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A T Haase

Publications and source records attributed to A T Haase.

101 records · Page 6Linked to original sources
PubMed1969

Mengovirus-induced cytopathic effect in L-cells: protective effect of interferon.

The effect of interferon on mengovirus-induced cytopathic effect (CPE) in L cells, the cut-off of host-cell protein synthesis, and production of mature virus were found to be dependent on the concentration of interferon. CPE and inhibition of host protein synthesis were not affected until the concentration of interferon was increased 100-fold over that required to reduce viral yields by 90%.

Animals↗
PubMedDate not supplied

Pathogenesis of lentivirus infections.

Following infection of animals or humans, lentiviruses play a prolonged game of hide and seek with the host's immune system which results in a slowly developing multi-system disease. Emerging knowledge of the disease processes is of some relevance to acquired immune deficiency syndrome (AIDS), which is caused by a virus possessing many of the characteristics of a lentivirus.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

Increased expression of nitric oxide synthase and dendritic injury in simian immunodeficiency virus encephalitis.

OBJECTIVES: Widespread dendritic injury may be one mechanism involved in the neurologic impairment that occurs in HIV-1 infection. The objectives of this study were to quantitate the extent of dendritic injury in a primate model of central nervous system (CNS) infection, investigate the role of nitric oxide (NO) as a mediator of neuropathologic changes, and evaluate the relation of these changes to cognitive and motor function. STUDY DESIGN/METHODS: Cognitive and motor function was assessed in rhesus macaque monkeys infected with simian immunodeficiency virus (SIV). In situ hybridization, immunohistochemistry, and quantitative image analysis were employed to assess the relations among productive infection, NO synthase (iNOS), and dendritic injury. RESULTS: Productive infection of cells of the macrophage lineage in CNS is associated with inflammation, increased expression of iNOS, and dendritic injury. The tests of cognitive and motor function employed were abnormal in both animals that had evidence of productive infection and those that did not. CONCLUSIONS: Increased NO accompanying productive infection and encephalitis may be one cause of neuronal injury in lentivirus infections of the CNS. Extension of tests of cognitive and motor function to late-stage AIDS in rhesus monkeys is needed to assess the potential role of NO-induced dendritic damage in lentiviral encephalopathy/AIDS dementia complex.

Animals↗