. Med. 133, Pincus, T., Rowe, W. P. & Lilly, F. (1971) J. Exp. Med. 133, Odaka, T. (1969) J. Virol. 3, Ware, L. M. & Axelrad, A. A. (1972) Virology 50, Stephenson, J. R. & Aaronson, S. A. (1972) Proc. Nat. Acad. Sci. USA 69, Rowe, W. P. & Hartley, J. W. (1972) J. Exp. Med. 136, Rowe, W. P. (1972) J. Exp. Med. 136, Steeves, R. A. & Eckner, R. J. (1970) J. Nat. Cancer Inst. 44, Lilly, F. & Steeves, R. A. (1973), Virology, in press. 11. Bassin, R. H., Tuttle, N. & Fischinger, P. J. (1970) Int. J. Cancer 6, Flamand, A. (1970) J. Gen. Virol. 8, Flamand, A. & Pringle, C. R. (1971) J. Gen. Virol. 11, Bassin, R. H., Tuttle, N. & Fischinger, P. J. (1971) Nature 229, Rowe, W. P., Pugh, W. E. & Hartley, J. W. (1971) Virology 42, Zavada, J. & Zavadova, Z. (1972) Nature New Biol. 240, Zavada, J. (1972) J. Gen. Virol. 15, Murphy, F. A. & Fields, B. N. (1967) Virology 33, Temin, H. M. (1967) J. Cell. Physiol. 69, Bader, J. P. (1972) Virology 48, Hanafusa, H. (1965) Virology 25, Payne, L. N. & Biggs, P. M. (1966) Virology 29, Piraino, F. (1967) Virology 32, Hartley, J. W., Rowe, W. P. & Huebner, R. J. (1970) J. Virol. 5, Steck, F. T. & Rubin, H. (1966) Virology 29, Steck, F. T. & Rubin, H. (1966) Virology 29, McSharry, J. J., Compans, R. W. & Choppin, P. W. (1971) J. Virol. 8, Duesberg, P. H., Martin, G. S. & Vogt, P. K. (1970) Virology 41,
Effect of the Fv-1 Locus on the Titration of Murine
JouRNAL OF VIRoLOGY, Dec. 1975, p. 1593-1598 Copyright X 1975 American Society for Microbiology Vol. 16, No. 6 Printed in U.SA. Effect of the Fv-1 Locus on the Titration of Murine Leukemia Viruses PAUL
More informationRole of Interferon in the Propagation of MM Virus in L Cells
APPLIED MICROBIOLOGY, Oct. 1969, p. 584-588 Copyright ( 1969 American Society for Microbiology Vol. 18, No. 4 Printed in U S A. Role of Interferon in the Propagation of MM Virus in L Cells DAVID J. GIRON
More informationMechanism of Restriction of Ecotropic and Xenotropic Murine
JOURNAL OF VIROLOGY, March 1977, p. 965-973 Copyright 1977 American Society for Microbiology Vol. 21, No. 3 Printed in U.S.A. Mechanism of Restriction of Ecotropic and Xenotropic Murine Leukemia Viruses
More informationTemperature-Sensitive Mutants Isolated from Hamster and
JOURNAL OF VIROLOGY, Nov. 1975, p. 1332-1336 Copyright i 1975 American Society for Microbiology Vol. 16, No. 5 Printed in U.S.A. Temperature-Sensitive Mutants Isolated from Hamster and Canine Cell Lines
More informationPersistent Infection of MDCK Cells by Influenza C Virus: Initiation and Characterization
J. gen. Virol. (199), 70, 341-345. Printed in Great Britain 341 Key words: influenza C virus/interferon/persistent infection Persistent Infection of MDCK Cells by Influenza C Virus: Initiation and Characterization
More informationQuantitative Assay of Paravaccinia Virus Based
APPrU MICROBIOLOGY, JUly 1972, p. 138-142 Copyright 1972 American Society for Microbiology Vol. 24, No. 1 Printed in U.S.A. Quantitative Assay of Paravaccinia Virus Based on Enumeration of Inclusion-Containing
More informationof an Infectious Form of Rous Sarcoma Virus*
Proceedings of the National Academy of Sciences Vol. 66, No. 2, pp. 314-321, June 1970 A Cell-Associated Factor Essential for Formation of an Infectious Form of Rous Sarcoma Virus* H. Hanafusa, T. Miyamoto,
More informationDefective Interfering Particles of Respiratory Syncytial Virus
INFECTION AND IMMUNITY, Aug. 1982, p. 439-444 0019-9567/82/080439-06$02.00/0 Vol. 37, No. 2 Defective Interfering Particles of Respiratory Syncytial Virus MARY W. TREUHAFTl* AND MARC 0. BEEM2 Marshfield
More informationDeterminants of the Host Range of Feline Leukaemia Viruses
J. gen. Virol. (1973), 20, I69-t75 Printed in Great Britain 169 Determinants of the Host Range of Feline Leukaemia Viruses By O. JARRETT, HELEN M. LAIRD AND D. HAY University of Glasgow, Leukaemia Research
More informationSuperinfection with Vaccinia Virus
