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Biomedical subjects

W P Rowe

Publications and source records attributed to W P Rowe.

At least 73 records · Page 4Linked to original sources
PubMed1976

Quantitative studies of integration of murine leukemia virus after exogenous infection.

Using a [3H]DNA probe prepared from AKR murine leukemia virus, we determined the number of copies of the AKR virus genome integrated into the cellular DNA after exogenous infection of NIH mouse, AKR mouse, and rat cells in tissue culture. NIH mouse cells, which lack a portion of the viral genome (referred to as Gross-AKR specific sequences), incorporated three to four copies of these sequences per haploid genome. AKR cells, in which the Gross-AKR specific sequences are already present as three to four copies per haploid genome, did not shwo any distinct change in copy number after infection. Rat cells, which lack DNA sequences homologous to murine leukemia virus, incorporated one copy of the viral genome per haploid genome. It is inferred that the presence of viral sequences may affect the efficiency of integration of exogenous provirus, and that there may be a limit to the number of copies that can be inserted.

AKR murine leukemia virus↗
PubMed1976

Changes in expression of murine leukemia virus antigens and production of xenotropic virus in the late preleukemic period in AKR mice.

We recently reported that thymocytes from 6-month-old preleukemic AKR mice express higher levels of murine leukemia virus (MuLV)-related antigens that thymocytes from 2-month-old mice. We have now found that the level of xenotropic MuLV (defined operationally as MuLV able to infect mink cell cultures) is also markedly increased in thymus of 6-month-old AKR mice and that this increase in virus correlates closely with increased MuLV-antigen expression. There is no increase of MuLV antigen or xenotropic virus in spleen or lymph nodes. Production of ecotropic MuLV remains unchanged with age in thymus, lymph nodes, and spleen. Thymic grafts from 6-month-old AKR mice, but not from 2-month-old mice, induce both amplified MuLV-antigen expression and xenotropic virus production in the thymus of young AKR recipients. Experiments with lethally irradiated AKR mice reconstituted with syngeneic bone marrow cells indicate that age-related changes in the thymus rather than in bone marrow precursor cells are responsible for MuLV-antigen amplification.

Aging↗
PubMed1976

Lymphocytic choriomeningitis virus infection in fetal, newborn, and young adult Syrian hamsters (Mesocricetus auratus).

The pathogenesis of lymphocytic choriomeningitis virus infection in fetal, newborn, and young adult hamsters was studied. Infected newborn hamsters initially developed a persistent viremia and viruria with titers often in excess of 10(4.0) mean infectious doses/0.03 ml of blood or urine. After week 12 two different patterns of infection became evident. Approximately one-half of the hamsters eventually cleared the infection, whereas the others developed a chronic progressive and ultimalely fatal disease characterized by continuous high-titered viremia and viruria and high titers of virus in their tissues. Complement-fixing antibody and, to a lesser degree, virus-neutralizing antibody coexisted with the viremia. Hamsters with persistently high levels of viremia and viruria developed chronic glomerulonephritis and widespread vasculitis, whereas hamsters that cleared their infections did not develop these lesions. Litters of hamsters born to viremic mothers were invariably infected. Litter sizes were small and breeding effectiveness was reduce; however, vertical, congenital infection was successfully passed through three generations. The course of infection in the congenitally infected hamsters was similar to that in newborn infected hamsters, with all animals producing complement-fixing antibody, some animals being capable of clearing the viremia and remaining healthy, and other animals having persistent viremia and fatal disease. Inoculated young adult hamsters did not become diseased, developed viremia and viruria which persisted up to 3 and 6 months, respectively, and developed complement-fixing antibody by 10 days after infection. The prolonged urinary excretion of large amounts of lymphocytic choriomeningitis virus by asymptomatic, chronically infected hamsters is an important public health consideration when dealing with potential human infection.

Aging↗
PubMed1976

Naturally occurring murine leukemia viruses in wild mice: characterization of a new "amphotropic" class.

