bbc.co.uk:

A study on children has found further evidence that ME, or Chronic Fatigue Syndrome, could be caused by a virus.

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sciencedaily.com:

A novel mechanism used by adenovirus to sidestep the cell's suicide program, could go a long way to explain how tumor suppressor genes are silenced in tumor cells and pave the way for a new type of targeted cancer therapy, report researchers at the Salk Institute for Biological Studies in the Aug. 26, 2010 issue of Nature.

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rndsystems.com:

Multiple sclerosis (MS) is an autoimmune neurological disorder that affects over 2 million people worldwide. Onset of the disease is thought to occur following exposure of genetically predisposed individuals to an unknown environmental trigger that activates myelin-specific T cells. These cells cross the blood-brain barrier to trigger an inflammatory attack that demyelinates axons in the central nervous system.  Polymorphisms in the vitamin D receptor are among the genetic variations that increase the risk of MS. The incidence of MS is also elevated in northern climates, where vitamin D deficiency is common. Since exposure of the skin to ultraviolet light aids in the conversion of inactive vitamin D to the active form, the short days, low UV intensity, and lack of exposed skin common to winter months, decrease the amount of active VitD3 that can be produced. Although the correlation between VitD3 deficiency and MS is intriguing, we are only now beginning to understand the biology that may explain this connection. In both human MS and in experimental autoimmune encephalomyelitis (EAE), the mouse model of the disease, VitD3 can influence specialized populations of cells that may play a critical role in protection against the disease. VitD3 promotes the formation of tolerogenic or “semi-mature” dendritic cells (DCs). These DCs induce the development of CD25–FoxP3+/–IL-10++ Tr1 cells, a subset of regulatory T cells (Treg), and downregulate the production of Th1 inflammatory cells. A pair of interacting co-inhibitory proteins, B7-H1 (also known as PD-L1) and PD-1, appear to be critical molecules in this process.

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PubMed:

Raltegravir is a potent inhibitor of XMRV, a virus implicated in prostate cancer and chronic fatigue syndrome

Abstract

BACKGROUND: Xenotropic murine leukemia-related retrovirus (XMRV) is a recently discovered retrovirus that has been linked to human prostate cancer and chronic fatigue syndrome (CFS). Both diseases affect a large fraction of the world population, with prostate cancer affecting one in six men, and CFS affecting an estimated 0.4 to 1% of the population.

PRINCIPAL FINDINGS: Forty-five compounds, including twenty-eight drugs approved for use in humans, were evaluated against XMRV replication in vitro. We found that the retroviral integrase inhibitor, raltegravir, was potent and selective against XMRV at submicromolar concentrations, in MCF-7 and LNCaP cells, a breast cancer and prostate cancer cell line, respectively. Another integrase inhibitor, L-000870812, and two nucleoside reverse transcriptase inhibitors, zidovudine (ZDV), and tenofovir disoproxil fumarate (TDF) also inhibited XMRV replication. When combined, these drugs displayed mostly synergistic effects against this virus, suggesting that combination therapy may delay or prevent the selection of resistant viruses.

CONCLUSIONS: If XMRV proves to be a causal factor in prostate cancer or CFS, these discoveries may allow for rational design of clinical trials.

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