JOURNAL OF VIROLOGY, Aug. 1975, p. 322-329 Copyright 1975 American Society for Microbiology Vol. 16, No. 2 Printed in U.S.A. Abortive Infection of a Rabbit Cornea Cell Line by Vesicular Stomatitis Virus:
More informationSOME PROPERTIES OF ECHO AND COXSACKIE VIRUSES IN TISSUE CULTURE AND VARIATIONS BY HEAT
THE KURUME MEDICAL JOURNAL Vol. 9, No. 1, 1962 SOME PROPERTIES OF ECHO AND COXSACKIE VIRUSES IN TISSUE CULTURE AND VARIATIONS BY HEAT SHIGERU YAMAMATO AND MASAHISA SHINGU Department of Microbiology, Kurume
More information(;[rowth Charaeteristies of Influenza Virus Type C in Avian Hosts
Archives of Virology 58, 349--353 (1978) Archives of Virology by Springer-Verlag 1978 (;[rowth Charaeteristies of Influena Virus Type C in Avian Hosts Brief Report By M ~R A~N D. AUSTIn, A. S. MONTO, and
More informationEnvelope Antigen Relationships among Three Hamster-specific Sarcoma Viruses and a Hamster-specific Helper Virus
J. gen. Virol. (197o), 9, I9-26 I9 Printed in Great Britain Envelope Antigen Relationships among Three Hamster-specific Sarcoma Viruses and a Hamster-specific Helper Virus By G. KELLOFF AND R. J. HUEBNER
More information125. Identification o f Proteins Specific to Friend Strain o f Spleen Focus forming Virus (SFFV)
No. 101 Proc. Japan Acad., 54, Ser. B (1978) 651 125. Identification o f Proteins Specific to Friend Strain o f Spleen Focus forming Virus (SFFV) By Yoji IKAWA,*} Mitsuaki YOSHIDA,*) and Hiroshi YosHIKURA**>
More informationLeukocytes and Interferon in the Host Response to Viral Infections
JOURNAL OF BACTERIOLOGY, June, 1966 Copyright 1966 American Society for Microbiology Vol. 91, No. 6 Printed in U.S.A. Leukocytes and Interferon in the Host Response to Viral Infections IL. Enhanced Interferon
More informationHelper-Dependent Properties of Friend Spleen
JOURNAL OF VIROLOGY, Sept. 1973, p. 523-533 Copyright ( 1973 American Society for Microbiology Vol. 12, No. 3 Printed in U.S.A. Helper-Dependent Properties of Friend Spleen Focus-Forming Virus: Effect
More informationEffects of Cell Culture and Laboratory Conditions on Type 2 Dengue Virus Infectivity
JOURNAL OF CLINICAL MICROBIOLOGY, Aug. 1979, p. 235-239 0095-1137/79/08-0235/05$02.00/0 Vol. 10, No. 2 Effects of Cell Culture and Laboratory Conditions on Type 2 Dengue Virus Infectivity JARUE S. MANNING*
More informationAmantadine in Tissue Culture'
JOURNAL OF BACTERIOLOGY, Sept., 1965 Copyright 1965 American Society for Microbiology Vol. 90, No. 3 Printed in U.S.A. Mode of Action of the Antiviral Activity of Amantadine in Tissue Culture' C. E. HOFFMANN,
More informationThe Infectious Cycle. Lecture 2 Biology W3310/4310 Virology Spring You know my methods, Watson --SIR ARTHUR CONAN DOYLE
The Infectious Cycle Lecture 2 Biology W3310/4310 Virology Spring 2016 You know my methods, Watson --SIR ARTHUR CONAN DOYLE The Infectious Cycle Virologists divide the infectious cycle into steps to facilitate
More informationISOLATION OF A SARCOMA VIRUS FROM A SPONTANEOUS CHICKEN TUMOR
ISOLATION OF A SARCOMA VIRUS FROM A SPONTANEOUS CHICKEN TUMOR Shigeyoshi ITOHARA, Kouichi HIRATA, Makoto INOUE, Masanori Veterinary Pathology, Faculty of Agriculture, Yamaguchi University* HATSUOKA, and
More informationxcelligence Real-Time Cell Analyzers
xcelligence Real-Time Cell Analyzers Application Note No. 9 A New Way to Monitor Virus-Mediated Cytopathogenicity Introduction One of the most important procedures in virology is the measurement of viral
More informationIntroduction.-Cytopathogenic viruses may lose their cell-destroying capacity
AN INHIBITOR OF VIRAL ACTIVITY APPEARING IN INFECTED CELL CULTURES* BY MONTO Hot AND JOHN F. ENDERS RESEARCH DIVISION OF INFECTIOUS DISEASES, THE CHILDREN'S MEDICAL CENTER, AND THE DEPARTMENT OF BACTERIOLOGY
More informationthe xenotropic sequences in the region of the env gene. The to the env gene of mouse xenotropic type C virus.
