Potential Involvement of Retroviral Elements in Human Dementias
Laura Manuelidis
Neuropathology Section, Yale University, School of Medicine, PO Box 3333, 333 Cedar Street, New Haven, Connecticut 06510, USA
Search for more papers by this authorGeoffrey Murdoch
Neuropathology Section, Yale University, School of Medicine, PO Box 3333, 333 Cedar Street, New Haven, Connecticut 06510, USA
Search for more papers by this authorElias E. Manuelidis
Neuropathology Section, Yale University, School of Medicine, PO Box 3333, 333 Cedar Street, New Haven, Connecticut 06510, USA
Search for more papers by this authorLaura Manuelidis
Neuropathology Section, Yale University, School of Medicine, PO Box 3333, 333 Cedar Street, New Haven, Connecticut 06510, USA
Search for more papers by this authorGeoffrey Murdoch
Neuropathology Section, Yale University, School of Medicine, PO Box 3333, 333 Cedar Street, New Haven, Connecticut 06510, USA
Search for more papers by this authorElias E. Manuelidis
Neuropathology Section, Yale University, School of Medicine, PO Box 3333, 333 Cedar Street, New Haven, Connecticut 06510, USA
Search for more papers by this authorJoan Marsh
Search for more papers by this authorSummary
Creutzfeldt-Jakob disease (CJD) is a dementia of humans caused by a class of infectious agents with several biological properties similar to those of conventional viruses. The molecular nature of this group of agents is enigmatic, for neither an agent-specific nucleic acid nor a non-host protein has yet been identified. Recent transmissions of familial CJD dementias to rodents suggest that this class of agent can be integrated into the germline. Furthermore, tissue culture studies indicate that CJD causes transformation of cells in a manner reminiscent of slowly oncogenic retroviruses. Currently characterized retroviral-like elements include many forms that do not have ‘typical’ retroviral ultra-structural morphology; several forms are also known to be resistant to various types of standard physicochemical inactivation. We suggest that CJD agents are either constituted by retroviral-like nucleic acids or interact with endogenous retroviral sequences to elicit a slowly progressive disease of the central nervous system. Several overlapping properties between infectious CJD and ‘non-infectious’ dementias, such as Alzheimer's disease, implicate potential common pathogenic mechanisms.
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