Murine sarcoma virus transformed mouse 3T3 cells, which are negative for murine leukemia virus and which yield sarcoma virus after superinfection with murine leukenmia virus, spotaneously give rise to flat variants front which murine sarcoma virus can no longer be rescued. The revertants support leukemia viruis growth and show an enhanced sensitivity to murine sarcoma superinfection and, like normal cells, do not release RNA-dependent DNA polymerase activity. Because revertants could be obtained with high frequency from progeny of single transformed cells, each cell that containts the sarconma virus genome seems to have the capacity to suppress or eliminate an RNA tumor virus native to its species of origin.
Abstract Cloned cat cells (CCC) transformed by the m1 isolate of Moloney murine sarcoma virus (MSV) have the properties of sarcoma-positive, leukemia-negative (S+L-) cells. Over the past 5 years, partially flat as well as very contact-inhibited variant clones were isolated from several clonal generations of S+L- cat cells. Partially flat subclones still contained the MSV genome and could serve as useful cell systems for quantal assays for a number of replicating retroviruses. The frequency of isolation of rescue-negative, very flat subclones diminished with sequential cloning cycles of S+L- cells. The rescuenegative revertant cells grew to low density in liquid media, were more similar to normal cells in soft-agar colony formation, and were intermediate in concanavalin A agglutinability when compared to normal or S+L- cells. Revertants could be retransformed by pseudotypes of MSV other than MSV coated with feline endogenous xenotropic virus. Feline endogenous xenotropic virus was readily induced from S+L- cells but was not inducible from some revertants by halogenated pyrimidines. Rescue-negative revertants could support the growth of a number of helper viruses. Chromosomes of parental CCC normal cells, MSV producer cells, S+L- cells, or revertants were all significantly hypodiploid. No stable pathognomonic changes were observed relative to type and chromosome number among the above. The MSV-coded precursor polyprotein with a molecular weight of 60,000 was detected in producer and S+L- cells but not detected in revertants. Producer and S+L- cells had multiple MSV src copies in their DNA, whereas revertants did not contain residual src DNA. The number of either feline endogenous xenotropic virus or feline leukemia virus-like DNA copies was not different among producer, S+L-, or revertant cells. Accordingly, all rescue-negative cat cell revertants tested have lost multiple copies of MSV proviral DNA.
Microbiology Society journals contain high-quality research papers and topical review articles. We are a not-for-profit publisher and we support and invest in the microbiology community, to the benefit of everyone. This supports our principal goal to develop, expand and strengthen the networks available to our members so that they can generate new knowledge about microbes and ensure that it is shared with other communities.
Journal Article SOME BACTERICIDAL AND VIRUCIDAL PROPERTIES OF IODINE NOT AFFECTING INFECTIOUS RNA AND DNA Get access YU-CHIH HSU, YU-CHIH HSU Search for other works by this author on: Oxford Academic PubMed Google Scholar SHIGEKO NOMURA, SHIGEKO NOMURA Search for other works by this author on: Oxford Academic PubMed Google Scholar CORNELIUS W. KRUSÉ CORNELIUS W. KRUSÉ Search for other works by this author on: Oxford Academic PubMed Google Scholar American Journal of Epidemiology, Volume 82, Issue 3, November 1965, Pages 317–328, https://doi.org/10.1093/oxfordjournals.aje.a120552 Published: 01 November 1965 Article history Received: 09 April 1965 Published: 01 November 1965
SUMMARY Mouse and cat cells were each examined for the mode of restriction of endogenous xenotropic oncornavirus. Murine xenotropic helper virus (MuX) and its pseudo-type of Moloney murine sarcoma virus (MSV(MuX)) were grown in cat cells to high titre. MuX alone did not replicate in any mouse cell tested including normal or transformed outbred Swiss 3T3 cells or SC-1 cells, but did grow in a variety of other mammalian cells. MSV(MuX) was not able to achieve that intracellular state from which it could be rescued by mouse leukaemia virus (MuLV) in any mouse cell tested with the exception of SC-1 cells. Detection of MSV(MuX) foci with appropriate helper virus was as sensitive in SC-1 cells as in the cells of several other species. Sequential passage of MSV(MuX) virus complex in SC-1 cells resulted in a loss of infectious sarcoma and helper viruses, but transformed, MSV rescuable cells were retained. If cat embryo cells were infected with either the feline endogenous xenotropic virus (FeX) or its MSV pseudotype (MSV(FeX)), two analogous states of restriction were observed. FeX alone did not replicate in cat cells as measured by release of progeny virus or by FeX group-specific antigen induction. Cat cells could be susceptible or insusceptible to the entry of MSV(FeX) as measured by MSV rescue with appropriate ecotropic feline leukaemia virus. The sensitivity of detection of MSV(FeX) foci in some cat cells in the presence of feline ecotropic virus was comparable to that exhibited by cells of other mammalian species. A single strain of cat cells underwent a change in its restrictive capacity for MSV(FeX) on prolonged passage. Late passage cat cells became very insusceptible to MSV(FeX) but not to other pseudotypes of MSV. Infectious FeX or its group-specific antigens were not detected in the insusceptible cells. The major glycoprotein of FeX did appear as a surface antigen of the insusceptible cells. It is apparent that two levels of cellular restriction can be distinguished in each of two mammalian cell systems by the susceptibility to penetration of MSV coated with endogenous xenotropic oncornavirus.
