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At least 289 records · Page 16Linked to original sources
PubMed1965

STUDIES ON PROTEIN AND NUCLEIC ACID METABOLISM IN VIRUS-INFECTED MAMMALIAN CELLS. THE FORMATION OF A VIRUS-SPECIFIC ANTIGEN IN KREBS II ASCITES-TUMOUR CELLS INFECTED WITH ENCEPHALOMYOCARDITIS VIRUS.

1. Krebs II mouse ascites-tumour cells infected with encephalomyocarditis virus were found to contain, in addition to mature virus, a virus-specific protein antigen. An assay, based on the ability of this antigen to block the neutralization of purified virus by its specific antiserum, was developed. 2. This antigen was present both in the culture fluid 17 hr. after the infection of cells with virus and intracellularly, where its titre increased at a time when viral capsid protein was being synthesized. Within the cell, it was mostly localized in the soluble cell sap. 3. In contrast with virus, the antigen did not agglutinate sheep erythrocytes, and its immunological properties were destroyed by digestion with trypsin. Ribonucleic acid was not detected in concentrated preparations of the antigen, nor was the titre of antigen affected by ribonuclease. 4. The antigen had a sedimentation coefficient (20 degrees ) of approx. 14s, and its diffusion coefficient, determined by the method of Allison & Humphrey (1960), was 3.2x10(-7) cm.(2)sec.(-1). The particle weight of the antigen was hence 420000+/-40000. 5. The capsid protein from purified encephalomyocarditis virus could be degraded by treatment with ethanolamine into a protein of sedimentation coefficient (20 degrees ) of approx. 4s. The 14s antigen, when similarly treated, yielded a protein of similar size. However, no such smaller antigen was detected in virus-infected cells. 6. It is concluded that the non-haemagglutinating antigen represents a polymeric form of the basic viral capsid-protein molecule and that it is synthesized in the cytoplasm of infected cells. It may be either an intermediate or a by-product in the process of viral capsid-protein synthesis.

Animals↗
PubMed1963

An electron microscope study of the development of SV40 virus.

Kidney cells, predominantly from Cercopithecus monkeys but also from baboons, were infected in vitro with the SV40 virus. The infectious cycle was studied with the electron microscope by means of thin sections of cells fixed from 3 hours up to 11 days after infection. The frequency of virus formation and various nuclear and cytoplasmic lesions in relation to the infection are described. The virus particles appear in the nucleus in close contact with the chromatin. In a small number of cells they have been observed as early as 10 to 12 hours after infection, but most often they appear 24 to 48 hours afterward. Their mean diameter is 33 mmicro. They have no membrane and are frequently arranged as crystal-like structures. In addition to the appearance of virus, one observes various lesions in the nucleoplasm and particularly in the nucleolus, which shows an early hypertrophy and produces unusual, dense condensations in contact with the nucleolonema. The importance of these nucleolar lesions and the relationship between the SV40 virus and the polyoma, common wart, and Shope papilloma viruses are discussed.

Cell Nucleolus↗
PubMed1965

AN ELECTRON MICROSCOPE STUDY OF THE DEVELOPMENT OF A MOUSE HEPATITIS VIRUS IN TISSUE CULTURE CELLS.

Samples taken at different intervals of time from suspension cultures of the NCTC 1469 line of mouse liver-derived (ML) cells infected with a mouse hepatitis virus have been studied with the electron microscope. The experiments revealed that the viruses are incorporated into the cells by viropexis within 1 hour after being added to the culture. An increasing number of particles are found later inside dense cytoplasmic corpuscles similar to lysosomes. In the cytoplasm of the cells from the samples taken 7 hours after inoculation, two organized structures generally associated and never seen in the controls are observed: one consists of dense material arranged in a reticular disposition (reticular inclusion); the other is formed by small tubules organized in a complex pattern (tubular body). No evidence has been found concerning their origin. Their significance is discussed. With the progression of the infection a system of membrane-bounded tubules and cisternae is differentiated in the cytoplasm of the ML cells. In the lumen of these tubules or cisternae, which are occupied by a dense material, numerous virus particles are observed. The virus particles which originate in association with the limiting membranes of tubules and cisternae are released into their lumen by a "budding" process. The virus particles are 75 mmicro in diameter and possess a nucleoid constituted of dense particles or rods limiting an electron transparent core. The virus limiting membrane is sometimes covered by an outer layer of a dense material. In the cells from the samples taken 14 to 20 hours after inoculation, larger zones of the cell cytoplasm are occupied by inclusion bodies formed by channels or cisternae with their lumens containing numerous virus particles. In the samples taken 20 hours or more after the inoculation numerous cells show evident signs of degeneration.

