Murine neurotropic retrovirus spongiform polioencephalomyelopathy: acceleration of disease by virus inoculum concentration

Brooks, Benjamin Rix; Swarz, Jeffrey R.; Narayan, Opendra; Johnson, Richard T.

doi:10.1128/iai.23.2.540-544.1979

Cited by 36 publications

(16 citation statements)

References 13 publications

(13 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The present study extends the observation that non-inflammatory spongiosis of the central nervous system is not pathognomonic for unconventional viral agents (Brooks et al, 1979;Gardner et al, 1973;McCarter et al, 1977;Oldstone et al, 1977). Our observations suggest that in this infection vacuolation does not result from a permissive infection of the vacuolated cells but may be the result of: 1 a non-permissive infection of neurons and/or glia, 2 the toxic effects of a viral protein or 3 the consequences of metabolic alteration in productively infected endothelial cells and pericytes during early stages of the disease.…”

Section: Discussionsupporting

confidence: 86%

“…Newborn NIH Swiss mice and BALB/c mice (Microbiological Associates, Bethesda, MD) were inoculated intracerebrally or intraperitoneally with 2 x lo4 plaque-forming units measured on XC Rous Sarcoma virus transformed rat kidney cells (XCpfu) or 2 x lo5 XCpfu of concentrated cloned, ecotropic, neurotropic retrovirus as previously described (Brooks et al, 1979;1980). Controls included newborn NIH Swiss mice and BALB/c mice inoculated with Hanks' balanced salt solution (HBSS) without phenol red.…”

Section: Animals and Virusmentioning

confidence: 99%

“…Recently, a reduction of the incubation period of the experimental disease from 2 months to 15 days was effected by concentration of purified retrovirus (Brooks et al, 1979). High titered inocula provided in vivo synchronization of infection allowing more detailed studies of the pathogenesis of the infection (Brooks et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Spongiform Polioencephalomyelopathy Caused by a Murine Retrovirus. Ii. Ultrastructural Localization of Virus Replication and Spongiform Changes in the Central Nervous System

Swarz

Brooks

Johnson

1981

Neuropathology Appl Neurobio

View full text Add to dashboard Cite

The development of murine retrovirus induced spongiform polioencephalomyelopathy was studied sequentially by electron microscopy. During the initial 30 days, viral infection of the central nervous system, as evidenced by viral budding from membranes, was limited to the endothelial cells and pericytes. Viral particles were observed in the lumen of blood vessels, extracellular spaces and astrocytic endfeet surrounding blood vessels, but no morphological evidence of productive infection was found in astrocytes or neurons during early development of vacuolation. The earliest lesions in the neuropil consisted of swelling of astroglia followed by vacuolation, initially in axons and dendrites and later in neuronal and astrocytic soma, where vacuoles appeared to arise from dilated cisternae of the Golgi apparatus. Vacuoles contained only amorphous debris and fragments of membranes. Virions budding aberrantly into vacuoles were seen only in mice surviving beyond 35 days. Numerous reactive astrocytes were observed, but inflammatory cells were absent. The ultrastructural changes were remarkably similar to those described in scrapie, Kuru, and Creutzfeldt-Jakob disease.

show abstract

Section: Discussionsupporting

confidence: 86%

Section: Animals and Virusmentioning

confidence: 99%

See 1 more Smart Citation

Spongiform Polioencephalomyelopathy Caused by a Murine Retrovirus. Ii. Ultrastructural Localization of Virus Replication and Spongiform Changes in the Central Nervous System

Swarz

Brooks

Johnson

1981

Neuropathology Appl Neurobio

View full text Add to dashboard Cite

show abstract

“…The spongiform lesions are seen in most but not all experimental and natural hosts and do not appear to be an obligatory correlate of clinical disease (5,10,11,13). Similar spongiform lesions have been observed in mice naturally or experimentally infected with some strains of murine leukemia virus (MuLV) (1,3,4,14,17). In these MuLV-infected mice, spongiform encephalomyelopathy was associated with the expression of high levels of MuLV p30 and gp7O antigens in the brain (6,9,17).…”

supporting

confidence: 61%

Retrovirus antigens in brains of mice with scrapie- and murine leukemia virus-induced spongiform encephalopathy

Hoffman¹,

Pitts²,

Rohwer³

et al. 1982

Infect Immun

View full text Add to dashboard Cite

Wild mouse ecotropic virus-induced spongiform encephalomyelopathy pathologically similar to scrapie was associated with the expression of retrovirus antigens in mouse brains. However, scrapie-infected mice with spongiform encephalopathy showed no increased expression of retrovirus antigens in brain. Thus, the pathogenesis of the scrapie spongiform lesion does not appear to involve activation of endogenous retrovirus.

show abstract

“…Inoculation by any route of the neurotropic LC MuLV into newborn (younger than 5 days) susceptible laboratory mice leads to a high incidence of paralysis, with a shortened latent period of a few weeks to several months depending on dose and mouse strain 14, 9,[29][30][31][32] [13]. The rapid induction of paralysis in vivo and the localization of the paralytogenic determinants to the envelope region should allow construction of chimeric MuLVs that will yield more precise mapping of this determinant and should further define the mechanism of retrovirally induced direct neuronal cell damage.…”

Section: Preventionmentioning

confidence: 99%

Neurotropic retroviruses of wild mice and macaques

Gardner

1988

Ann Neurol.

View full text Add to dashboard Cite

A neurotropic retrovirus causes a naturally occurring lower-limb paralysis in wild mice, characterized by a noninflammatory spongiform change located primarily in the lower spinal cord. The causative agent is an ecotropic murine leukemia virus, unique to certain wild mice in southern California. The disease is readily transmitted to newborn susceptible laboratory mice. The paralytogenic property is attributed to direct viral injury to motor neurons and glial cells and is associated with unique amino acids in the murine leukemia virus envelope gp70. This murine model may have relevance to both human T-lymphotropic virus type I, and human immunodeficiency virus infection of human brain. It presents a practical model for testing antiviral agents aimed at retrovirus infection of the mammalian central nervous system. Simian acquired immunodeficiency syndrome type D retrovirus causes a silent infection of the brain in infected macaques. Viral nucleic acids are detected in the brain parenchyma in the absence of viral antigen, neurological symptoms, and neuropathology. Infected choroid plexus epithelial cells are the source of cell-free virus in the cerebrospinal fluid of viremic monkeys. This model adds yet another example of retroviral infection of the central nervous system and points to the choroid plexus as a potential source of infectious virus.

show abstract

Murine neurotropic retrovirus spongiform polioencephalomyelopathy: acceleration of disease by virus inoculum concentration

Abstract: A 10-fold reduction in the incubation period of murine neurotropic retrovirus spongiform polioencephalomyelopathy was effected by a 1,000-fold concentration of the cloned virus inoculum.

Cited by 36 publications

References 13 publications

Spongiform Polioencephalomyelopathy Caused by a Murine Retrovirus. Ii. Ultrastructural Localization of Virus Replication and Spongiform Changes in the Central Nervous System

Spongiform Polioencephalomyelopathy Caused by a Murine Retrovirus. Ii. Ultrastructural Localization of Virus Replication and Spongiform Changes in the Central Nervous System

Retrovirus antigens in brains of mice with scrapie- and murine leukemia virus-induced spongiform encephalopathy

Neurotropic retroviruses of wild mice and macaques

Contact Info

Product

Resources

About