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Saturday, December 20, 2014

Chronic Fatigue Syndrome (HHV-6?) in Pets

Abnormal Signs Found in Animals of Myalgic Encephalo-myelitis/Chronic Fatigue Syndrome Patients:A Look at 463 Animals

Read More: http://informahealthcare.com/doi/abs/10.1300/J092v06n02_08?journalCode=wcfs

Conclusions: A large number of animals of ME/CFS patients have atypical or unusual diseases which at least mimic ME/CFS. Most of the 127 ME/CFS patients surveyed have significant animal interactions.


Read More: http://informahealthcare.com/doi/abs/10.1300/J092v06n02_08?journalCode=wcfs

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Pathogenic effects of human herpesvirus 6 in human lymphoid tissue ex vivo.

http://www.ncbi.nlm.nih.gov/pubmed/12857897

Abstract

Human herpesvirus 6 (HHV-6) is a potentially immunosuppressive agent that has been suggested to act as a cofactor in the progression of human immunodeficiency virus disease. However, the lack of suitable experimental models has hampered the elucidation of the mechanisms of HHV-6-mediated immune suppression. Here, we used ex vivo lymphoid tissue to investigate the cellular tropism and pathogenic mechanisms of HHV-6. Viral strains belonging to both HHV-6 subgroups (A and B) were able to productively infect human tonsil tissue fragments in the absence of exogenous stimulation. The majority of viral antigen-expressing cells were CD4(+) T lymphocytes expressing a nonnaive phenotype, while CD8(+) T cells were efficiently infected only with HHV-6A. Accordingly, HHV-6A infection resulted in the depletion of both CD4(+) and CD8(+) T cells, whereas in HHV-6B-infected tissue CD4(+) T cells were predominantly depleted. The expression of different cellular antigens was dramatically altered in HHV-6-infected tissues: whereas CD4 was upregulated, both CD46, which serves as a cellular receptor for HHV-6, and CD3 were downmodulated. However, CD3 downmodulation was restricted to infected cells, while the loss of CD46 expression was generalized. Moreover, HHV-6 infection markedly enhanced the production of the CC chemokine RANTES, whereas other cytokines and chemokines were only marginally affected. These results provide the first evidence, in a physiologically relevant study model, that HHV-6 can severely affect the physiology of secondary lymphoid organs through direct infection of T lymphocytes and modulation of key membrane receptors and chemokines.

Association between anticonvulsant hypersensitivity syndrome and human herpesvirus 6 reactivation and hypogammaglobulinemia.

http://www.ncbi.nlm.nih.gov/pubmed/14967790

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