Proc. Natl. Acad. Sci. U$A Vol. 74, No. 10, pp. 4671-4675, October 1977 Microbiology Friend strain of spleen focus-forming virus is a recombinant between ecotropic murine type C virus and the env gene
More informationEnhanced Growth of a Murmne Coronavirus in Transformed Mouse Cells
INFECI1ON AND IMMUNITY, Oct. 1972, p. 501-507 Copyright 1972 American Society for Microbiology Vol. 6, No. 4 Printed in U.S.A. Enhanced Growth of a Murmne Coronavirus in Transformed Mouse Cells LAWRENCE
More informationhemagglutinin and the neuraminidase genes (RNA/recombinant viruses/polyacrylamide gel electrophoresis/genetics)
Proc. Natl. Acad. Sci. USA Vol. 73, No. 6, pp. 242-246, June 976 Microbiology Mapping of the influenza virus genome: Identification of the hemagglutinin and the neuraminidase genes (RNA/recombinant viruses/polyacrylamide
More informationBY F. BROWN, B. CARTWRIGHT AND DOREEN L. STEWART Research Institute (Animal Virus Diseases), Pirbright, Surrey. (Received 22 August 1962) SUMMARY
J. gen. Microbial. (1963), 31, 179186 Prinied in Great Britain 179 The Effect of Various Inactivating Agents on the Viral and Ribonucleic Acid Infectivities of FootandMouth Disease Virus and on its Attachment
More informationActivation of Nonexpressed Endogenous Ecotropic Murine Leukemia Virus by Transfection of Genomic DNA into Embryo Cells
JOURNAL OF VIROLOGY, Mar. 1983, P. 950-955 0022-538X/83/030950-06$02.00/0 Copyright 1983, American Society for Microbiology Vol. 45, No. 3 Activation of Nonexpressed Endogenous Ecotropic Murine Leukemia
More informationNEUTRALIZATION OF REOVIRUS: THE GENE RESPONSIBLE FOR THE NEUTRALIZATION ANTIGEN* BY HOWARD L. WEINER~ AN~ BERNARD N. FIELDS
NEUTRALIZATION OF REOVIRUS: THE GENE RESPONSIBLE FOR THE NEUTRALIZATION ANTIGEN* BY HOWARD L. WEINER~ AN~ BERNARD N. FIELDS (From the Department of Microbiology and Molecular Genetics, Harvard Medical
More informationEVALUATION OF THE EFFECTIVENESS OF A 7% ACCELERATED HYDROGEN PEROXIDE-BASED FORMULATION AGAINST CANINE PARVOVIRUS
Final report submitted to Virox Technologies, Inc. EVALUATION OF THE EFFECTIVENESS OF A 7% ACCELERATED HYDROGEN PEROXIDE-BASED FORMULATION AGAINST CANINE PARVOVIRUS Syed A. Sattar, M.Sc., Dip. Bact., M.S.,
More informationPERSISTENT INFECTIONS WITH HUMAN PARAINFLUENZAVIRUS TYPE 3 IN TWO CELL LINES
71 PERSISTENT INFECTIONS WITH HUMAN PARAINFLUENZAVIRUS TYPE 3 IN TWO CELL LINES Harold G. Jensen, Alan J. Parkinson, and L. Vernon Scott* Department of Microbiology & Immunology, University of Oklahoma
More informationvirus-i (RAV-1) or Rous associated virus-2 (RAV-2), do not transform but do produce
ISOLATION OF NONINFECTIOUS PARTICLES CONTAINING ROUS SARCOMA VIRUS RNA FROM THE MEDIUM OF ROUS SARCOMA VIRUS-TRANSFORMED NONPRODUCER CELLS* BY HARRIET LATHAM ROBINSONt VIRUS LABORATORY, UNIVERSITY OF CALIFORNIA,
More informationBrief Definitive Report
Brief Definitive Report HEMAGGLUTININ-SPECIFIC CYTOTOXIC T-CELL RESPONSE DURING INFLUENZA INFECTION BY FRANCIS A. ENNIS, W. JOHN MARTIN, ANY MARTHA W. VERBONITZ (From the Department of Health, Education
More informationInduction of Interferon in Chick Cells by Temperaturesensitive Mutants of Sindbis Virus
J. gen. ViroL 0974), 25, 381-39o Printed in Great Britain 38I Induction of Interferon in Chick Cells by Temperaturesensitive Mutants of Sindbis Virus By G. J. ATKINS, M. D. JOHNSTON, LINDA M. WESTMACOTT
