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Biomedical subjects

S Rasheed

Publications and source records attributed to S Rasheed.

At least 109 records · Page 6Linked to original sources
PubMed1979

Different rat-derived transforming retroviruses code for an immunologically related intracellular phosphoprotein.

Kirsten sarcoma virus (Ki-MSV) and Harvey sarcoma virus (Ha-MSV) are mouse-rat recombinant viruses that were originally isolated by experimental inoculation of rats with helper-independent mouse type C viruses. We have recently identified in cells transformed by Ki-MSV or Ha-MSV, a phosphoprotein, p21, coded for by Ki-MSV and Ha-MSV [Shih, T.Y., Weeks, M.O., Young, H.A. & Scolnick, E.M. (1979) Virology 95, in press]. The p21, which is not a virion structural protein, was identified with antisera prepared by transplantation in rats of syngeneic Ha-MSV- or Ki-MSV-transformed nonproducer cells. In this study, we have applied the same methodology to examine a purely rat sarcoma virus (RaSV), which was isolated in cell culture by using helper-independent rat type C viruses [Rasheed, S., Gardner, M.B. & Huebner, R.J. (1978) Proc. Natl. Acad. Sci. USA 75, 2972-2976]. We report here that this new, purely rat sarcoma virus apparently codes for a p29, which shares immunological determinants and common V-8 protease-generated peptides with the p21 of Ha-MSV. The data suggest that the RaSV has acquired genetic information with similar coding capacity to some rat genetic information with similar coding combinant viruses, Ki-MSV and Ha-MSV. Based on data obtained on the p21 of a mutant of Ki-MSV temperature-sensitive for the maintenance of transformation, we suggest that the gene in RaSV that codes for the p29 is also required for the maintenance of RaSV-induced fibroblast transformation.

Animals↗
PubMed1979

Inhibition of spontaneous transformation of rat embryo cells releasing endogenous type C virus by virus-specific antiserum.

Noninbred Sprague-Dawley rat embryo cell clones predictably undergo transformation after 20-30 in vitro passages following spontaneous release of endogenous rat leukemia virus (RaLV). In the presence of RaLV-specific antiserum, virus production and infectivity were reduced and transformation was delayed from 6 to 25 weeks. Transformation was not associated with an increased expression of Kirsten murine sarcoma virus-related src gene RNA.

Animals↗
PubMed1979

Reversion of Kirsten sarcoma virus transformed human cells: elimination of the sarcoma virus nucleotide sequences.

The virus-specific nucleotide sequences in the RNA and DNA of a Kirsten mouse sarcoma virus (Ki-MSV)-transformed non-producer human osteosarcoma cell clone and two subclones of these cells that reverted to a normal phenotype have been analysed by hybridization of sarcoma virus-specific complementary DNA (cDNA) to cellular RNA or DNA. Whereas the transformed clone had acquired de novo Ki-MSV sequences in the RNA and DNA of the cells, both the revertant cell lines seemed to have lost most or all of this information from the cellular nucleic acids. The DNA from the revertant cells lacked the sequences represented either in the Ki-MSV-specific cDNA or in the total cDNA of the leukaemia-sarcoma virus complex. Thus, the reversion of the virus-transformed human cells to normal morphology is associated with the loss of most or all of the proviral sequences from the cellular DNA.

Base Sequence↗
PubMed1978

In vitro isolation of stable rat sarcoma viruses.

A Sprague-Dawley (SD-1) rat embryo culture, at low passage level, released an endogenous ecotropic type C virus (SD-RaLV) and after about 20 further passages it underwent spontaneous transformation. The SD-RaLV, released from the transformed cells, did not cause rapid transformation of other rat embryo cells. However, when the transformed cells were repeatedly cocultivated with three different chemically transformed and serially transplanted rat tumor cell lines (sarcoma, carcinoma, and hepatoma), rapidly fibroblast-transforming "sarcoma" viruses (RaSV) were recovered after each attempt. RaSV was not recovered from one of these tumor cell lines before transplantation, nor could focus-forming virus be rescued from these same tumor cells by cocultivation with other cells releasing heterologous type C viruses. Foci were induced on normal rat kidney and several other rat embryo cell strains within 7-15 days and both productive and nonproductive NRK clones were derived. The productive clones were positive for rat specific p30 antigen and the RaSVs released were serially transmitted to other rat embryo cells. RaSV genome was rescued from the nonproductive clones by superinfection with SD-RaLV, wild rat type C virus, and several heterologous type C viruses. These observations appear to represent naturally occurring transformation-specific (src) genes being recovered in vitro in the form of stable "sarcoma" viruses. These viruses differ from the Kirsten and Harvey strains of murine sarcoma virus in that they apparently contain no MuLV sequences and are of purely rat origin.

