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Biomedical subjects

M M Lieber

Publications and source records attributed to M M Lieber.

At least 235 records · Page 13Linked to original sources
PubMed1975

Isolation from the asian mouse Mus caroli of an endogenous type C virus related to infectious primate type C viruses.

Treatment of a cell line derived from the Asian feral mouse Mus caroli with 5-bromodeoxyuridine induces an infectious, xentropic type C virus. This virus shares strongly cross-reactive reverse transcriptase (RNA-dependent DNA polymerase) and p30 antigens and crossinterferes with type C viruses isolated from a woolly monkey (SSAV) and gibbon apes (GALV). By similar criteria, the caroli virus is much less related to previously described type C viruses of the laboratory mouse, Mus musculus. Induction of virus from 10 of 13 single cell clones indicates that the virus is endogenous in Mus caroli cells. Thre results suggest that infectious primate type C viruses arose by trans-species infection(s) of certain primates with endogenous type C viruses from MUs caroli or a closely related Mus species.

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PubMed1975

Endogenous primate and feline type C viruses.

1. Endogenous type C viruses have been detected in a wide variety of mammalian species. Multiple copies of related, but not identical, virogene sequences can be found in the DNA of these species. 2. The endogenous type C virogenes are subject to the pressures of natural selection, and closely related species possess related virogene sequences. These genes evolve as cellular entities diverging from one another in a manner which correlates well with taxonomic relatedness of the species. 3. The endogenous type C viruses of baboons and domestic cats are related, but they can be distinguished by biologic and immunologic criteria and by partial nucleic acid sequence homology. Virogene sequences in the DNA of Old World monkeys and domestic cats also show a degree of relatedness not shared by the unique sequence DNA of these species. The data suggest that progenitors of domestic cats were exogenously infected by a type C virus that also gave rise to present-day endogenous type C viruses of Old World monkeys. 4. The genomes of exogenously infectious viruses replicating in permissive host cells appear to evolve much more rapidly than endogenous virogenes which replicate as cellular genes. Laboratory strains of efficiently oncogenic type C viruses are presumed to be derived from activated endogenous viruses which have been selected for virulence and which, in certain cases, have acquired the capacity to replicate in the host's own cells. 5. The ubiquitous presence of endogenous type C viruses among vertegrates and their preservation throughout millions of years of evolution suggests that these genes express normal physiologic functions which provide a selective advantage to the species.

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PubMed1975

Nucleic acid homology of murine xenotropic type C viruses.

Two major subclasses of xenotropic (X-tropic) murine type C viruses can be distinguished by nucleic acid hybridization. The most frequently encountered subclass (MuLV-X-alpha) includes isolates from BALB/c, C57BL/6J, C58/J, AKR/J, CBA/J, and DBA/2J inbred strains and from the Asian feral mouse subspecies Mus musculus molossinus. The other subclass (MuLV-X-beta) consists of viruses isolated from the NIH Swiss and NZB/BINJ strains. Thus, significant polymorphism exists among the endogenous type C virogenes of a single species, Mus musculus. MuLV-X-alpha genes are found in strains that also have endogenous mouse-tropic viruses (either N-tropic, B-tropic, or both), whereas the MuLV-X-beta subclass is restricted to mouse strains from which mouse-tropic viruses have not yet been isolated. The results are consistent with a model which proposes that mouse-tropic endogenous viruses are derived from the MuLV-X-alpha subclass.

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PubMed1974

A distinct class of inducible murine type-C viruses that replicates in the rabbit SIRC cell line.

The existence of the selectively permissive rabbit cell line SIRC allows definition of a new class of endogenous murine type-C virus. Continuous clonal lines of transformed cells derived from the BALB/c mouse-embryo cell line BALB/3T3 contain at least two distinct classes of endogenous type-C viral genomes. Spontaneously released endogenous viruses grow well on the mouse cell line NIH/3T3 (N-tropic viruses) but not on the rabbit cell line SIRC. Type-C viruses induced by treatment with BrdU grow well on SIRC (S-tropic viruses) but not in NIH/3T3 or BALB/3T3. BrdU-treated AKR mouse-embryo cells also release an S-tropic virus. N-tropic and S-tropic viruses both have the mouse intraspecies gs-1 and viral RNA-directed DNA polymerase antigenic determinants. DNA.RNA hybridization techniques reveal that the two host-range classes of endogenous viruses are only partially related to each other. Cell transformation facilitates the spontaneous release of the N-tropic viruses; treatment with thymidine analogues induces the production of the S-tropic viruses. Thus, the two classes of viral genomes appear to be subject to different cellular controls.

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PubMed1974

Nucleic acid homology of murine type-C viral genes.

The nucleic acid sequence homology between various murine, endogenous type-C viruses (three host range classes of BALB/c virus, the AT-124 virus, and the CCL 52 virus) and two laboratory strains of murine leukemia virus (Rauscher and Kirsten) was determined by DNA:RNA hybridization. The viral sequences exhibit varying degrees of partial homology. DNA:DNA hybridizations were performed between [(3)H]DNA probes prepared from N- and X-tropic BALB/c endogenous viruses and cellular DNAs from BALB/c, NIH Swiss, and AKR inbred mouse strains as well as from California feral mice and the Asian mouse subspecies Mus musculus molossinus and M. musculus castaneus. All of these strains of mice are shown to possess multiple (six to seven per haploid genome), partially related copies of type-C virogenes in their DNAs. Thermal melting profiles of the DNA:RNA and DNA:DNA hybrids suggest that the partial homology of the viral nucleic acid sequences is the result of base alterations throughout the viral genomes, rather than the loss of discrete segments of viral sequences.

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