More informationDistinctive Characteristics of Crude Interferon from Virus-infected Guinea-pig Embryo Fibroblasts
J. gen. Virol. (1984), 65, 843-847. Printed in Great Britain 843 Key words: IFN/guinea-pig/acid-labile Distinctive Characteristics of Crude Interferon from Virus-infected Guinea-pig Embryo Fibroblasts
More informationPlaque Assay of Sendai Virus in Monolayers of a Clonal Line
JOURNAL OF CUNICAL MICROBIOLOGY, Feb. 1976. p. 91-95 Copyright 1976 American Society for Microbiology Vol. 3, No. 2 Printed in U.SA. Plaque Assay of Sendai Virus in Monolayers of a Clonal Line of Porcine
More informationThe Effect of Environment on the Replication of Poliovirus in Monkey Kidney Cells
J. gen. Mimobiol. (1961), 25, 421428 Printed in Great Britain 421 The Effect of Environment on the Replication of Poliovirus in Monkey Kidney Cells BY G. FURNESS" Department of Microbiology, University
More informationAdenovirus Manual 1. Table of Contents. Large Scale Prep 2. Quick MOI Test 4. Infection of MNT-1 Cells 8. Adenovirus Stocks 9
Adenovirus Manual 1 Table of Contents Large Scale Prep 2 Quick MOI Test 4 TCID 50 Titration 5 Infection of MNT-1 Cells 8 Adenovirus Stocks 9 CAUTION: Always use filter tips and bleach everything!!! Adenovirus
More informationFormation of an Infectious Virus-Antibody Complex with Rous
JOURNAL OF VIROLOGY, Mar. 1976, p. 163-167 Copyright 1976 American Society for Microbiology Vol. 17, No. 3 Printed in U.S.A. Formation of an Infectious Virus-Antibody Complex with Rous Sarcoma Virus and
More informationEffect of Exogenous Interferon on Rubella Virus Production in Carrier Cultures of Cells Defective in Interferon Production
INFECTION AND IMMUNITY, Aug. 1970, p. 132-138 Copyright 1970 American Society for Microbiology Vol. 2, No. 2 Printed in U.S.A. Effect of Exogenous Interferon on Rubella Virus Production in Carrier Cultures
More informationMechanism of Pock Formation by Shope Fibroma
JOURNAL OF BACTERIOLOGY, Sept., 1966 Copyright ( 1966 American Society for Microbiology Vol. 92, No. 3 Printed in U.S.A. Mechanism of Pock Formation by Shope Fibroma Virus on Monolayers of Rabbit Cells
More informationRADIATION LEUKEMIA IN C57BL/6 MICE I. Lack of Serological Evidence for the Role of Endogenous Ecotropic Viruses in Pathogenesis*
RADIATION LEUKEMIA IN C57BL/6 MICE I. Lack of Serological Evidence for the Role of Endogenous Ecotropic Viruses in Pathogenesis* BY JAMES N. IHLE, ROBERT McEWAN AND KATHLEEN BENGALI (From the Basic Research
More informationHost Cell Range and Growth Characteristics of
INFECTION AND IMMUNITY, Mar. 1973, p. 398-4 Copyright 1973 Americau Society for Microbiology Vol. 7, No. 3 Printed in U.S.A. Host Cell Range and Growth Characteristics of Bovine Parvoviruses' R. C. BATES'
More informationINTRABULBAR INOCULATION OF JAPANESE ENCEPHALITIS VIRUS TO MICE
THE KURUME MEDICAL JOURNAL Vol. 15, No. 1, 1968 INTRABULBAR INOCULATION OF JAPANESE ENCEPHALITIS VIRUS TO MICE TOSHINORI TSUCHIYA Department of Microbiology, and Department of Ophthalmology, Kurume University
More informationCytomegalovirus Based upon Enhanced Uptake of Neutral
JOURNAL OF CUNICAL MICROBIOLOGY, JUlY 1976, p. 61-66 Copyright 1976 American Society for Microbiology Vol. 4, No. 1 Printed in U.S.A. Plaque Reduction Neutralization Test for Human Cytomegalovirus Based
More informationTHE CYTOPATHOGENIC ACTION OF BLUETONGUE VIRUS ON TISSUE CULTURES AND ITS APPLICATION TO THE DETECTION OF ANTIBODIES IN THE SERUM OF SHEEP.