A new class of murine leukemia viruses, isolated from wild Mus musculus trapped in California, is described. These viruses, designated "amphotropic," replicate in mouse, rabbit, mink, human, guinea pig, and rat cells, but not in hamster, quail, or duck cells. They show N-tropism for mouse cells, and do not trigger the XC cell response. They are distinct by interference and virus neutralization testing from the previously recognized mouse-tropic and xenotropic MuLV classes. Mouse-tropic viruses occuring along with three of the four amphotropic isolates were found to be distinguishable by virus neutralization from other mouse-tropic murine leukemia virus strains of laboratory mouse origin.

Animals↗
PubMed1976

Adenoviridae.

The elevation of the genus Adenovirus to a family named Adenoviridae is described. This family at the present stage contains two genera, mammalian adenoviruses--Mastadenovirus--and avian adenoviruses--Aviadenovirus. The two genera are separated primarily on the basis of difference in immunological properties of the virions.

Adenoviridae↗
PubMed1975

Correlation of early murine leukemia virus titer and H-2 type with spontaneous leukemia in mice of the BALB/c times AKR cross: a genetic analysis.

Tissue extracts from 6-wk old mice of the AKR strain (H-K) show high levels of infectious murine leukemia virus, and these mice show a near 100% incidence of spontaneous leukemia. In F1 mice of the cross, BALB/c times AKR (H-2K/H-2K), both the occurrence of virus and the incidence of spontaneous leukemia are suppressed to very low values, due largely to the presence of the FV-1b allele inherited from the BALB/c parent. Mice of the (BALB/c times AKR) F-1 times AKR backcross generation were observed for possible correlations between virus expressions at 6 wk of age, H-2 type and leukemia incidence. H-2 type showed at most a weak influence on the occurrence of infectious virus, but there was a very strong correlation between the level of virus expression and the occurrence of leukemia and a strong correlation between H-2 type and leukemia. In addition, there was a highly significant nonrandom distribution of virus-negative mice among the backcross litters, suggesting a maternal effect on virus expression.

Animals↗
PubMed1975

Definitive evidence that the murine C-type virus inducing locus Akv-1 is viral genetic material.

DNA of the AKR mouse contains a set of murine leukemia virus sequences that are not present in DNA of the NIH Swiss mouse. NIH mice partially congenic for the AKR murine-leukemia-virus-inducing locus Akv-1 contain this set of sequences, and, in a three-point cross segregating for Akv-1 on an NIH background, the sequences segregated with Akv-1. It is concluded that the Akv-1 locus contains viral sequences.

AKR murine leukemia virus↗
PubMed1975

Qualitative and quantitative studies of AKR-type murine leukemia virus sequences in mouse DNA.

Utilizing a single-stranded [3H]DNA probe highly representative of AKR viral 70S RNA, we have performed association kinetics experiments with cellular DNA in vast excess from 3 high-, 5 low- and 4 non-virus-yielding mouse strains. Our hybridization studies indicate that in the strains so far tested, the complete genome of the AKR-type MLV is present in the DNA of the embryos of both high- and low-virus-yielding mouse strains, while DNA of non-virus strains contains only a part of the genome. Furthermore, at least two populations of virus-specific DNA sequences can be identified (more abundant and less abundant species) according to their rate of association. Low-virus-yielding mouse strains contain a smaller number (1-2 copies) of the less abundant species, and thus a lower number of complete viral genome than do high-virus strains (3-4 copies). Non-virus-yielding strains are lacking these less abundant sequences in their genome. DNA from wild Mus musculus also contained viral sequences, the sample tested showing association kinetics identical to the non-virus-producing strains. Thus there is a good correlation between completeness of the AKR-type MLV genome in cellular DNA and the capacity of the cells to release AKR-type MLV. Mice of a non-virus-yielding strain made partially congenic for the AKR virus-inducing locus Akv-1 contained the complete virus genome, confirming that this locus consists of structural genes of the virus.

AKR murine leukemia virus↗
PubMed1975

Studies of FBJ osteosarcoma virus in tissue culture. II. Autoinhibition of focus formation.

