An international group of HHV-6 experts, investigators and clinicians have  published a comprehensive review of chromosomally integrated HHV-6 (ciHHV-6).  The article, entitled “Chromosomally Integrated human herpesvirus-6: questions and answers,” is written in response to the widespread confusion in the medical community on how to test or diagnose the condition, as well as how to treat a patient with ciHHV-6 who may or may not have symptoms consistent with HHV-6 reactivation.

Written in a question/answer format, the group hopes that this article will help spread the word about ciHHV-6, a condition that affects nearly 1% of the worldwide population. The group advises physicians to use whole blood PCR tests to identify these patients and not to rely on serum or plasma tests to diagnose the condition. They suggest that any patient with greater than 500,000 DNA copies per ml in whole blood probably has HHV-6. Rarely, a patient with graft versus host disease or drug induced hypersensitivity syndrome will have a viral load above 500,000 copies, but this is transient and the viral load diminishes quickly. In an individual with ciHHV-6, the viral load will consistently be over 500,000 copies per ml in whole blood.

If you’d like to learn more about chromosomally integrated HHV-6, please visit our web page on ciHHV-6, or download the article at the link above.

A group of physicians from the University Hospital in Reims, France, have reported a case of fatal HHV-6 myocarditis in an immunocompetent patient.  Although the initial bloodwork and heart biopsies tested came back negative for the presence of HHV-6 infection, post-mortem frozen tissues showed evidence of chronic HHV-6 infection in regions of the heart that had not been biopsied in the initial screening process. This report demonstrates that HHV-6 can establish a nearly undetectable chronic active myocarditis in the immunocompetent, and in the absence of diagnosis and treatment, may eventually result in heart failure and death.

The authors emphasize the importance of endomyocardial biopsy and molecular analysis on frozen tissue—as opposed to fixed tissues—as HHV-6 was not detected in either serum or in paraffin fixed tissues of this patient, who died of an HHV-6 infection. The antibody titers for HHV-6 were not elevated. Endomyocardial biopsies are not performed for most myocarditis cases in the United States, although they are done routinely in many European countries.

HHV-6 infection has been reported to cause cardiac complications in both the immunocompromised and the immunocompetent, including myocarditis (Mahrholdt 2006) dilated cardiomyopathy (Comar 2009) and “idiopathic” left ventricle dysfunction (Kühl 2005). Despite a recent increase in publications that report HHV-6 myocarditis in immunocompromised patients, however, the virus’s role in the pathology of acute chronic myocarditis remains poorly defined.

Uwe Kühl, who leads a large cardiology practice at Charite-University in Berlin, treats HHV-6 positive myocarditis with valganciclovir and has achieved considerable success. His associate Dirk Lassner reported on these results at the 2011 International Conference on HHV-6 & 7. View video.

Click here to learn more about HHV-6 and Heart Disease.

A new study shows that multiple sclerosis patients with HHV-6 have higher risk of relapse and poor response to IFN-beta treatment. In a two year study, a group from the top hospital in Spain demonstrated that HHV-6 was found more often during relapses than during remission. Patients with higher HHV-6 DNA loads in the serum did not fare well, while those who had clearance of HHV-6 fared much better. The prevalence of HHV-6 in whole blood diminished from 64.8% before interferon treatment started, to 41.4% at the end of the 24 month trial. Of interest, there was no correlation between EBV DNA loads in the serum and disease progression.

Interferon beta (IFN-beta) is a common treatment in MS. Although the conventional wisdom is that the mechanism of action is “unkown”,  interferon is a natural antiviral that is often used for treatment of hepatitis  and enteroviruses. Interferon naturally inhibits viral replication, and in fact interferon was originally tested in MS patients because of its antiviral propertites.

The authors suggest that the exacerbations in MS could be explained by an immune reaction to the active replication, and that HHV-6 could be involved in MS through several mechanisms including a) increased death of HHV-6 infected neurons, astrocytes and oligodendrocytes, b) viral interference with the phosphorylation of myelin basic protein or c) increasing the glutamate level in the spinal fluid. HHV-6 is able to induce inflammation and demyelination. It has also been suggested that HHV-6 can interfere with the remyelination process.

The authors suggest further trials with other potential antivirals.

http://www.ncbi.nlm.nih.gov/pubmed/21518144