Onderstepoort Journal of Veterinary Research, Volume 27, Number 2, October, 1956. The Government Printer. THE CYTOPATHOGENIC ACTION OF BLUETONGUE VIRUS ON TISSUE CULTURES AND ITS APPLICATION TO THE DETECTION
More informationPathogenesis of Simian Foamy Virus Infection in Natural and Experimental Hosts
INCTION AD ImmuNrry, Sept. 1975, p. 470-474 Copyright 0 1975 American Society for Microbiology Vol. 12, No. 3 Printed in U.S.A. Pathogenesis of Simian Foamy Virus Infection in Natural and Experimental
More information~Lentivirus production~
~Lentivirus production~ May 30, 2008 RNAi core R&D group member Lentivirus Production Session Lentivirus!!! Is it health threatening to lab technician? What s so good about this RNAi library? How to produce
More informationHost Defense Mechanisms Against Influenza Virus: Interaction of Influenza Virus with Murine Macrophages In Vitro
INFECTION AND IMMUNITY, Dec. 1978, p. 758-762 0019-9567/78/0022-0758$02.00/0 Copyright 1978 American Society for Microbiology Vol. 22, No. 3 Printed in U.S.A. Host Defense Mechanisms Against Influenza
More informationMarkers of Rubella Virus Strains in RK13 Cell Culture
JOURNAL OF VIROLOGY, Feb. 1969, p. 157-163 Copyright 1969 American Society for Microbiology Vol. 3, No. 2 Printed in U.S.A. Markers of Rubella Virus Strains in RK13 Cell Culture ALICE FOGEL' AND STANLEY
More informationNUTRITIONAL REQUIREMENTS FOR THE PRODUCTION OF POLIOVIRUS
NUTRITIONAL REQUIREMENTS FOR THE PRODUCTION OF POLIOVIRUS TYPE II, COXSACKIE B3, AND VACCINIA VIRUSES BY CONTINUOUS ANIMAL CELL CULTURES' R. L. TYNDALL AND E. H. LUDWIG Department of Bacteriology, The
More informationDuring Murine Cytomegalovirus Infection
INFECTION AND IMMUNITY, Sept. 1980, p. 1050-1054 0019-9567/80/09-1050/05$02.00/0 Vol. 29, No. 3 Antivirus Antibody-Dependent Cell-Mediated Cytotoxicity During Murine Cytomegalovirus Infection JODY E. MANISCHEWITZ
More informationAli Alabbadi. Bann. Bann. Dr. Belal
31 Ali Alabbadi Bann Bann Dr. Belal Topics to be discussed in this sheet: Particles-to-PFU Single-step and multi-step growth cycles Multiplicity of infection (MOI) Physical measurements of virus particles
More informationThermal Inactivation Studies of a Coronavirus, Transmissible Gastroenteritis Virus
J. gen. Virol. (1981), 56, 235-240. Printed in Great Britain 235 Key words: coronavirus/transmissible gastroenteritis virus~heat inactivation Thermal Inactivation Studies of a Coronavirus, Transmissible
More informationReplication Defective Enterovirus Infections: Implications for Type I Diabetes
Replication Defective Enterovirus Infections: Implications for Type I Diabetes N. M. Chapman Department of Pathology & Microbiology University of Nebraska Medical Center Enterovirus Genome and 2 Capsid
More informationSeparation of sarcoma virus-specific and leukemia virus-specific genetic sequences of Moloney sarcoma virus (mechanism of transformation)
Proc. Nat. Acad. Sd. USA Vol. 72, No. 11, pp. 4650-4654, November 1975 Microbiology Separation of sarcoma virus-specific and leukemia virus-specific genetic sequences of Moloney sarcoma virus (mechanism
More informationIsolation of Different Serotypes in Human Heteroploid
JOURNAL OF CLINICAL MICROBIOLOGY, Feb. 1977, p. 202-207 Copyright 1977 American Society for Microbiology Vol. 5, No. 2 Printed in U.S.A. Demonstration of Dual Rhinovirus Infection in Humans by Isolation
More informationProduction of Interferon Alpha by Dengue Virus-infected Human Monocytes
J. gen. Virol. (1988), 69, 445-449. Printed in Great Britain 445 Key words: IFN-ct/dengue virus/monocytes Production of Interferon Alpha by Dengue Virus-infected Human Monocytes By ICHIRO KURANE AND FRANCIS
More informationIsolation and Properties of Moloney Murine Leukemia Virus Mutants: Use of a Rapid Assay for Release of Virion Reverse Transcriptase
JOURNAL OF VIROLOGY, Apr. 1981, p. 239-248 0022-538X/81/040239-10$02.00/0 Vol. 38, No. 1 Isolation and Properties of Moloney Murine Leukemia Virus Mutants: Use of a Rapid Assay for Release of Virion Reverse
More informationTHERMOINACTIVATION OF HF AND M STRAINS OF HERPES SIMPLEX VIRUS IN VARIOUS CONDITIONS
THE KURUME MEDICAL JOURNAL Vol. 16, No. 2, 1969 THERMOINACTIVATION OF HF AND M STRAINS OF HERPES SIMPLEX VIRUS IN VARIOUS CONDITIONS HIDEFUMI KABUTA, SHIGERU YAMAMOTO, MIZUKO TANIKAWA AND YOH NAKAGAWA
More informationSize of Virus-Specific RNA in B-34, a Hamster Tumor Cell Producing Nucleic Acids of Type C Viruses from Three Species
