Subject(s)
Athletic Injuries/microbiology , Bacterial Translocation , Fusobacterium Infections/microbiology , Fusobacterium nucleatum/isolation & purification , Lumbar Vertebrae/injuries , Meningitis, Bacterial/microbiology , Spinal Fractures/complications , Anti-Infective Agents/therapeutic use , Bacteremia/drug therapy , Bacteremia/etiology , Bacteremia/microbiology , Bacterial Typing Techniques/methods , Colon/microbiology , Culture Media , Diabetes Mellitus, Type 2/complications , Diagnosis, Differential , Dura Mater/injuries , False Negative Reactions , Fusobacterium Infections/cerebrospinal fluid , Fusobacterium Infections/drug therapy , Fusobacterium Infections/etiology , Fusobacterium nucleatum/growth & development , Humans , Leukocytosis/cerebrospinal fluid , Leukocytosis/etiology , Low Back Pain/etiology , Male , Meningitis, Bacterial/cerebrospinal fluid , Meningitis, Bacterial/drug therapy , Meningitis, Bacterial/etiology , Metronidazole/therapeutic use , Middle Aged , Off-Road Motor Vehicles , Psoas Abscess/microbiology , Wound Infection/diagnosisABSTRACT
Human cytomegalovirus (HCMV) cloned EcoRI fragments R and b hybridized strongly, under standard high-stringency conditions, to uninfected cellular DNA of human, murine, or sea urchin origin. Less hybridization was detected with fragments, A, C, E, WL(F), WN(H), I, M, O, P, Q, V, c, d, and e. Southern blot analysis of the HCMV-related human DNA localized the major sites of hybridization of HCMV EcoRI fragments R, b, and d to defined regions of the 28S rRNA gene.
Subject(s)
Cytomegalovirus/genetics , DNA, Viral/analysis , Animals , Humans , Mice , Nucleic Acid Hybridization , Sea UrchinsABSTRACT
We have detected nucleotide sequences related to the transforming gene (v-myc) of avian myelocytomatosis virus MC-29 in the DNA genome of human cytomegalovirus (HCMV) strain AD169. Cloned DNA representing the entire 1.5-kilobase-pair oncogene v-myc and subfragments of this gene were hybridized to EcoRI-cleaved HCMV virion DNA and cloned subgenomic HCMV DNA fragments. Only a 0.5-kilobase-pair Pst I-Sal I subfragment representing the 5' end of the coding sequence of the v-myc oncogene hybridized to the HCMV DNA. We have localized these v-myc-related sequences to five regions in the long unique segment of the HCMV genome corresponding to EcoRI fragments C, I, P, R, and b and to regions within the EcoRI junction fragments F and H at or near the repeats bounding the short unique segment. There was no hybridization of these HCMV sequences to other retroviral oncogenes tested including v-src, v-myb, v-erb, v-ST-fes, v-fos, v-ras (Harvey), v-mos, and v-abl.
Subject(s)
Avian Sarcoma Viruses/genetics , Cloning, Molecular , Cytomegalovirus/genetics , Genes, Viral , Oncogenes , Base Sequence , DNA Restriction Enzymes , DNA, Viral/genetics , Humans , Nucleic Acid Hybridization , Species SpecificityABSTRACT
Antigenic determinants of mouse mammary tumor virus (MuMTV) from the low-mammary-tumor-incidence strain BALB/cNIV were compared by competition radioimmunoassay with those of MuMTV's isolated from several high- and low-mammary-tumor-incidence mouse strains, using rabbit hyperimmune sera against BALB/cNIV MuMTV and against MuMTV from the high-mammary-tumor-incidence strain BALB/cfC3H. Using anti-BALB/cfC3H serum in competition radioimmunoassay, BALB/cNIV MuMTV lacked antigenic determinants present on MuMTV's from the BALB/cfC3H, C3H, and GR strains. With anti-BALB/cNIV serum in competition radioimmunoassay, type-specific antigenicity was detected with BALB/cNIV MuMTV. We found class-specific antigenicities on BALB/cNIV MuMTV that were shared with RIII and C3Hf MuMTV's BALB/cNIV MuMTV was reportedly derived from the C3Hf strain by infection of BALB/c mouse mammary tissue after transplantation into a (BALB/c X C3Hf)F1 hybrid followed by retransplantation into the BALB/c strain (D. R. Pitelka, K. B. DeOme, and H. A. Bern. Proc. Am Assoc. Cancer Res. 6:51, 1965). However, BALB/cNIV MuMTV contained type-specific antigens not present on C3Hf MuMTV. The possible origin of these determinants is discussed.
Subject(s)
Mammary Neoplasms, Experimental/microbiology , Mammary Tumor Virus, Mouse/immunology , Animals , Antibodies, Neoplasm , Antibodies, Viral , Dose-Response Relationship, Immunologic , Epitopes , Female , Mammary Tumor Virus, Mouse/pathogenicity , Mice , RadioimmunoassayABSTRACT
Studies of mouse mammary tumor virus (MMTV) have been impeded by the lack of an in vitro infectivity assay. We have developed a rapid, quantitative in vitro assay for MMTV infectivity based on the detection of positively staining foci by immunoperoxidase. This assay and a 50% end-point titration of MMTV infectivity gave identical virus titers. Infection of a rat hepatoma cell line, a feline kidney cell line, and a normal murine mammary gland cell line by virus from the mouse mammary tumor GR3A cell line was linear with respect to virus concentration. The infectious titers obtained in both homologous and heterologous cell lines were not significantly different, demonstrating a lack of host range specificity. Virus infectivity was inactivated by heating at 55 degrees C and by ultraviolet irradiation. Rabbit anti-MMTV serum neutralized the infectivity with a 50% neutralization end point of 1:5000. Applications of this assay to the study of the immunological, biological, and biochemical characteristics of MMTV are discussed.
