Isotype Distribution and Specificity of the Antibody Response to Primary Moloney Murine Sarcoma Virus Infection in BALB/c Mice

1989 ◽  
Vol 2 (2) ◽  
pp. 89-101
Author(s):  
THOMAS J. POWELL ◽  
BRIAN GAUPP ◽  
J. MILLER EPPS ◽  
R.V. SRINIVAS ◽  
EDDIE W. LAMON
Keyword(s):  
Virus Infection ◽  
Antibody Response ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Moloney Murine Sarcoma Virus ◽  
Murine Sarcoma

scholarly journals Alternate utilization of two regulatory domains within the Moloney murine sarcoma virus long terminal repeat.

1985 ◽  
Vol 5 (8) ◽  
pp. 1959-1968 ◽  
Author(s):  
B J Graves ◽  
S P Eisenberg ◽  
D M Coen ◽  
S L McKnight
Keyword(s):  
Long Terminal Repeat ◽  
Transcriptional Activation ◽  
Substantial Effect ◽  
Positive Control ◽  
Terminal Repeat ◽  
Temporal Shift ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Moloney Murine Sarcoma Virus ◽  
Murine Sarcoma

The Moloney murine sarcoma virus long terminal repeat (LTR) harbors two distinct positive activators of transcription, namely, a distal signal and an enhancer. In this report we demonstrate that infection by herpes simplex virus (HSV) can markedly affect the utilization of these two Moloney murine sarcoma virus transcription signals. We investigated the HSV-mediated trans-acting effects with two goals in mind: first, to gain insight into LTR function, and second, to probe the mechanisms used by HSV to establish its own transcription cascade. In mock-infected cells, LTR-mediated expression was heavily dependent on the Moloney murine sarcoma virus enhancer but was effectively distal signal independent. HSV infection mobilized the use of the LTR distal signal and concomitantly alleviated enhancer dependence. Indeed, enhancer function may actually be inhibited by HSV trans-acting factors. These results suggest that the two positive control signals of the Moloney murine sarcoma virus LTR facilitate transcriptional activation by two different pathways. We further observed that the identity of the structural gene driven by the LRT, as well as the state of integration of a transfected template, can exert a substantial effect on the response of a template to HSV infection. According to these findings, we propose a tentative model to account for the initial temporal shift of the HSV transcriptional cascade.

Immunosuppression by Murine Sarcoma Virus (Moloney)

1970 ◽  
Vol 1 (3) ◽  
pp. 288-292
Author(s):  
S. P. Chan ◽  
W. A. Hook ◽  
W. Turner ◽  
M. A. Chirigos
Keyword(s):  
Antibody Response ◽  
Survival Time ◽  
Primary Tumor ◽  
Sheep Erythrocyte ◽  
Humoral Antibody ◽  
Secondary Tumors ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Erythrocyte Antigen ◽  
Murine Sarcoma

Infection of mice with the murine sarcoma virus (Moloney) markedly suppressed the humoral antibody response to sheep erythrocyte antigen injected 10 days after infection, when tumor size was maximal, and on day 26, when primary tumors had partially regressed. Humoral antibody response was also inhibited when antigen was injected at the time secondary tumors and metastases were evident. No significant suppression of humoral antibody was seen when mice were injected with sheep erythrocyte antigen 5 days after virus infection. Inhibition of the cellular immune response of murine sarcoma virus (Moloney)-infected mice, as measured by the increased survival time of skin grafts, was also determined. Mice that were infected 5 days prior to grafting demonstrated prolonged survival of grafts, suggesting a suppression of cellular immunity. These mice had a graft survival time 14 days greater than noninfected controls. No significant prolongation of graft survival was seen in mice grafted at the times of maximum primary tumor growth, of primary tumor regression, or when secondary tumors had appeared.

Alternate utilization of two regulatory domains within the Moloney murine sarcoma virus long terminal repeat

1985 ◽  
Vol 5 (8) ◽  
pp. 1959-1968
Author(s):  
B J Graves ◽  
S P Eisenberg ◽  
D M Coen ◽  
S L McKnight
Keyword(s):  
Long Terminal Repeat ◽  
Transcriptional Activation ◽  
Substantial Effect ◽  
Positive Control ◽  
Terminal Repeat ◽  
Temporal Shift ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Moloney Murine Sarcoma Virus ◽  
Murine Sarcoma

The Moloney murine sarcoma virus long terminal repeat (LTR) harbors two distinct positive activators of transcription, namely, a distal signal and an enhancer. In this report we demonstrate that infection by herpes simplex virus (HSV) can markedly affect the utilization of these two Moloney murine sarcoma virus transcription signals. We investigated the HSV-mediated trans-acting effects with two goals in mind: first, to gain insight into LTR function, and second, to probe the mechanisms used by HSV to establish its own transcription cascade. In mock-infected cells, LTR-mediated expression was heavily dependent on the Moloney murine sarcoma virus enhancer but was effectively distal signal independent. HSV infection mobilized the use of the LTR distal signal and concomitantly alleviated enhancer dependence. Indeed, enhancer function may actually be inhibited by HSV trans-acting factors. These results suggest that the two positive control signals of the Moloney murine sarcoma virus LTR facilitate transcriptional activation by two different pathways. We further observed that the identity of the structural gene driven by the LRT, as well as the state of integration of a transfected template, can exert a substantial effect on the response of a template to HSV infection. According to these findings, we propose a tentative model to account for the initial temporal shift of the HSV transcriptional cascade.

The long terminal repeat of an endogenous intracisternal A-particle gene functions as a promoter when introduced into eucaryotic cells by transfection

1984 ◽  
Vol 4 (10) ◽  
pp. 2128-2135
Author(s):  
K K Lueders ◽  
J W Fewell ◽  
E L Kuff ◽  
T Koch
Keyword(s):  
Long Terminal Repeat ◽  
Promoter Activity ◽  
Terminal Repeat ◽  
Flanking Sequence ◽  
Murine Sarcoma Virus ◽  
Sarcoma Virus ◽  
Mouse Cells ◽  
Moloney Murine Sarcoma Virus ◽  
Intracisternal A Particle ◽  
Murine Sarcoma

We describe experiments designed to determine whether an endogenous intracisternal A-particle (IAP) gene randomly selected from a mouse embryo library has the potential to be transcriptionally active. Assays for IAP gene transcription were done with permanently transformed rat cells and transiently transfected monkey and mouse cells. The rat cells, which had integrated IAP gene copies, contained IAP RNA. A start site within the IAP 5' long terminal repeat (LTR) was localized by S1 mapping. The promoter activity of the IAP LTR was also measured in cells 48 h after the introduction of recombinant plasmids in which bacterial chloramphenicol acetyl transferase (CAT) encoding sequences were under the control of the LTR. The IAP LTR promoted CAT activity in mouse and monkey cells. In mouse L-cells, the levels of CAT activity were 10 to 25% of those promoted by an analogous recombinant containing the Moloney murine sarcoma virus LTR as the promoter. In contrast to the Moloney murine sarcoma virus LTR, the IAP LTR was five- to eightfold more active in monkey cells than in mouse cells. The 5' and 3' LTRs were equally active, and promoter activity was dependent on having the orientation of the LTRs with respect to the CAT gene the same as their orientation with respect to the IAP gene. A 5'-flanking sequence containing a member of the highly repetitive R-sequence family increased CAT activity in COS cells 11-fold when present along with the LTR. Our results indicate that the LTR of an endogenous mouse IAP gene can function as an efficient promoter in heterologous as well as homologous cells.

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