JOURNAL OF VIROLOGY, OCt. 1975, p. 832-837 Copyright i 1975 American Society for Microbiology Vol. 16, No. 4 Printed in U.S.A. Size of Virus-Specific RNA in B-34, a Hamster Tumor Cell Producing Nucleic
More informationBrief DeNnitive Report
Published Online: 1 July, 1981 Supp Info: http://doi.org/10.1084/jem.154.1.199 Downloaded from jem.rupress.org on August 25, 2018 Brief DeNnitive Report VIRUS-SPECIFIC INTERFERON ACTION Protection of Newborn
More informationAssociated Antigens (membrane immunoflui
Proc. Nat. Acad. Sci. USA Vol. 72, No. 5, pp. 1671-1675, May 1975 Augmentation of Lymphocyte Cytotoxicity by Antibody to Herpesvirus saimiri Associated Antigens (membrane immunoflui e/lymphoma/disease
More informationM. MIYAKI, ET AL. AC, PJ and normal cells were seeded ml kanamycin. The fibroblasts were detached from the dish by treatment at room temperature
INCREASED SENSITIVITY OF FIBROBLASTS OF SKIN FROM PATIENTS WITH ADENOMATOSIS COLI AND PEUTZ-JEGHERS' SYNDROME TO TRANSFORMA- TION BY MURINE SARCOMA VIRUS*1 Michiko MIYAKI,*2 Noriko AKAMATSU,*2 Makoto ROKUTANDA,*2
More informationReplication in Tissue Culture
JOURNAL OF VIROLOGY, Jan 1977, p. 277-283 Copyright C 1977 American Society for Microbiology Vol. 21, No. 1 Printed in U.S.A. Effect of Cyclophosphamide In Vitro and on Vaccinia Virus Replication in Tissue
More informationSUSCEPTIBILITY OF SUCKLING MICE TO VARIOLA VIRUS
SUSCEPTIBILITY OF SUCKLING MICE TO VARIOLA VIRUS RONALD G. MARSHALL AND PETER J. GERONE U. S. Army Chemical Corps, Fort Detrick, Frederick, Maryland Received for publication December, 6 ABSTRACT MARSHALL,
More informationInfection of Chick Embryo Fibroblasts With Template Active RNA From Avian Myeloblastosis Virus
J. gen. ViroL (I97O), 6, I63-I68 Prh, ted in Great Britain I63 Infection of Chick Embryo Fibroblasts With Template Active RNA From Avian Myeloblastosis Virus By I. HLO2;ANEK*I" AND VLASTA SOVOV,~ Institute
More informationLarge Scale Infection for Pooled Screens of shrna libraries
Last modified 01/11/09 Large Scale Infection for Pooled Screens of shrna libraries Biao Luo, Glenn Cowley, Michael Okamoto, Tanaz Sharifnia This protocol can be further optimized if cells being used are
More informationApplication of μmacs Streptavidin MicroBeads for the analysis of HIV-1 directly from patient plasma
Excerpt from MACS&more Vol 8 1/2004 Application of μmacs Streptavidin MicroBeads for the analysis of HIV-1 directly from patient plasma L. Davis Lupo and Salvatore T. Butera HIV and Retrovirology Branch,
More informationReceived 3 September 2002/Accepted 15 January 2003
JOURNAL OF VIROLOGY, Apr. 2003, p. 4646 4657 Vol. 77, No. 8 0022-538X/03/$08.00 0 DOI: 10.1128/JVI.77.8.4646 4657.2003 Copyright 2003, American Society for Microbiology. All Rights Reserved. Ability of
More informationNEUTRALIZATION OF VISNA VIRUS BY HUMAN SERA
THE ENTEROVIRUS DEPARTMENT, STATENS SERUMINSTITUT, COPENHAGEN, DENMARK NEUTRALIZATION OF VISNA VIRUS BY HUMAN SERA By HALLD~R THORMAR~ and HERDIS VON MACNUS Received 28.ix.62 In a previous paper (12) the
More information7.012 Quiz 3 Answers
MIT Biology Department 7.012: Introductory Biology - Fall 2004 Instructors: Professor Eric Lander, Professor Robert A. Weinberg, Dr. Claudette Gardel Friday 11/12/04 7.012 Quiz 3 Answers A > 85 B 72-84
More informationSupplementary Figures
Inhibition of Pulmonary Anti Bacterial Defense by IFN γ During Recovery from Influenza Infection By Keer Sun and Dennis W. Metzger Supplementary Figures d a Ly6G Percentage survival f 1 75 5 1 25 1 5 1
More informationEffect of Mutation in Immunodominant Neutralization Epitopes on the Antigenicity of Rotavirus SA-11
J. gen. Virol. (1985), 66, 2375-2381. Printed in Great Britain 2375 Key words: rotaviruses/antigenieity/antiserum selection Effect of Mutation in Immunodominant Neutralization Epitopes on the Antigenicity
More informationTHE ROLE OF INTERFERON IN VACCINIA VIRUS INFECTION OF MOUSE EMBRYO TISSUE CULTURE
THE ROLE OF INTERFERON IN VACCINIA VIRUS INFECTION OF MOUSE EMBRYO TISSUE CULTURE BY LOWELL A. GLASGOW, M.D., A~rD KARL HABEL, M.D. (From the Laboratory of Biology of Viruses, National Institute of Allergy
More informationEffect of Magnesium on Replication of Rhinovirus HGP'
JOURNAL OF VIROLOGY, June 1967, p. 489-493 Copyright 1967 American Society for Microbiology Vol. 1, No. 3 Printed in U.S.A. Effect of Magnesium on Replication of Rhinovirus HGP' MILAN FIALA' AND GEORGE
More informationG. W. WOOD J. C. MUSKETT and D. H. THORNTON MAFF, Central Veterinary Laboratory, New Haw, Weybridge, Surrey, U.K.
