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HHV-6A and HHV-6B are double stranded DNA viruses within the betaherpesvirinae subfamily and of the genus Roseolovirus. HHV-6B primary infection is the cause of the common childhood illness exanthema subitum (also known as roseola infantum or sixth disease).
Histological slide of the human herpes virus-6 showing infected cells, with inclusion bodies in both the nucleus and the cytoplasm.
During 1986, Syed Zaki Salahuddin, Dharam Ablashi, and Robert Gallo cultivated peripheral blood mononuclear cells from patients with AIDS and lymphoproliferative illnesses. HHV-6A includes several adult-derived strains and its disease spectrum is not well defined, although it is thought by some to be more neurovirulent.[13][14] HHV-6B is commonly detected in children with roseola infantum, as it is the etiologic agent for this condition.
HHV-6A and HHV-6B were recognized by the International Committee on Taxonomy of Viruses (ICTV) as distinct species in 2012.
The diameter of an HHV-6 virion is about 2000 Angstroms.[8] The virion's outer portion consists of a lipid bilayer membrane that contains viral glycoproteins and is derived from that of the host. During maturation of HHV-6 virions, human cell membranes are used to form viral lipid envelopes (as is characteristic of all enveloped viruses).
The origin of replication (often labeled as "oriLyt" in the literature) is where DNA replication begins.[20] The direct repeat termini (DRL and DRR) possess a repeated TTAGGG sequence, identical to that of human telomeres. The unique segment contains seven major core gene blocks (U27-U37, U38-U40, U41-U46, U48-U53, U56-U57, U66EX2-U77, and U81-U82),[20] which is also characteristic of herpesviruses. This article needs more links to other articles to help integrate it into the encyclopedia. When an extracellular HHV-6 virion comes across human cells, it encounters the human receptor protein cluster of differentiation 46 (CD46). The extracellular region of CD46 contains four short consensus repeats of about 60 amino acids that fold into a compact beta-barrel domain surrounded by flexible loops.[22] As has been demonstrated for CD46 with other ligands, the CD46 protein structure linearizes upon binding HHV-6. During the year 2011, Researchers at the National Institutes of Health attempted to elucidate the then unknown method whereby HHV-6a gains entry into the nervous system.
Active infections involve the linear dsDNA genome circularizing by end to end covalent linkages.
Other betaherpesviruses establish latency as a nuclear episome, which is a circular DNA molecule (analogous to plasmids).
Researchers during 2011 discovered that reactivation can positively be triggered in vitro by histone deacetylase inhibitors.
The classical presentation of primary HHV-6b infection is as exanthema subitum (ES) or "roseola", featuring a high temperature followed by a rash. There are inconsistencies with the correlations between age and seropositivity: According to some reports there is a decrease of seropositivity with the increase of age, while some indicate no significant decline, and others report an increased rate of seropositivity for individuals age 62 and older. Transmission is believed to occur most frequently through the shedding of viral particles into saliva. Vertical transmission has also been described, and occurs in approximately 1% of births in the United States.[6][43] This form is easily identifiable as the viral genome is contained within every cell of an infected individual.
Diagnosis for the virus, particularly HHV-6B, is vital for the patient because of the infectiona€™s adverse effects. The virus periodically re-activates from its latent state, with HHV-6 DNA being detectable in 20-25% of healthy adults in the United States. Multiple sclerosis (MS) is an autoimmune and inflammatory disorder of the nervous system that results in demyelination of axons in the brain and spinal cord. Interestingly, MS prevalence increases in populations as they are farther from the Equator.[50][51] Incidence is three times higher in those born 42 degrees latitude north and above than in those born 37 degrees north and below. To explain the data above, two hypotheses were proposed.[52] The first is known as the Poliomyelitis hypothesis and suggests that infection at a young age confers immunity but adult infection increases MS risk. The Epstein-Barr virus (EBV) paradox is also noteworthy, as HHV-6 has been reported to transactivate EBV.[30] Individuals are at a 10-fold less risk of MS if they are seronegative for EBV. Analysis of the epidemiological, serological, and immunological data above supports the association between an infectious agent and MS. The first study to specifically investigate HHV-6-related demyelination appeared in the literature during 1996, when a previously healthy 19-month-old child developed acute encephalopathy. The molecular mimicry hypothesis, in which T cells are essentially confusing an HHV-6 viral protein with myelin basic protein, first appeared around this time. A few months later, researchers in the United States created a synthetic peptide with a sequence identical to that of an HHV-6 peptide.