Electrons↗
PubMed1962

The propagation of the virus of epizootic hemorrhagic disease of deer in newborn mice and HeLa cells.

The New Jersey strain of EHD virus has been propagated in newborn Swiss mice by the intracerebral route and is regularly lethal beyond the first serial mouse passage. A complement-fixing antigen prepared from the brains of infected mice reacts positively with the sera of deer recovered from infection with either the New Jersey or South Dakota strain of virus, but not with the serum of normal deer. The mouse-passaged virus induced an inapparent infection in an experimental deer. The virus can also be grown serially in HeLa cell culture and induces a characteristic cytopathic effect. It is neutralizable in such cultures to high titer by the sera of deer recovered from EHD (New Jersey strain) and to lower titer by the serum of a deer recovered from EHD (South Dakota strain). Normal deer serum does not neutralize the virus in tissue culture. The HeLa cell-passaged virus induced typical lethal EHD in an experimental deer and virus could be recovered from most of the tissues of this animal in HeLa cell culture. An unexplained prozone of inhibition of cytopathogenicity at low dilutions was observed in cultures of some of the organs. The fact that EHD virus exhibited a limited sensitivity to sodium desoxycholate suggests that it may belong in the arbor virus group.

Animals↗
PubMed1964

STUDIES ON PERSISTENT INFECTIONS OF TISSUE CULTURES. V. THE INITIAL STAGES OF INFECTION OF L(MCN) CELLS BY NEWCASTLE DISEASE VIRUS.

The initial stages of infection of L(MCN) cell populations with standard Newcastle disease virus (NDV(ST)) were analyzed in an effort to elucidate the steps leading to survival of the cultures and to the indefinite persistence of the infectious process at a low level. Cells were exposed in suspension to NDV at varying multiplicities and the monolayer cultures derived from such cells assayed at intervals for cellular growth rates, percentage of infected cells as determined by immunofluorescence, yields of viral progeny and of interferon, and, on occasion, resistance to superinfection with vesicular stomatitis virus. The percentage of cells calculated to be initially infected on the basis of adsorption data was found to match closely the percentage of immunofluorescent cells resulting from the first infectious cycle (up to 24 hours). Cells initially infected with NDV(ST) produced a mixed progeny of infectious virus (from 15 to 40 pfu/cell) and about 10 times as many non-infectious particles in 24 hours [NDV(L(MCN))], but little or no interferon. If all cells were infected the cultures ultimately died. At multiplicities of infection (m) of 2 or less the cultures survived with increasing ease as the percentage of infected cells was reduced. The number of pfu per infected cell was of the above order during the first 3 days; it declined thereafter. Limited secondary spread of the infection was noted by 48 hours and no further cycling was noted thereafter. As m decreased from 2.0 to 0.1 there was an increase in the yields of interferon and the time at which peak titers were reached. Addition of anti-NDV serum 2 hours after infection prevented measurable production of interferon. In contrast, following exposure of cells to NDV(L(MCN)) at multiplicities ranging from 20.0 to 0.2 (based on infectious virus) all cultures survived, no secondary spread was noted, the number of pfu per infected cells was reduced at the higher multiplicities, and the yields of interferon were similar and maximal by 24 hours and not affected by anti-NDV serum added after an adsorption period of 2 hours. It is concluded that the non-infectious virus particles in the progeny released from NDV(ST)-infected cells induce resistance in remaining cells or, if adsorbed simultaneously with infectious virus, abort the intracellular infectious process. In both instances interferon is produced which may then render additional cells resistant. The non-infectious component is considered an incomplete or defective product of viral replication and not merely thermally inactivated virus. NDV(ST) partially or completely inactivated at 37 degrees C induced neither cellular resistance nor synthesis of interferon. The incomplete viral component behaved in all respects like ultraviolet-inactivated NDV(ST) except that it was significantly more efficient in inducing interferon synthesis. On the basis of the presented data a scheme has been devised and discussed which appears to explain satisfactorily the events which take place on initial infection of L(MCN) cells with NDV and which lead to the persistence of the infectious process.

Animals↗