J. Comp. Path. 1986 vol. 96 OBSERVATIONS ON THE ABILITY OF AVIAN REOVIRUS VACCINMATION OF HENS TO PROTECT THEIR PROGENY AGAINST THE EFFECTS OF CHALLENGE WITH HOMOLOGOUS AND HETEROLOGOUS STRAINS By G. W.
More informationTransfection of Sf9 cells with recombinant Bacmid DNA
Transposition Bacmid DNA Mini Culturing baculo cells Transfection of Sf9 cells with recombinant Bacmid DNA Amplification of the virus Titration of baculo stocks Testing the expression Transposition 1.
More informationChang Gung University co-commissioned final report. Research Ttitle: Antiviral mechanism study for 254 UVC robot system
co-commissioned final report Research Ttitle: Antiviral mechanism study for 254 UVC robot system Project/Research Number:: Execution duration: 2014.10.16-2015.01.16 Principle Investigator: Professor Shin-Ru
More informationRetroviruses. containing 10% fetal calf serum and 0.24 U of insulin (Eli Lilly & Co.) per ml. Viruses. All virus preparations were clarified culture
JOURNAL OF VIROLOGY, Sept. 1982, p. 1055-1060 0022-538X/82/091055-06$02.00/0 Copyright 1982, American Society for Microbiology Vol. 43, No. 3 In Situ Hybridization: General Infectivity Assay for Retroviruses
More informationHemagglutinin Mutants of Swine Influenza Virus Differing in
INFECTION AND IMMUNITY, Oct. 1979, p. 197-201 0019-9567/79/10-0197/05$02.00/0 Vol. 26, No. 1 Hemagglutinin Mutants of Swine Influenza Virus Differing in Replication Characteristics in Their Natural Host
More informationThe Influence of Ultraviolet-inactivated Sendai Virus on Marek's Disease Virus Infection in Tissue Culture
J. gen. Virol. 097o), 9, 45-5 o 45 Printed in Great Britain The Influence of Ultraviolet-inactivated Sendai Virus on Marek's Disease Virus Infection in Tissue Culture By I. HLO~ANEK* Houghton Poultry Research
More informationGenetic Complementation among Poliovirus Mutants Derived
JOURNAL OF VIROLOGY, Dec. 1986, p. 1040-1049 0022-538X/86/121040-10$02.00/0 Copyright C) 1986, American Society for Microbiology Vol. 60, No. 3 Genetic Complementation among Poliovirus Mutants Derived
More informationVirus-Induced Hamster Tumor Cells
JOURNAL OF VIROLOGY, OCt. 1973. p. 931-936 Copyright 1973 American Society for Microbiology Vol. 12, No. 4 Printed in U.S.A. Properties of Noninfectious and Transforming Viruses Released by Murine Sarcoma
More informationNonproducing State of Rous Sarcoma Cells:
JOURNAL OF VIROLOGY, Aug. 1967, p. 729-737 Copyright 1967 American Society for Microbiology Vol. 1, No. 4 Printed in U.S.A. Nonproducing State of Rous Sarcoma Cells: Its Contagiousness in Chicken Cell
More informationNOTES CONTAMINATION OF CYNOMOLGUS MONKEY KIDNEY CELL CULTURES BY HEMAGGLUTINATING SIMIAN VIRUS (SV 5)
Japan. J. Med. Sci. Biol., 18, 151-156, 1965 NOTES CONTAMINATION OF CYNOMOLGUS MONKEY KIDNEY CELL CULTURES BY HEMAGGLUTINATING SIMIAN VIRUS (SV 5) Since the extensive use of cynomolgus monkey kidney cell
More informationSubeellular Distribution of Newly Synthesized Virus-Specific Polypeptides in Moloney Murine Leukemia Virus- Infected Cells
JOURNAL OF VIROLOGY, Jan. 1979, p. 385-389 0022-538X/79/01-0385/05$02.00/0 Vol. 29, No. 1 Subeellular Distribution of Newly Synthesized Virus-Specific Polypeptides in Moloney Murine Leukemia Virus- Infected
More information(From the Laboratory of Cell Biology, National Institute of Allergy and Infectious Diseases, National Instil/utes of Health, Bahesda, Maryland)
Published Online: 1 September, 1959 Supp Info: http://doi.org/10.1084/jem.110.3.445 Downloaded from jem.rupress.org on December 1, 2018 THE EFFECT OF CELL POPULATION DENSITY ON THE AMINO ACID REQUIREMENTS
More informationTRANSPORT OF AMINO ACIDS IN INTACT 3T3 AND SV3T3 CELLS. Binding Activity for Leucine in Membrane Preparations of Ehrlich Ascites Tumor Cells