A high-titered non-focus-forming virus, FBJ-MuLV (murine leukemia virus), present in FBJ tumor preparations, inhibited significantly the expression and production of FBJ-MuSV (murine sarcoma virus) in tissue culture. This "autoinhibition" was comparable to that observed when a 3- to 4-log excess of infectious MuLV was added to standard MuSV. The degree of inhibition was influenced by the tropism of the MuLV (or the ease of spread and propagation of MuLV in certain cells), multiplicity of infection by MuLV, amount of excess MuLV, and ability of the MuSV-transformed cells to replicate independently. The FBJ MuLV-MuSV complex may be a model system for the detection of sarcoma viruses in spontaneous tumors in various animals where inhibition by excess nontransforming virus could be an important biologic phenomenon.

Animals↗
PubMed1974

Evidence that the AKR murine-leukemia-virus genome is complete in DNA of the high-virus AKR mouse and incomplete in the DNA of the "virus-negative" NIH mouse.

The AKR mouse has a high titer of murine leukemia virus early in life, and virus-negative cells derived from embryos of this mouse strain can be activated to yield murine leukemia virus by treatment with 5-iododeoxyuridine. In contrast to this high-virus strain, the NIH Swiss mouse has a low incidence of leukemia and no murine leukemia virus has been isolated from it (virus-negative). We have investigated this difference between AKR and NIH mice by examining the sequences specific for murine leukemia virus in nucleic acids of these mice. A single-stranded viral-DNA probe synthesized in vitro using murine-leukemia-virus from the AKR mouse contains at least 87% of the sequences present in the 70S viral RNA; most of these sequences are in proportions similar to their content in the 70S RNA. Using this probe in nucleic acid hybridization experiments, we have shown that NIH-mouse-cell DNA and AKR-mouse-cell DNA differ with respect to sequences specific for AKR murine-leukemia-virus: NIH-mouse-cell DNA lacks some of the virus-specific sequences present in AKR-mouse-cell DNA, and there are two distinct sets of virus-specific sequences in AKR-mouse-cell DNA, whereas there is only one set in NIH-mouse-cell DNA.RNA from virus-negative AKR-mouse cells grown in tissue culture contains some, but not all, virus-specific RNA sequences; however, within 48 hr after initiating treatment of these cells with 5-iododeoxyuridine, the complete viral genome is represented in cellular RNA.

Animals↗
PubMed1974

Initiation of oncogenic transformation of mouse lymphocytes in vitro by Abelson leukemia virus.

While C-type RNA viruses are known to induce leukemias and lymphomas, oncogenic transformation of lymphoid cells by them in vitro has not been reported. In this study, splenocytes from female BALB/c mice were infected in vitro with Abelson virus, a C-type RNA virus that induces nonthymic lymphomas and plasmacytomas in mice. The cells were transplanted into recipients of different karyotype, either male BALB/c mice or hybrid BALB/c x AL/N (CALF1) mice, which bear the Rb(5.19)1Wh translocation. Transplants of eight of the resulting tumors (one plasmacytoma and seven lymphomas) contained cells of donor BALB/c karyotype, indicating that transformation of splenocytes occurred in vitro.

Animals↗
PubMed1974

AKR murine leukemia virus genome: frequency of sequences in DNA of high-, low-, and non-virus-yielding mouse strains.

Studies with a single-stranded DNA probe complementary to the RNA of mouse-tropic AKR murine leukemia virus indicate that the complete genome of the AKR-type murine leukemia virus is present in the DNA of high- and low-virus-yielding mouse strains, while DNA of non-virus-yielding strains contains only a part of the genome. Furthermore, in those strains where the genome is complete, two populations of virus-specific DNA sequences can be identified (more abundant and less abundant species) according to their rate of association with the probe. Low-virus-yielding mouse strains contain fewer copies of the less abundant species and, consequently, fewer complete viral genomes than do high-virus-yielding strains. Thus, in the ten strains tested, there is a good correlation between completeness of the genome of AKR-type murine leukemia virus in cellular DNA and the capacity of the cells to release infectious AKR-type murine leukemia virus. Moreover, the number of complete viral genomes correlates with the frequency of infectious virus production by virus-positive strains. DNA from wild Mus musculus also contained viral sequences, the sample tested showing reassociation kinetics identical to the non-virus-producing strains.

Animals↗
PubMed1974

Arenaviruses.

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Antigens, Viral↗