HHV-6 can cause fatal myocarditis http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=88596

HHV-6 infects human aortic and heart microvascular endothelial cells, increasing their ability to secrete proinflammatory chemokines http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12115999&dopt=Abstract

Mary Schweitzer on the tragic death of Casey Fero http://phoenix-cfs.org/Tragic%20death%20-%20Schweitzer.htm

Paul Cheney on CFS and the heart http://www.cfsresearch.org/cfs/cheney/15.htm

HHV-6 infects human aortic and heart microvascular endothelial cells, increasing their ability to secrete proinflammatory chemokines. Endothelial cells are important targets for (herpesvirus infection. To evaluate the biological effects of human herpesvirus-6 (HHV-6) infection, adult heart microvascular and aortic endothelial cells were examined for in vitro susceptibility to HHV-6 and for the alterations induced by viral infection on the production of monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8). Analysis by reverse transcription-polymerase chain reaction and by in situ polymerase chain reaction showed that HHV-6 replicates in endothelium in the absence of cytopathic effects, and that viral sequences were present in 20% umbilical vein and in 10% aortic and 1% microvascular endothelium. HHV-6 infection upregulated the production of MCP-1 and IL-8, with differences observed between aortic and microvascular endothelium. These findings demonstrate that endothelial cells represent a potential reservoir for HHV-6 infection, and the altered pattern of chemokine production can lead to attraction of immunocompetent cells and to the development of inflammatory processes. (Pathol Int. 2002 Jan ;52 (1):31-9 11940204)


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