The 61-amino-acid agnoprotein is a nonessential polypeptide encoded by the late leader region of simian virus 40 which appears to play a role in viral assembly. A 2-base-pair (bp) insertion mutant (in2379) was created by altering the coding region of this protein. This mutation prevents the synthesis of the agnoprotein and, in contrast to the more extensive deletion mutations previously described in this region, might be expected to have a lesser effect on the template for late viral transcription. In fact, the 2-bp insertion mutant grew significantly less well than most mutants containing larger deletions in the agnoprotein region and frequently gave rise to stock containing second-site alterations in the same region. These observations suggested that the defect in mutant in2379 extends beyond the loss of the agnoprotein. Characterization of a number of second-site mutants indicated that all of them grew more efficiently than the original 2-bp insertion mutant. Based on the nucleotide sequence of these mutants, we suggest possibilities for the deleterious effect induced by the insertion in mutant in2379.
I. Brain and spinal cord of mouse infected and paralyzed with poliomyelitis virus Lansing strain were inserted into bananas and were orally administered to 9 cynomolgus monkeys. Tokyo strain virus (type 2) was also administered to 6 monkeys in the same way. None of of all the 15 monkeys manifested the signs of apparent infection by the oral administration of the virus.II. Viremia was recognized on 6 of 15 monkeys during the period ranging from the very day of the virus administration to 4-5 days after it. Also of 3 among 7 groups the viruses were positive in stool specimens only on the next day of the virus administration.III. Two monkeys which had inoculated with cow serum γ-globulin were both viremia negative, and their stool specimens were also virus negative.IV. Noticable increase of neutralizing antibody of the monkey sera was not observed after the oral administration of the viruses.
A continuous cell culture designated SS5 was established from a lymph node biopsy specimen taken from a male with Hodgkin's disease. The cells grew in suspension as aggregates, in pairs, and singly. During their logarithmic growth the cell doubling time was approximately 24 hours. Chromosome studies were carried out on cells from the patient's bone marrow, the lymph node biopsy before culture, and again after 4 months' culture. On direct examination, the bone marrow and lymph node showed no abnormalities. After 4 months in culture, 89% of the cells examined had 46 chromosomes and were pseudodiploid. There were a low incidence of polyploidy (0.4%) and a low incidence of cells with aberrations (4%). Electron microscope examination showed that the cells carried two kinds of virus-like particles: the herpes-type virus which has been described for cultured Burkitt's tumor cells, and other particles of about the same size with morphology suggestive of a different type of virus. Since the herpes-type virus will not replicate in monolayer cultures, we could separate the two types by inoculating WI38 monolayer cultures with a cell-free concentrate from the SS5 line. Virus replication on passages in the WI38 cells was obvious by specific cellular changes, but only occasional virus-like particles were demonstrable by electron microscopy in the early passages. After 20 passages, abundant virus became evident as extracellular particles. When virus from the WI38 culture was introduced into a human lymphocyte suspension culture, massive virus budding from the cell membrane became evident. The virus ranged from 90–150 mμ, with most about 120 mμ in diameter, and produced a filamentous component 15 mμ in diameter. The filaments were shown to become the nucleoid of the budding virus. The virus was similar immunologically to simian virus SV5.
'%3e%3ccircle r='20' fill='%23008'/%3e%3ccircle r='17.5' fill='%23fff'/%3e%3ccircle r='3.5' fill='%23008'/%3e%3cg id='d'%3e%3cg id='c'%3e%3cg id='b'%3e%3cg id='a' fill='%23008'%3e%3ccircle r='.875' transform='rotate(7.5 -8.75 133.5)'/%3e%3cpath d='M0 17.5.6 7 0 2l-.6 5L0 17.5z'/%3e%3c/g%3e%3cuse xlink:href='%23a' transform='rotate(15)'/%3e%3c/g%3e%3cuse xlink:href='%23b' transform='rotate(30)'/%3e%3c/g%3e%3cuse xlink:href='%23c' transform='rotate(60)'/%3e%3c/g%3e%3cuse xlink:href='%23d' transform='rotate(120)'/%3e%3cuse xlink:href='%23d' transform='rotate(-120)'/%3e%3c/g%3e%3c/svg%3e)
