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Biomedical subjects

J G Stevens

Publications and source records attributed to J G Stevens.

108 records · Page 6Linked to original sources
PubMed1973

Latent herpes simplex virus in the central nervous system of rabbits and mice.

Herpes simplex virus (HSV) type 1 induces a long-standing latent infection in the central nervous system of mice and rabbits. The infection was extablished in the brain stems of rabbits after corneal inoculation of the virus, and in the spinal cords of mice after rear footpad infection. In these animals, infectious virus could not be recovered by direct isolation from tissues; it was detected only after the tissues were maintained as organ cultures in vitro.

Animals↗
PubMed1973

Pathogenesis of herpetic neuritis and ganglionitis in mice: evidence for intra-axonal transport of infection.

The pathogenesis of acute herpetic infection in the nervous system has been studied following rear footpad inoculation of mice. Viral assays performed on appropriate tissues at various time intervals indicated that the infection progressed sequentially from peripheral to the central nervous system, with infectious virus reaching the sacrosciatic spinal ganglia in 20 to 24 hr. The infection also progressed to ganglia in mice given high levels of anti-viral antibody. Immunofluorescent techniques demonstrated that both neurons and supporting cells produced virus-specific antigens. By electron microscopy, neurons were found to produce morphologically complete virions, but supporting cells replicated principally nucleocapsids. These results are discussed in the context of possible mechanisms by which herpes simplex virus might travel in nerve trunks. They are considered to offer strong support for centripetal transport in axons.

Animals↗
PubMed1971

Latent herpes simplex virus in spinal ganglia of mice.

Herpes simplex virus establishes a persistent, latent infection in spinal ganglia after mice have recovered from posterior paralysis. Infectious virus is replicated when these ganglia are explanted and maintained as organ cultures in vitro.

Animals↗
PubMed1971

Restriction of herpes simplex virus by macrophages. An analysis of the cell-virus interaction.

Macrophages restrict herpes simplex virus replication and can prevent the development of herpetic disease in mice. In an attempt to define the nature of this restriction, an analysis of virus-specified macromolecular syntheses in infected macrophages was undertaken. The significant results were the following: All cells were killed, but the infection was considered to be abortive since the level of infectious virus in macrophage cultures dropped steadily to a level beyond detection by 25 hr after infection. This restriction appeared to be specific for macrophages; the virus replicated efficiently in other mouse cells. DNA with a density characteristic for herpes simplex virus DNA was extracted from infected cultures, and the proportion of macrophages synthesizing DNA increased from less than 1% to greater than 50% by 6 hr after infection. Studies employing polyacrylamide gel electrophoresis indicated that the major viral-specific proteins were induced in macrophage cultures. In addition, all cells showing cytopathic changes characteristic of herpes virus infection also contained viral antigens which could be detected by fluorescent antibody techniques and, by 15 hr after infection, most contained nascent capsids lacking central dense cores. It is suggested that an error in DNA metabolism may be the primary cause of restriction.

Animals↗
PubMed1969

Changes in nuclear basic proteins during pseudorabies virus infection.

As a preliminary study to investigation of the possible role played by basic proteins in the genetic regulation of virus-infected cells, acid-extractable proteins synthesized during pseudorabies virus infection were investigated. The synthesis of histones was found to decrease in a gradual manner, and arrest was complete by 6 hr after infection. Five virus-induced acid-extractable proteins appeared in nuclei of infected cells after 4 hr of infection. Four of these proteins were virus structural proteins; one was not. All these proteins contained tryptophan and, therefore, were not "classic" histones.

Animals↗
PubMed1968

Labile coat: reason for noninfectious cell-free varicella-zoster virus in culture.

Experiments designed to determine why cell-free varicella-zoster virus replicated in cell culture is noninfectious were performed. Electron micrographs in which varicella-zoster virus (a herpesvirus) was compared to herpes simplex virus in primary human amnion cell cultures showed that the viruses were morphologically indistinguishable inside the nucleus. However, extranuclear varicella-zoster viruses were distinguished from herpes simplex virus by the presence of pleomorphism, incomplete coats, and a resultant loss of central dense cores. This result indicates that varicella-zoster virus possesses a labile coat which is degraded outside the nucleus. It is suggested that the labile coat is a principal reason for the lack of cell-free infectious virus in this system.

Amnion↗
PubMedDate not supplied

Latent infections by herpes simplex virus in experimental animals.

Studies in experimental animals, initially the rabbit and more recently the mouse, have been a great importance in establishing present day concepts concerning the phenomenon of herpesvirus latency. These early observations coupled with more recent knowledge of virological consequences following surgical manipulation of the trigeminal tract have led to a general hypothesis for the natural history of herpetic infections: The infection follows a circuit from skin, mucous membrane, or eye (the primary infection) to the corresponding sensory ganglia via associated nerves. Virus becomes latent in the ganglia and later, as a result of one of the many provocations known to be associated with recurrence of herpetic lesions, is reactivated and travels via the nerve to the surface and again produces lesions. Current research investigating this hypothesis is reviewed.

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