Simian Adenovirus SA7 Research Articles

Transformation of rodent cells by simian adenovirus SA-7.

A clone of the hamster cell line NIL-2 cells and primary rat embryo cells were transformed by simian adenovirus SA-7. The transformed NIL-2 cells formed foci of multilayered growth in monolayer cultures under agar and colonies when suspended in agar medium. The transformed rat cells formed foci under liquid medium. Cell lines were derived from both NIL-2 and rat transformed cells. A virus stock containing 1.8 × 109 particles and 2.5 × 108 PFU/ml contained 8 × 103 FFU/ml in NIL-2 cells and 4.6 × 102 FFU/ml in rat embryo cells. Approximately 3.1 × 104 infectious units were required to induce one focus in NIL-2 cells and 5.4 × 105 infectious units were required in rat embryo cells. The transformed NIL-2 cells contained SA-7-specific tumor antigens and RNA. They formed colonies in agar and induced tumors in hamsters with characteristic adenovirus-induced tumor pathology.

Large- and small-plaque variants of oncogenic Simian Adenovirus SA7(C8).

AbstractPreparations of simian adenovirus SA7, strain C8, highly oncogenic for hamsters, contain a mixture of large‐ and small‐plaque variants. The variants do not differ in their adsorption rates, virus yield per cell, sensitivity to sulfated agar polysaccharides or antigenic properties, as determined by neutralization tests. However, the small‐plaque variant releases infectious virus from cells at a slower rate than the large‐plaque variant. It is also more oncogenic for hamsters than the large‐plaque variant, but the tumors induced by the two variants do not differ morphologically. The variants seem to induce a transplantation antigen of similar or related antigenicity. Fewer cells are required for transplantation of tumors induced by the original virus and the small‐plaque variant than for transplantation of tumors induced by the large‐plaque variant.

Morphology of tumors induced in hamsters by simian adenoviruses.

AbstractSubcutaneous hamster tumors induced by Simian adenovirus SA7, strains C8, B105 and C626, were found to be poorly differentiated sarcomas having morphological features which distinguish them from tumors induced at the same site by papovaviruses and the Rous sarcoma virus. In general, the adenovirus‐induced tumors were morphologically alike, C8‐induced sarcomas showing some differences. Tumors induced by this strain in the subcutaneous tissue, muscles, peritoneum and mediastinum were morphologically identical. Tumors found in the brain were mainly malignant ependymomas and choroid plexus carcinomas, generally originating in neuroectoderm.The oncogenicity of adenovirus SA7 (C8) in meso‐ and ectodermal cells has thus been demonstrated.

Base composition of the DNA of oncogenic simian adenovirus SA7 and homology with human adenovirus DNA's

Base composition of the DNA of oncogenic simian adenovirus SA7 and homology with human adenovirus DNA's

Transformation of newborn hamster cells with simian adenovirus SA7.

AbstractNewborn Syrian hamster skin cells can be transformed in vitro by simian adenovirus SA7. The transformation occurs within 6–8 days of treatment with virus and the transformed cells give rise to tumour development when they are re‐inoculated into weanling hamsters.

Simian adenovirus SA7 DNA: chemical, physical, and biological studies.

Experimental Procedures.-M11aterials: A 13SC-1 cell line was obtained from lDr. RI. N. Hull; CV-1 was provided by Dr. Leroy McLaren. Simian adenovirus type SA7 was obtained from Dr. R. N. Hull. Snake venom phosphodiesterase, papaini (2X crvstallized), and electrophoretically purified pancreatic DNase I were purchased from Worthington Biochemical Corporation. RNase, sniake venom (Crotalus adamanteus), subtilisin, and alpha-chymotrypsin were obtained from Sigma Chemical Company. P'2-orthophosphate was obtained from the New England Nuclear Corporation. Cesium chloride was purchased from the American Potash Corporation and the Gallard Schlesinger Company. SV40 tumor antiserum was provided by Dr. W. Rowe; and SV40 tumor antigen was obtained from Flow Laboratories (Rockville, Maryland). Virus and cell culture: All cells were routinely propagated in Eagle's (MEM) medium with 10% fetal calf serum. The virus pools were produced by infecting monolayer cultures at a multiplicity of infection of 1-10 in MEM with 5% fetal calf serum and harvesting the infected cells at 36-48 hr postinfection. Virus purification: The virus was concentrated and purified by a procedure to be described in detail elsewhere.5 Briefly, the infected cells were disrupted by sonication; and the resulting virus suspension was treated sequentially with a combination of RNase, DNase, and snake venom followed by subtilisin anid alpha-chymotrypsin. The virus was then concentrated by centrifugation onto a CsCl cushion in a Spinco SW25.1 rotor at 25,000 rpm for 2 hr. The collected virus ban-d was centrifuged at least two times to equilibrium in a CsCl gradient. The final viruts bands were stored at 4?C in 35% CsCl or dialyzed against 0.15 411 NaCl containinig 0.01 Ml sodium phosphate, p1,1 7, and 0.001 M1 ethylenediaminietetraacetate (ED)TA) and stored frozen at 90C. Extraction of viral DNA: 1B3eta-mereaptoethanol (20 ,l) and papain (I mg) were added to each milliliter of dialyzed virus containing approximately 10 mg of virus. The mixture was incubated for 10-12 mini at 37?C or until visible clearing was obtained. Twenlty mg/ml of solid sodium dodecyl sulfate (SDS) was then added and incubation continued for 7 mimi at 37?C. This mixture was extracted at room temperature with an equal volume of phenol containing 0.2% 8-hydroxyquinoline. The aqueous phase was reextracted two times with fresh phenol. Traces of phenol were removed either by dialysis against 0.1 X SSC (SSC = 0.15 Ml NaCl + 0.015 M sodium citrate), or by precipitation and spooling of the DNA witb ethanol. The final preparation was stored in SSC with a drop of chloroform at 4?C. Density of DNA: The buoyant densities of native and alkali-treated viral DNA were determined in an equilibrium density gradient of CsCl containing 0.01 M tris(hydroxymethyl)aminomethane (tris) buffer, pH 7.4. Alkali-denatured DNA was prepared by exposing DNA, in 0.1 X SSC, to 0.2 N NaOH for 10 min at room temperature followed by neutralization with HCl. In each experiment, Micrococcus lysodeikticus or E. coli DNA was added as a standard. Centrifugations were performed at 25?C and 44,770 rpm in the Spinco model E ultracentrifuge equipped with ultraviolet absorptionl optics. Photographs were analyzed with a Spinco Analytrol densitometer.

Effects of ultraviolet irradiation on the transforming and plaque-forming capacities of simian adenovirus SA7.

Effects of ultraviolet irradiation on the transforming and plaque-forming capacities of simian adenovirus SA7.