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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.
The NIH grant funding databases CRISP, Explorer, and REPORTer were each thoroughly reviewed for research grants with individual viruses (or specific viral proteins such as the KSHV oncoprotein K13) mentioned in their TITLE or ABSTRACT (if available). This significant investment of funding allocated toward research on EBV, CMV, and KSHV has produced a wealth of knowledge regarding the pathogenic mechanisms, epidemiology, and gene product functions for each of these herpesviruses, leading to the development of steadily improved diagnostic tools and new virus-specific therapeutic approaches in a rather short timeframe. All NIH extramural grants given to study HHV-6 & 7 between 2000-2012 have been provided below. 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. Practical Oral Care for People With Developmental Disabilities – This booklet presents an overview of physical, mental, and behavioral challenges common in patients with developmental disabilities and offers strategies for providing oral care. This external link provides additional information that is consistent with the intended purpose of this site. Linking to a non-federal site does not constitute an endorsement by NIH or any of its employees of the sponsors or the information and products presented on the site. Help people who are suffering from genital herpes by volunteering for NIAID clinical studies on ClinicalTrials.gov.
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Scientists at NIAID and the National Center for Advancing Translational Sciences, two components of the National Institutes of Health (NIH), have identified key proteins required by two different herpesviruses to initiate infection. Sensory ganglia from mice latently infected with herpes simplex virus-1 are stained for reactivating virus. Like all members of the herpesvirus family, these viruses establish life-long dormant infections in people and can reactivate at any time to cause disease. When a herpesvirus infects a cell, its DNA is wrapped into histone-protein structures, called nucleosomes, that can either enhance or repress the initial stage of infection. The scientists demonstrated that during the early stages of infection, HCMV and HSV-1 require two classes of host enzymes, called LSD1 and JMJD2, to modify the histone structures and activate the first wave of viral gene expression. In the previous work, NIAID scientists demonstrated that inhibiting LSD1 using a type of anti-depression drug called an MAO inhibitor blocked HSV-1 infection. Importantly, as these and potentially other related viruses use common enzymes to initiate infection, such as LSD1 and JMJD2, the novel inhibitors in this study may have the capacity to treat other viral infections.
The scientists are continuing their studies of ML324 in animal models of infection and viral reactivation from latency. 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. Funding information was gathered on NIH extramural grants given to study HHV-4 (EBV), HHV-5 (CMV), HHV-6, HHV-7, and HHV-8 (KSHV) from 2000—2012 (graph above, chart below).
Unfortunately, no comparable investment has been made in Roseolovirus research, and as a result, researchers have needed to rely on private funding and limited resources to continue their important work on HHV-6 & HHV-7 over the past several years, and vital information regarding the biological and pathogenic nature of these viruses has not progressed to the point many hoped it would by this time.
For additional information on grants given for each virus in the review, download a copy of the entire detailed analysis HERE. 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. Based upon these findings, the groups demonstrated that inhibiting the activities of these proteins with a novel drug blocks herpesvirus infection and reactivation from dormancy.


At left, the large red neuron illustrates reactivating virus, and surrounding smaller red cells show the spread of infection from the neuron to support cells. They include herpes simplex virus (HSV) types 1 and 2, which cause oral and genital herpes, and human cytomegalovirus (HCMV), which can cause significant complications in immune-compromised people, such as organ transplant recipients who take anti-rejection drugs. Building on work published in 2009, the NIH scientists focused on identifying the cellular enzymes required to prevent these structures from repressing viral gene expression, thus allowing infection to proceed. Therefore, they tested synthetic small-molecule compounds to identify a drug that would inhibit the second group of enzymes, the JMJD2 family. While these drugs are an important advance in the treatment of herpesvirus infections, they do not prevent early-stage infection, which can result in inflammation and tissue damage.
Additionally, they are investigating other required host proteins that may also serve as potential targets for antiviral development. Targeting the JMJD2 histone demethylases to epigenetically control herpesvirus infection and reactivation from latency.
Inhibition of the histone demethylase LSD1 blocks ?-herpesvirus lytic replication and reactivation from latency. The HHV-6 Foundation gives modest Pilot Grants to investigators interested in pursuing research on HHV-6 to this end.
In contrast, targeting the initiation stage of infection may prove to be more effective in controlling infection-related tissue damage and transmission. This NIH study provides additional evidence in support of emerging therapeutic strategies that aim to modulate human host proteins to fight infections.



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