Human herpesvirus 6A, 6B and 7: Infectious substances pathogen safety data sheet

Section I – Infectious agent

Name

Human betaherpesvirus 6A, 6B, and 7

Agent type

Virus

Taxonomy

Family

Orthoherpesviridae

Genus

Roseolovirus

Species

Roseolovirus humanbeta6a, Roseolovirus humanbeta6b, Roseolovirus humanbeta7

Synonym or cross-reference

Human betaherpesvirus 6 (HHV-6) collectively refers to the 6A and 6B variants^{Footnote 1}. HHV-6 was previously designated as human B-lymphotropic virus^{Footnote 2}. Also known as roseolovirus, roseola infantum, exanthema subitum, and sixth disease^{Footnote 3}^{Footnote 4}.

Characteristics

Brief description

Human betaherpesvirus 6A (HHV-6A), human betaherpesvirus 6B (HHV-6B), and human betaherpesvirus 7 (HHV-7) are enveloped, double-stranded DNA viruses, 150 to 200 nm in diameter^{Footnote 5}. Herpesviruses are made of four main components: the genome, capsid, tegument, and envelope. The tegument contains thousands of protein and RNA molecules surrounding the icosahedral capsid and is contained within the viral envelope^{Footnote 6}. Genomes of HHV-6 and HHV-7 are 159-162 kb and 145-153 kbp in size, respectively^{Footnote 5}^{Footnote 7}. The overall G+C content of both HHV-6 and HHV-7 are 43%^{Footnote 8}. HHV-6 (A and B) and HHV-7 have telomere-like repeats that flank the ends of the genome to facilitate its integration into the telomeric region of host chromosomal DNA during latency^{Footnote 7}^{Footnote 9}^{Footnote 10}.

Properties

HHV-6 (A and B) and HHV-7 have a biphasic life cycle. Latency for HHV-6 involves integration of viral DNA into host chromosomal DNA. During latency, viral and host DNA is passed down to host daughter cells without infectious virus production. Integration of HHV-6 (A and B) DNA into germline cells enables the virus to be passed down to progeny, referred to as inherited chromosomally integrated HHV-6 (iciHHV-6)^{Footnote 11}. For these individuals, every nucleated cell in the body contains a copy of the HHV-6 (A or B) genome^{Footnote 7}. HHV-6 establishes latent infection in peripheral blood mononuclear cells, while HHV-7 establishes latent infection in CD4+ lymphocytes^{Footnote 5}^{Footnote 12}. Upon reactivation, the HHV-6 (A and B) and HHV-7 revert to the lytic cycle in tissues, in which viruses are actively produced. During the lytic cycle, the host may or may not be symptomatic.

HHV-6 (A and B) and HHV-7 are lymphotropic viruses that have a predilection for CD4+ T lymphocytes^{Footnote 1}. HHV-6A uses cellular receptor CD46, whereas HHV-6B primarily uses CD134 and to a lesser extent CD46^{Footnote 1}^{Footnote 7}^{Footnote 13}. HHV-6A and HHV-6B differ in their ability to infect other cell types^{Footnote 1}. HHV-7 infects CD4+ T lymphocytes and uses the CD4 receptor^{Footnote 5}. Proteins encoded by HHV-6 and HHV-7 have immunomodulatory capacities to increase survival by evading the host immune response and changing the environment of the host cell^{Footnote 5}.

HHV-6 (A and B) and HHV-7 have been found in many tissues of the body including the brain^{Footnote 14}^{Footnote 15}, eye^{Footnote 16}^{Footnote 17}, bone marrow^{Footnote 5}^{Footnote 18}, lymphoid tissue^{Footnote 19}^{Footnote 20}, salivary glands^{Footnote 21}^{Footnote 22}, lungs^{Footnote 23}^{Footnote 24}, gastrointestinal tract^{Footnote 25}^{Footnote 26}, and liver^{Footnote 27}^{Footnote 28}.

Section II – Hazard identification

Pathogenicity and toxicity

HHV-6A seems to largely cause asymptomatic primary infection in young children^{Footnote 5}^{Footnote 29}. HHV-6B and HHV-7 cause exanthema subitum, also known as roseola infantum, usually in children under 2 years of age. Primary HHV-7 infection tends to occur at a later age, with 75% of children being seropositive by age 5^{Footnote 3}^{Footnote 4}^{Footnote 30}^{Footnote 31}^{Footnote 32}^{Footnote 33}. Symptoms of HHV-6B- and HHV-7-associated exanthema subitum are clinically indistinguishable and generally include fever, febrile seizure, rhinorrhea, diarrhoea, and a maculopapular skin rash that persists for 1 to 4 days^{Footnote 4}^{Footnote 31}^{Footnote 34}^{Footnote 35}. HHV-6B and HHV-7 infections may also be asymptomatic^{Footnote 30}^{Footnote 35}. Although infrequent, manifestations of HHV-6 (A and B) and HHV-7 may involve the central nervous system (CNS)^{Footnote 36}^{Footnote 37}^{Footnote 38}. Neurological complications of HHV-6B and HHV-7 include encephalitis, meningoencephalitis^{Footnote 39}, status epilepticus^{Footnote 40}, convulsions^{Footnote 31}, motor and psychomotor impairment, and intellectual disabilities, with prevalence rates of neurological complications of up to 50%^{Footnote 41}. HHV-6 infection has also been associated with brain tumours^{Footnote 42}.

