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Biomedical subjects

R T JOHNSON

Publications and source records attributed to R T JOHNSON.

At least 19 recordsLinked to original sources
PubMed1964

THE PATHOGENESIS OF HERPES VIRUS ENCEPHALITIS. II. A CELLULAR BASIS FOR THE DEVELOPMENT OF RESISTANCE WITH AGE.

The resistance to herpes virus encephalitis which develops with age was studied in mice using fluorescent antibody staining. Adult mice remained susceptible to intracerebral inoculation, and the infection of the central nervous system was identical with that found in immature mice. A "barrier" to the spread of virus inoculated extraneurally developed with maturation, and the limitation of spread appeared to coincide with the infection of peritoneal and tissue macrophages. In vitro, suckling and adult mouse macrophages were infected with equal ease. However, suckling mouse macrophages infected other cells in contact with them, while infected adult mouse macrophages did not. Studies failed to reveal the nature of this change in macrophages which developed with age. The role of macrophages in the pathogenesis of herpes virus encephalitis is discussed. The hypothesis is made that an alteration in the macrophages of the maturing mouse plays an important role in its development of resistance to herpes virus encephalitis.

Aging↗
PubMed1964

THE PATHOGENESIS OF HERPES VIRUS ENCEPHALITIS. I. VIRUS PATHWAYS TO THE NERVOUS SYSTEM OF SUCKLING MICE DEMONSTRATED BY FLUORESCENT ANTIBODY STAINING.

The pathogenesis of herpes simplex virus encephalitis and myelitis was studied in suckling mice using routine titration procedures and fluorescent antibody staining for the identification of infected cells. After intracerebral inoculation virus was shown to disperse rapidly in the cerebrospinal fluid (CSF), multiply in meninges and ependyma, and then invade the underlying parenchyma infecting both neurons and glia. Following extraneural inoculation virus gained access to the central nervous system (CNS) by both hematogenous and neural pathways. After intraperitoneal and intranasal inoculation virus was found to multiply in viscera and produce viremia; foci of CNS infection then developed around small cerebral vessels. After subcutaneous and intranasal inoculation neural spread of virus was demonstrated along corresponding peripheral and cranial nerves. This spread resulted from the centripetal infection of endoneural cells (Schwann cells and fibroblasts). Antigen was not found in axons even after infection of the corresponding ganglion cell perikaryon. Subsequent spread within the CNS was unrelated to neural tracts, and there was no evidence of axonal spread of virus in the host-virus system studied. These findings are discussed in relation to previous and current theories of the viral "blood-brain barrier" and neural pathways of infection.

Animals↗