MP and Infectious Diseases of the CNS

A great many infectious agents, especially virus, selectively bind to lipid rafts of the host cell to gain entry, and conversely, new virions are released in MP, such as retrovirus [85]. Biochemical details of the budding process are now better understood, as given, for example, by Nabhan et al. [86]. Release of the virions may be prompted by immune mechanisms responding to immune complex (IC) and can be complement-mediated. Examples include pseudorabies virus, cholera, rotavirus, shigella, HIV, and Newcastle disease virus [87-92]. These facts suggest inhibiting MP release might be a therapeutic target in slowing the dissemination of virions; see 6.

Tantalizing evidence for a viral trigger in the etiology of several neurodegenerative diseases (MS, ALS, AD, PD, others) is well known. Mechanisms of brain damage by virus-induced neuroinflammation were recently reviewed [93], as was HIV-associated dementia [94]. However, the latter paid little attention to a possible role of MP, although several studies have shown correlations of MP to HIV (HTLV- 1) progression, including from our laboratory [95].

Viral theories of neurodegenerative diseases have recently shifted focus to human endogenous retroviruses (HERV), for example, in amyotrophic lateral sclerosis (ALS) [96]. A number of papers have shown that HERV transcripts occur on MP, e.g., [97]. Several other reports of HERV transport by MP are in the field of reproductive medicine and as cited above [85].

 
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