Myelin basic protein (MBP) regularly exchanges phosphate groups with the environment, and its ability to do so has implications for proper myelin sheath integrity.


Among individuals with MS, these target threonines have been found to be phosphorylated less often. Some of the genes expressed by HHV-6 manipulate host levels of various cytokines (see section on gene products).
For many, but not all, patients who meet criteria for CFS, the illness begins with an acute, infectious-like syndrome. Other studies have employed assays that can detect active infection: primary cell culture, PCR of serum or plasma, or IgM early antigen antibody assays.
In summary, active infection with HHV-6 is present in a substantial fraction of patients with CFS. Hashimoto's thyroiditis is the most common thyroid disease and is characterized by abundant lymphocyte infiltrate and thyroid impairment. HHV-6 has been detected in lymphomas, leukemias, cervical cancers, and brain tumors.[13] Various medulloblastoma cell lines as well as the cells of other brain tumors have been demonstrated to express the CD46 receptor.
Another product of HHV-6, the immediate early protein U95, has been shown to bind nuclear factor-kappa B. Researchers consistently report having found HHV-6 DNA in tissues that were removed from patients with MTLE.
The virus is a common cause of liver dysfunction and acute liver failure, and has recently been linked to periportal confluent necrosis. In a recent study,[88] the immune stimulant AHCC was recently found to reduce saliva viral loads of HHV-6 in cancer patients.
This was necessitated by the discovery that the herpes viruses of fish and molluscs are only distantly related to those of birds and mammals. Below this membrane envelope is a tegument which surrounds an icosahedral capsid, composed of 162 capsomeres.
Variability in the number of telomeric repeats is observed in the range of 15-180.[22][23] These termini also contain pac-1 and pac-2 cleavage and packing signals that are conserved among herpesviruses. These conserved genes code for proteins that are involved in replication, cleavage, and packing of the viral genome into a mature virion.[22] Additionally, they code for a number of immunomodulatory proteins. Please help improve this article by adding links that are relevant to the context within the existing text. While their precise interaction has not yet been determined, the second and third SCR domains have been demonstrated as required for HHV-6 receptor binding and cellular entry. This process was first reported for the herpes simplex virus.[23] Once circularized, HHV-6 begins to express what are known as "immediate early" genes. In fact, herpes comes from the Greek word herpein, meaning "to creep." Herpesviruses are 'to creep' in that they may enter a latent stage, inactively infecting their human host. However, one study (1997) indicated that a rash is not a distinguishing feature of HHV-6 infection, with rates similar to non-HHV-6 infections (10-20% of febrile children in both groups). HHV-6 primary infections account for up to 20% of infant emergency room visits for fever in the United States[40][41] and are associated with several more severe complications, such as encephalitis, lymphadenopathy, myocarditis and myelosuppression. After primary infection, latency is established in salivary glands, hematopoietic stem cells, and other cells, and exists for the lifetime of the host.
Symptoms that point to this infection, such as rashes, go unnoticed in patients that receive antibiotics because they can be misinterpreted as a side-effect of the medicine.[12] HHV-6B is known to be associated with the childhood disease roseola infantum, as well as other illnesses caused by the infection. In the immunocompetent setting, these re-activations are often asymptomatic, but in immunosuppressed individuals there can be serious complications.
The history of MS in the context of HHV-6 began during 1995 when Peter Challoner, a scientist at PathoGenesis Corporation of Seattle, began looking for non-human genetic sequences in the brains of MS patients.
Individuals are also less likely to present with MS as an adult if their childhood was spent in a low incidence region. The second is known as the Prevalence hypothesis, and suggests that MS is caused by a pathogen that is more common in regions with high rates of MS.
