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Intensive care (ICU) patients with co-infections of HHV-6 and CMV are 7.5x more likely to die or have an extended stay in the hospital. Japanese investigators published findings suggesting that HHV-6B plays a pathogenic role in epilepsy by enhancing gene expression that induces neuroinflammation and sclerosis in the temporal lobe. A pivotal study, led by Michael Boeckh at the Fred Hutchinson Cancer Research Center, has determined that occult infections contribute to 57% of all cases of “idiopathic” pneumonia syndrome (IPS), a condition previously assumed to be non-infectious. Delirium associated with HHV-6B reactivation in cord blood transplant patients: time for an antiviral prophylaxis trial?
A prospective study authored by Joshua Hill and Danielle Zerr determined that higher than average HHV-6B DNA levels increased the odds of developing delirium after cord blood transplantation (CBT) by almost three fold.
Michael VanElzakker, a researcher affiliated with the Tufts University PTSD neuroimaging laboratory as well as the Massachusetts General Hospital Psychiatric Neuroscience division, has published a novel hypothesis on the possible etiology of Chronic Fatigue Syndrome (CFS). For years, CFS researchers have been looking in plasma and blood cells for a pathogenic agent that causes the myriad of symptoms experienced by patients with the condition.
Herpesviruses and certain intracellular bacteria establish latency in the vagus nerve and reactivate during periods of stress or illness, causing the release of proinflammatory cytokines.
To test his hypothesis, VanElzakker suggests that vagus nerve biopsy samples should be sought from CFS patients who have died prematurely from other causes. Potential therapeutic options, he says, include virus-specific antiviral treatments, glial cell inhibitors such as lbudilast (used for asthma and stroke in Japan) and vagus nerve stimulation. VanElzakker points out that one potential problem with antivirals are that these drugs are not effective within immunoprivileged sites such as the vagal paraganglia. For more information, read the full paper and visit the Foundation’s webpage on HHV-6 & CFS. ABOUT THE HHV-6 FOUNDATIONThe HHV-6 Foundation in a non-profit entity founded to encourage scientific exchange between investigators and to provide pilot grants for promising scientific and clinical research on the under- appreciated viruses HHV-6A and HHV-6B. The Foundation sponsors international conferences and supports scientists and clinicians seeking to clarify the role of the two HHV-6 viruses in disease.
A fifth case of limbic encephalitis associated with GAD antibodies and HHV-6 infection has been reported, this time in an immunocompetent woman with chromosomally integrated HHV-6, epilepsy, and psychosis.
Tetsushi Yoshikawa and Yoshiki Kawamura just published an important study linking HHV-6B in brain tissues to sclerosis in mesial temporal lobe epilepsy. Investigators at the University of Bonn Medical Center in Germany have screened 346 fresh-frozen brain tissue resections from temporal lobe epilepsy (TLE) patients for all nine herpesviruses as well as for RNA viruses including Paramyxovirinae, Phleboviruses, Enteroviruses, and Flavivirus, using qPCR.


Pitt Niehusmann has completed the largest study to date on the question of whether viruses play a role in refractory mesial temporal lobe epilepsy (MTLE), with 346 samples analyzed.
Immunocompetent adults are not supposed to get HHV-6 encephalitis or status epilepticus (SE) and HHV-6 testing is rarely performed in these patients. A report published by a group from the University of Minnesota details the case of a 59-year-old male who developed non-convulsive status epilepticus and hyponatremia in addition to HHV-6 reactivation following umbilical cord blood transplantation. Case report describes child with multiple episodes of febrile status epilepticus, followed by chorea and developmental regression, caused by human herpes virus-6 encephalitis.
A group from Spain has confirmed the existence of a novel epilepsy syndrome featuring generalized seizures and epileptic encephalopathy after HHV-6-associated PALE (posttransplant limbic encephalitis) in children. A ten-year NIH-funded study has determined that a third of infants with prolonged seizures and fever suffer from either a new or reactivated roseola virus infection. A group from the Royal Children’s Hospital in Melbourne, Australia has reported the development of epilepsy after HHV-6 posttransplant limbic encephalitis (PALE) among children receiving stem cell transplantation with cord blood (CBT).
Research groups in China, Germany and the US each publish compelling evidence that HHV-6 plays a role in epilepsy. On the other hand, single infections with either HHV-6 or CMV did not significantly impact outcome.
HHV-6 DNA levels were significantly higher in the resected tissue of epilepsy patients with sclerosis compared to those without it. In the paper, published in Medical Hypotheses, VanElzakker suggests that CFS may be the result of a pathological infection of the vagus nerve. However, according to VanElzakker, they may have been looking in the wrong place (plasma) and need to search instead in the tissues of the peripheral and central nervous system.
HHV-6 is a highly neurotropic virus and potent inducer of cytokines such as IL-6 and NFkB, which many groups have proposed as an etiological theory for the role of HHV-6 in neurological conditions such as seizures and epilepsy.
In addition, he also suggests that radiolabeled antibodies may be effectively designed and used to detect these CNS-localized infections.
Vagus nerve stimulation is currently used for refractory epilepsy, a condition that has been associated with HHV-6B reactivation. Also, any antiviral therapy would need to be broad spectrum since diagnosis of the specific pathogen(s) is challenging. Since the HHV-6A and HHV-6B can smolder in the brain and other organs without circulating in the peripheral blood or plasma, identifying chronic infection is a challenge.


The patient’s condition improved (with a drop in GAD antibody titers and stabilization of psychotic symptoms) in response to three weeks of antiviral therapy but relapsed when antiviral therapy was withdrawn. Jin-Mei Li at West China Hospital has identified a possible synergy between a polymorphism of Apolipoprotein E (ApoE) and HHV-6B infection, resulting in a higher viral load and seizure frequency in these patients.
A new case report from Baylor suggests that testing for HHV-6 in these patients may be worthwhile. Although VanElzakker proposes that any neutoropic virus or bacteria could trigger CFS, HHV-6 is at the top of his list. During infection, the sensory vagus nerve sends a signal to the brain to initiate “sickness behavior,” an involuntary response characterized by fatigue, fever, myalgia, depression, and other symptoms that are often observed in patients with CFS. If this low-level “chronic” infection is localized to the vagus nerve it would be undetectable in the plasma, but could be demonstrated through analyzing tissue biopsies of the vagus nerve, VanElzakker suggests. Radiolabeled antibodies are currently employed in fields such as tumor imaging, where they assist in locating clusters of specific virus in vivo. An antiviral such as valacyclovir (Valtrex), for example, works well against HSV-1 but has limited if any effect on CMV or HHV-6.
However, VanElzakker proposes that when sensory vagal ganglia or paraganglia are themselves infected with any virus or bacteria, these symptoms would be exaggerated. HHV-6 is well-known for invading the hippocampus and other parts of the limbic system, and also establishes residence in the human sensory ganglia along with other neurotropic herpesviruses including HSV-1 and VZV (Hufner 2007). Two infectious disease specialists, Jose Montoya and Martin Lerner, have published previous studies suggesting that valganciclovir therapy may be effective for the subset of CFS patients suspected of having smoldering or low-level infections of HHV-6, EBV and CMV.
He notes that many of the symptoms of sickness behavior (such as fatigue, sleep changes, myalgia, cognitive impairment, depression and zinc depletion) are also mediated by proinflammatory cytokines and observed in CFS.
Ampligen, a drug that has undergone clinical assessment for use among CFS patients, also has antiviral properties. Of interest, lbudilast is a phoshpodiesterase inhibitor and several drugs in this pharmaceutical class have been shown to inhibit CMV replication.




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