Animals↗
PubMed1978

In vitro lymphocyte transformation by Epstein-Barr virus (EBV)-like viruses isolated from Old-World non-human primates.

EBV-like viruses and lymphoid cell lines have been isolated from baboons and an orangutan. The cell lines have properties of B- or undifferentiated lymphocytes and have antigens and DNA related to those of EBV. The baboon virus has a broad in vitro transformation host range among lymphocytes of Old-World simian species whereas the orangutan isolate has a narrower host range. Baboon and orangutan viruses as well as EBV have shown transforming activity for gibbon lymphocytes. Baboon virus is infectious for rhesus monkeys and baboons but has not induced neoplastic disease in these species.

Animals↗
PubMed1977

Human bladder carcinoma: characterization of two new tumor cell lines and search for tumor viruses.

Two newly established human bladder carcinoma cell lines, designated HT-1197 and HT-1376, were characterized. Cells of both cultures exhibited fine structural microvilli and tonofibrils indicative of their epithelial origin. In addition, desmosomes were also present in HT-1197. Marker chromosomes present in HT-1197 and HT-1376 distinguished these from each other and from other known human tumor cell lines. Both cultures grew in soft agar, induced fibrinolytic activity, and were tumorigenic in mice and hamsters. No type C or other virus expression was detected in these cell lines nor in other human urothelial tumors tested.

Animals↗
PubMed1977

Characterization of purely ecotropic and amphotropic naturally occurring wild mouse leukemia viruses.

Two new strains of murine leukemia virus, one (strain 4996) purely ecotropic and the other (strain 1313) purely amphotropic, were isolated from spontaneous lymphomas in aged wild mice (Mus musculus). The 4996 virus is the first wild mouse field isolate which consists solely of ecotropic virus without the concomitant presence of amphotropic virus. The 1313 isolate is distinct in host range from seven other previously described wild mouse amphotropic isolates and is also the only murine leukemia virus shown to replicate in chicken cells.

AKR murine leukemia virus↗
PubMed1976

Acceleration of transformation of rat embryo cells by rat type C virus.

Sprague-Dawley and Fischer rat embryo cells became spontaneously transformed about 20 passages after release of endogenous ecotropic type C virus (SD-RaLV and F-RaLV). The virus-producing transformed cells showed loss of contact inhibition, increased growth rate, and tumorigenicity in vivo. Exogenous infection of other Fischer rat embryo cultures in early passage with SD-RaLV and F-RaLV markedly accelerated their rates of transformation.

Animals↗
PubMed1976

Spontaneous release of endogenous ecotropic type C virus from rat embryo cultures.

Type C viruses were isolated from embryo cultures of two different rat strains, Sprague-Dawley and Fischer. Both viruses (termed rat leukemia virus, RaLV) were released spontaneously from rat embryo cells, have a density of 1.14 to 1.15 g/cm(3) based on equilibrium sedimentation in sucrose gradients, contain 60-70S RNA, RNA-directed DNA polymerase, and rat type C virus-specific 30,000 molecular-weight-protein determinants. Molecular hybridization studies using the Sprague-Dawley RaLV 60-70S RNA show that the virus-specific nucleotide sequences are present in the DNA of rat embryos. Both Sprague-Dawley and Fischer RaLV can rescue the murine sarcoma virus genome from Kirsten murine sarcoma virus-transformed nonproducer cells and are neutralized by antisera to the RPL strain of RaLV. In contrast to previous RaLV's, these viruses propagate in their own cells of origin as well as in cells of heterologous rat strains.

Animals↗
PubMed1976

Amphotropic host range of naturally occuring wild mouse leukemia viruses.

Seven murine leukemia virus field isolates (uncloned) from wild mice (Musmusculus) of four widely separated areas in southern California show an unusually wide in vitro host range. They replicate well in human, feline, canine, guinea pig, rabbit, rat, and mouse cells, whereas bovine, hamster, and avian cells are resistant. Since this host range includes that of both mouse tropic (ecotropic) and xenotropic murine leukemia viruses, they are designated as "amphotropic". No purely xenotropic virus component is detectable in these field isolates. They may represent the "wild" or ancestral viruses from which the ecotropic and xenotrophic murine leukemia virus strains of laboratory mice have been derived.

Animals↗
PubMed1976

Lower motor neuron disease in wild mice caused by indigenous type C virus and search for a similar etiology in human amyotrophic lateral sclerosis.

In certain genetically susceptible populations of wild mice a progressive motor neuron disease with a long latent period is caused by indigenous type C leukemia virus. Neuronal damage appears to be due primarily to a direct neurotropic effect of the virus and not to an immunogenic mechanism. The disease can be prevented by antiviral genetic means. Search for a similar virus in humans with ALS has been negative.

Amyotrophic Lateral Sclerosis↗