However, among individuals who are positive, those that acquire EBV infection later in life are at a 3-fold greater risk for MS. EBV antibodies in healthy individuals remain constant, whereas antibody levels in individuals who later develop MS begin to increase and plateau between 20 and 30 years of age, regardless of age of onset. However, the exact mechanism of a possible viral influence on the manifestation of MS is less clear. Levels of myelin basic protein were elevated in his cerebrospinal fluid, suggesting that demyelination was occurring.[56] This link was almost forgotten, until four years later when an MS-related study was published showing an HHV-6 prevalence of 90% among demyelinated brain tissues. Early on in the development of this hypothesis (2002), Italian researchers used the HHV-6a variant along with bovine myelin basic protein to generate cross-reactive T cell lines.


More specifically, two threonine residues on MBP have been identified as the phosphorylation targets of glycogen synthase kinase and mitogen-activated protein kinase. In fact, HHV-6 produces a transmembrane protein, known as U24, that is also a phosphorylation target of the kinases mentioned previously. OECs have been investigated thoroughly in relation to spinal cord injuries, amyotrophic lateral sclerosis, and other neurodegenerative diseases.
For instance, infected cells have increased levels of interleukin-8, which is believed to induce MMP-9 epression. Cases of CFS can follow well-documented infections with several infectious agents.[65] A study of 259 patients with a "CFS-like" illness published shortly after HHV-6 was discovered used primary lymphocyte cultures to identify people with active replication of HHV-6.
Moreover, HHV-6 is known to infect cells of the nervous system and immune system, organ systems with demonstrable abnormalities in CFS. For instance, HHV-8 is linked to Kaposi's sarcoma,[77] the Epstein-Barr virus to Burkitt's lymphoma, and HPV to cervical cancer.
Individuals who do not properly produce this protein experience a higher incidence of cancer, a phenomenon known as Li-Fraumeni syndrome. Within this region of the brain exists three structures: the amygdala, hippocampus, and parahippocampal gyrus. Because of possible confusion with viruses derived from reptiles, the family name was changed in the third report (1979) to herpesviridae. The unique segment also possesses a block of genes (U2-U19) that are conserved among HHV-6, HHV-7, and Cytomegaloviruses (the betaherpesviruses). When various anatomical regions were assayed for their viral load, olfactory tissues were found to have the highest HHV-6 content.
These gene products are believed to be transcription activators[6] and may be regulated by the expression of viral micro RNAs.[25] Subsequent expression of "early genes" then occurs and activates, for instance, viral DNA polymerases.
HHV-6 infections more frequently present with high temperatures (over 40C), at a rate of around two thirds compared to less than half in the non-HHV-6 patients. Studies report varying rates of prevalence of HHV-6 in saliva (between 3% - 90%),[12] and have also described the salivary glands as an in vivo reservoir for HHV-6. HHV-6 re-activation causes severe disease in transplant recipients and can lead to graft rejection, often in consort with other betaherpesviridae. The possibility of a causative infectious agent in association with MS has been evaluated through the lens of these epidemiological findings. This pathogen would be widespread and cause an asymptomatic (latent) infection in most individuals. These were compared to the T cells of individuals with MS as well as those of controls, and no significant difference was found between the two. These activated T cells also recognized and initiated an immune response against a synthetically created peptide sequence that is identical to part of human myelin basic protein.
Our kinases act on an HHV-6 protein due to a shared sequence of seven amino acids (MBP92a€“104=IVTPRTPPPSQGK; U241a€“13=MDPPRTPPPSYSE).
Despite this association, it remains unproven that reactivated HHV-6 infection is a cause of CFS.
One of HHV-6a€™s gene products, the U14 protein, binds P53 and incorporates it into virions. A number of the unique segment genes are associated with, for instance, the HCMV US22 family. He also noticed a higher concentration of infected cells in areas where demyelination had occurred.[49] His research was likely the first published study to suggest a link between HHV-6 and MS.
Only rarely and years after the primary infection does this hypothetical agent cause the neurological symptoms of MS. During their research, they found that the levels of these cross-reactive T cells are significantly elevated in MS patients.[58] Their research concluded by suggesting that HHV-6 may indeed be a causative agent for MS.
Although up to 100% of the population are exposed (seropositive) to HHV-6, most by 3 years of age, there are rare cases of primary infections in adults. A third hypothesis essentially combines these two and also suggests the involvement of multiple pathogens.
In the United States, these have been linked more with HHV-6a, which is thought to be more pathogenic and more neurotropic and has been linked to several central nervous system-related disorders.



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