Growth Of Newcastle Disease Virus Research Articles

Intrinsic Interference: a New Type of Viral Interference

The hemadsorption-negative plaque test has revealed a new type of viral interference, termed intrinsic interference. Several unrelated types of noncytopathic viruses were shown to induce in infected host cells a state of interference unique in being directed solely against superinfection by Newcastle disease virus (NDV). The NDV-refractory state arises only in those individual cells of a population actually infected by the inducing virus, and presumably results from the action of a protein(s) coded for by the viral genome. Thus, intrinsic interference differs fundamentally from that mediated by an extrinsic protein detectable under conditions favoring resistance to a broad spectrum of viruses and characteristic of interference induced by interferon, the latter being coded for by the cell genome. Intrinsic interference is defined as a viral genome-induced cellular state of resistance to challenge by high multiplicities of NDV, coexistent with a state of susceptibility to a broad spectrum of other viruses, similarly tested at high multiplicities. The capacity to induce intrinsic interference was demonstrated with rubella virus, Sindbis virus (arbovirus, group A), West Nile virus (arbovirus, group B), poliovirus (MEF, type 2), the lactic dehydrogenase virus (Riley's agent), and an unidentified nonhemadsorbing, noncytopathic adventitious virus. A state of intrinsic interference was also observed in the V5 line of mouse cells carrying a murine leukemia virus, probably resulting from some heretofore unsuspected contaminating virus. The molecular basis for intrinsic interference is not known, but it appears to involve a step in the NDV growth cycle beyond that of viral attachment, entry, and eclipse.

Growth of Newcastle disease virus in a HVJ carrier culture of HeLa cells

Growth of Newcastle disease virus (NDV) in a HVJ carrier culture of HeLa cells (HeLa HVJ) was investigated. Although most of the cells of the carrier culture contained HVJ antigen, its presence did not interfere with the growth of superinfecting NDV. When HeLa HVJ cells were infected with NDV at a low multiplicity of infection, the yield of progeny virus was higher, and the cytopathic changes were more extensive than those in normal HeLa cells. Plaques produced by NDV on HeLav HVJ cell monolayers were clearer and larger than those on HeLa cells. HeLa HVJ cells could be distinguished from normal HeLa cells both with respect to production of interferon and sensitivity to its action. Production of interferon which normally appeared in HeLa cell culture infected with NDV could not be demonstrated in HeLa HVJ cell culture. The cells of HeLa HVJ were less susceptible to the antiviral action of interferon than normal HeLa cells.

A radiological study of cell-virus interaction in the Rous sarcoma.

Abstract Rous sarcoma virus (RSV) and Newcastle disease virus (NDV) are in activated exponentially by X-rays and ultraviolet (UV) light. While both viruses are similar in their sensitivity to X-rays, RSV is about ten times more resistant to UV light than is NDV. The capacity of chick fibroblasts to initiate the growth of RSV is as sensitive to inactivation by both X-rays and UV light as is their ability to divide and form colonies, while their capacity to initiate the growth of NDV is many times more radioresistant. A common radiosensitive target controls the ability of cells to divide and to initiate the production of RSV. Once the cells have started to produce virus, they may upon irradiation lose their ability to divide and yet continue to produce virus. The results suggest that the genome of the Rous sarcoma virus must be integrated with that of the cell before virus production can begin.

Infection and growth of Newcastle disease virus (NDV) in cultures of chick embryo lung epithelium

The present report constitutes a quantitative study of various stages of infection of chick embryo lung epithelium in vitro with Newcastle disease virus (NDV). The virus was assayed throughout these experiments by the plaque technique. The velocity constant for adsorption was determined as well as the true multiplicity of infection. One-step growth curves were carried out in which both the virus liberated into the medium, and that remaining associated with the cells (cell-associated virus or CAV) were measured. It was found that extracellular virus and CAV were equal in amount during the period of exponential virus increase, and the apparent release time (i.e. the time required for release of a newly formed virus particle into the medium after it has gained the property of infectivity) was calculated as about 80 minutes. Further study showed that practically all of this time was spent at the cell surface. In fact, there was no compelling evidence for infective virus at any place other than the cell surface. X-ray inactivation studies showed that both CAV and released virus occur as independent particles rather than in clumps. The small fraction of inoculated virus which retains its infectivity upon coming in contact with susceptible cells and which can be found associated with these cells during the latent period is largely resistant to serum inactivation. These particles are somehow protected from serum neutralization by their association with subcellular particulates, but do not participate in the infectious cycle unless liberated by homogenization and plated on another cell layer.

Growth of Newcastle disease virus in the embryonated egg.

Summary1. Data are presented to support the contention that the growth of Newcastle disease virus in the developing chick embryo occurs in cycles of 4 hr. The apparent 4-hr latent period in the production of virus following the inoculation of an infective dose does not correspond to the lag phase in the multiplication of bacterial cells, but rather indicates an intercellular development of virus particles that cannot be determined by any of the present technics for measuring viral activity. The maximum adsorption of virus onto susceptible cells occurs within 10 minutes after its introduction into the embryonated egg. 2. The existence of an unequal development of infective and hemagglutinating titers during the growth of Newcastle disease virus is described and an attempted explanation for this discrepancy is made on the hypothesis that the hemagglutination unit results from a maturation of the infectious particles and cannot therefore be detected early in its growth.