Journal of Supramolecular Structure 4:441 (401)-447 (407) (1976) TRANSPORT OF AMINO ACIDS IN INTACT 3T3 AND SV3T3 CELLS. Binding Activity for Leucine in Membrane Preparations of Ehrlich Ascites Tumor Cells
More informationSelection of Temperature-Sensitive Mutants During Persistent Infection: Role in Maintenance. of L Cells
JOURNAL OF VIROLOGY, Sept. 1973, p. 481-491 Copyright ( 1973 American Society for Microbiology Vol. 12, No. 3 Printed in U.S.A. Selection of Temperature-Sensitive Mutants During Persistent Infection: Role
More informationAssay of Human Interferon in Vero Cells by Several Methods
JOURNAL OF CLINICAL MICROBIOLOGY, Apr. 1979, p. 471-475 0095-1137/79/04-0471/05$02.00/0 Vol. 9, No.4 Assay of Human Interferon in Vero Cells by Several Methods PAULO C. P. FERREIRA, MARIA L. P. PEIXOTO,
More informationEffect of Complement and Viral Filtration on the
APPLIED MICROBIOLOGY, JUlY 1968, p. 1076-1080 Copyright @ 1968 American Society for Microbiology Vol. 16, No. 7 Printed in U.S.A. Effect of Complement and Viral Filtration on the Neutralization of Respiratory
More informationVIRAL TITER COUNTS. The best methods of measuring infectious lentiviral titer
VIRAL TITER COUNTS The best methods of measuring infectious lentiviral titer FLUORESCENCE CYCLES qpcr of Viral RNA SUMMARY Viral vectors are now routinely used for gene transduction in a wide variety of
More informationInhibition of Enterovirus Cytopathic Effects by 2- (a-hydroxybenzyl)-benzimidazolel
JOURNAL OF BACTROLOGY, Mar., 1966 Copyright ( 1966 American Society for Microbiology Vol. 91, No. 3 Printed in U.S.A. nhibition of nterovirus Cytopathic ffects by 2- (a-hydroybenzyl)-benzimidazolel ROSTOM
More information5. Influence of multiplicity of infection (MOI) on synchronous baculovirus infections 5.1. Introduction
5. Influence of multiplicity of infection (MOI) on synchronous baculovirus infections 5.1. Introduction The symptoms of baculovirus infection vary greatly between cells in the same cell culture, even if
More informationElectron Microscope Studies of HeLa Cells Infected with Herpes Virus
244 STOKER, M. G. P., SMITH, K. M. & Ross, R. W. (1958). J. gen. Microbiol. 19,244-249 Electron Microscope Studies of HeLa Cells Infected with Herpes Virus BY M: G. P. STOKER, K. M. SMITH AND R. W. ROSS
More informationLoss of Proviral DNA Sequences in a Revertant of Kirsten Sarcoma Virus-transformed Murine Fibroblasts
J. gen. Virol. (I979), 44, 245-249 245 Printed in Great Britain Loss of Proviral DNA Sequences in a Revertant of Kirsten Sarcoma Virus-transformed Murine Fibroblasts (Accepted 22 February I979) SUMMARY
More informationInhibition of Human Herpesviruses by Combinations of Acyclovir and Human Leukocyte Interferon
INFECTION AND IMMUNITY, June 1981, p. 995-999 0019-9567/81/060995405$02.00/0 Vol. 32, No. 3 Inhibition of Human Herpesviruses by Combinations of Acyclovir and Human Leukocyte Interferon MYRON J. LEVIN*
More informationThe Glycoprotein of Vesicular Stomatitis Virus Is the Antigen That Gives Rise to and Reacts with Neutralizing Antibody
JOURNAL OF VIROLOGY, Dec. 1972, p. 1231-1235 Copyright 1972 American Society for Microbiology Vol. 10, No. 6. Printed in U.S.A. The Glycoprotein of Vesicular Stomatitis Virus Is the Antigen That Gives
More informationRapid Sensitive Assay for Interferons Based on the
APPLIED MICROBIOLOGY, Sept. 1970, p. 317-322 Copyright ( 1970 American Society for Microbiology Vol. 20, No. 3 Printed in U.S.A. Rapid Sensitive Assay for Interferons Based on the Inhibition of MM Virus
More informationRole of Carbohydrate in Biological Functions of Friend
JOURNAL OF VIROLOGY, Jan. 1977, p. 35-40 Copyright 0 1977 American Society for Microbiology Vol. 21, No. 1 Printed in U.S.A. Role of Carbohydrate in Biological Functions of Friend Murine Leukemia Virus
More information