Herpes and Alzheimer’s Disease: Subversion in the Central Nervous System and How It Might Be

In this study, we have investigated interactions of a TK- mutant of virulent HSV type 2 (HSV-2) (syn+) and a nonneuroinvasive HSV-1 (syn) in mice. The main advances have been made through studies in humans and in mice, investigating the likelihood of reactivation of the latent virus in brain. These viral lesions, situated in the central nervous system (CNS) portion of the root, consist of severe myelin destruction accompanied by mononuclear cell infiltration and partial sparing of axons. However, recent advances in viral vector technology coupled with efficient delivery methods have opened up new avenues that show promise at the preclinical testing stage. Both immunocompetent and immunocompromised individuals may be affected. Get a printable copy (PDF file) of the complete article (1.3M), or click on a page image below to browse page by page. Nonpathogenic HSV-1 gene transfer vectors have been generated by elimination of viral functions necessary for replication.

These viruses efficiently invade the peripheral nervous system and establish lifelong latency in neurons resident in peripheral ganglia. It has many natural biological features which make it attractive for gene delivery to a variety of tissues. While this response is necessary to quell virus replication, drive the pathogen into a “latent” state, and likely hinder viral reactivation, collateral damage can ensue with demonstrable cell death and foci of tissue pathology in the central nervous system (CNS) as a result of the release of inflammatory mediators including reactive oxygen species. Latent infections of peripheral nervous tissue are characterized by the ability to recover infectious virus from explant cultures of most of the latently infected ganglia. The research was performed at Brown and at the Marine Biological Laboratory at Woods Hole, Mass., using squid taken from local waters. The basic idea of gene transfer arose in the late 1950s, after the discovery that viruses have an intrinsic capability to transfer their genetic material into infected cells. To achieve this, HSV-1 has evolved a complex strategy in which the particular character of its interaction with certain host cells assures its continued persistence and spread in the human community.


It publishes high-impact research reports, commentaries, perspectives, reviews, colloquium papers, and actions of the Academy. Latent infections of peripheral nervous tissue are characterized by the ability to recover infectious virus from explant cultures of most of the latently infected ganglia1–4. It publishes high-impact research reports, commentaries, perspectives, reviews, colloquium papers, and actions of the Academy. This gene transfer technology is based on the use of a virus as a gene delivery vehicle. Using gene array analysis, we have examined the changes that occur in cellular mRNA levels in mouse trigeminal ganglia following explantation, a stimulus that results in HSV-1 reactivation from latency. It has many natural biological features which make it attractive for gene delivery to a variety of tissues. Patients with symptoms suggestive of herpes viruses infections coexisting with peri-phe-ral nervous system manifestations, especially Guillain-Barré syndrome, mononeuropathy, plexopathy and radiculopathy, should be screened for the herpes viruses infections in the differential diagnosis.

Both primary infection and recurrence may lead to neurologic infection and disease. Longitudinal section of the optic nerves and chiasma showed that both myelinated axons and neuroglial cells crossed at the chiasma. Virus can also spread to the CNS via retrograde transport through the oculomotor nucleus that innervates extraocular muscles of the eye. History of medicine. We report a 36-year-old woman with cerebral vasculitis and ischemic stroke secondary to herpes simplex virus (HSV). While this response is necessary to quell virus replication, drive the pathogen into a “latent” state, and likely hinder viral reactivation, collateral damage can ensue with demonstrable cell death and foci of tissue pathology in the central nervous system (CNS) as a result of the release of inflammatory mediators including reactive oxygen species. Here, we investigated the acute and prolonged complement system activity in HSE patients, by using enzyme-linked immunosorbent assays (ELISAs) for numerous complement components (C).

Advances in imaging technology have greatly enhanced our ability to diagnose the illness noninvasively. In this context, a number of viral vectors has been used in recent years to introduce and express genes into the CNS. Most cases of neonatal HSV disease are caused by HSV type 2, whereas virtually all cases of HSE are caused by HSV type 1. These include a natural tropism for neurons, a large viral genome allowing the insertion of multiple exogenous genes, and the ability to establish asymptomatic life-long latent infections. History. Using gene array analysis, we have examined the changes that occur in cellular mRNA levels in mouse trigeminal ganglia following explantation, a stimulus that results in HSV-1 reactivation from latency. IL-6 is a pro-inflammatory cytokine that has previously been associated with herpes simplex virus type 1 reactivation.

Herpes zoster is a viral disease characterized by a painful skin rash with blisters in a limited area on one side of the body, often in a stripe.

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