HHV-6 encephalitis is associated with a mortality rate of approximately 20%, and survivors suffer significant morbidity^{Footnote 43}. Sequelae in children with meningoencephalitis or encephalitis associated with HHV-6B infection include visual impairment, speech impairment, and paralysis on one side of the body^{Footnote 38}^{Footnote 44}.

Following primary infection, HHV-6 (A and B) and HHV-7 establish persistent latent infection. Reactivation of HHV-6B, HHV-7, and to a far lesser degree HHV-6A has been associated with many health conditions. Pityriasis rosea is a self-limiting skin condition that is related to HHV-6 and/or HHV-7 reactivation^{Footnote 45}. Reactivation of HHV-7 has been associated with myocarditis in children^{Footnote 46}, while reactivation of HHV-6B has been linked to dilated cardiomyopathy and cardiac dysfunction^{Footnote 47}^{Footnote 48}. In some cases, HHV-6 and HHV-7 reactivation is associated with a rare and serious adverse drug reaction referred to as drug rash with eosinophilia and systemic symptoms (DRESS)^{Footnote 49}^{Footnote 50}^{Footnote 51}. HHV-6 and HHV-7 reactivation is frequent in Kawasaki disease patients^{Footnote 52}. Reactivation of HHV-6A is associated with progressive multiple sclerosis and Hashimoto’s thyroiditis^{Footnote 53}^{Footnote 54}^{Footnote 55}. HHV-6 (A and B) reactivation frequently occurs in ocular inflammatory diseases^{Footnote 17}. Reactivation of HHV-6A and HHV-7 has been associated with Alzheimer’s disease^{Footnote 56}. Immunocompromised individuals are at higher risk for developing health conditions after reactivation^{Footnote 57}.

HHV-6B and HHV-7 reactivate in approximately 30-60% of hematopoietic stem cell transplant (HSCT) recipients, and less frequently in solid organ transplant recipients^{Footnote 5}^{Footnote 13}^{Footnote 58}^{Footnote 59}^{Footnote 60}^{Footnote 61}^{Footnote 62}. HHV-6 reactivation in immunocompromised individuals, such as transplant recipients, is associated with encephalitis, and graft rejection in solid organ transplant patients^{Footnote 58}^{Footnote 63}^{Footnote 64}^{Footnote 65}.

Epidemiology

HHV-6 (A and B) and HHV-7 are ubiquitous worldwide. Prevalence of HHV-6B and HHV-7 in adults is approximately 80-96% and 75-98%, respectively^{Footnote 66}^{Footnote 67}^{Footnote 68}^{Footnote 69}^{Footnote 70}. Prevalence of HHV-6A varies widely according to region^{Footnote 29}^{Footnote 67}^{Footnote 69}. Due to the similar immunology response to testing, and a lack of serological assays to differentiate HHV-6A and HHV-6B, determining the prevalence of HHV-6A and HHV-6B in various populations is difficult^{Footnote 23}. The vast majority of primary HHV-6 and HHV-7 infections occur in early childhood. Seroprevalence is over 75% for HHV-6 in children up to 2 years of age^{Footnote 71}. HHV-6 or HHV-7 are associated with approximately 32% of cases of acute encephalitis in children^{Footnote 72}.

CNS involvement is more frequent when primary HHV-7 infection occurs in older children^{Footnote 73}. Rare genetic disorders in otherwise healthy children may predispose them to encephalopathy during primary HHV-6B or HHV-7 infection^{Footnote 38}^{Footnote 74}. Hematopoietic stem cell transplantation (HSCTs) are risk factors for HHV-6 and HHV-7-associated encephalitis^{Footnote 38}^{Footnote 58}. HHV-6 reactivation in HSCT patients was associated with poor clinical outcomes including decreased overall survival and increased incidence of acute graft-versus-host disease^{Footnote 59}. HHV-6 reactivation is also commonly observed in pregnant women, and iciHHV-6 results in higher risk of pre-eclampsia in fetuses and spontaneous abortion in pregnant women^{Footnote 75}.

Outbreaks of HHV-6 infection were reported in Brazil between October and December 1997, infecting children aged less than 7 years old at daycare centers. Serum samples were collected from 401 of 730 children, and seroprevalence of HHV-6 was found to be 63.8%^{Footnote 76}.

Host range

Natural host(s)

Humans^{Footnote 5}.

Other host(s)

Non-human primates, rabbits, and mice have been experimentally infected with HHV-6 (A and B)^{Footnote 77}^{Footnote 78}^{Footnote 79}^{Footnote 80}.

Infectious dose

Unknown.

Incubation period

Incubation period is approximately 1 to 2 weeks^{Footnote 36}.

Communicability

HHV-6 (A and B) and HHV-7 are found in human saliva^{Footnote 21}^{Footnote 22}^{Footnote 81}. Person-to-person transmission is likely to occur primarily via saliva through close contact with mucous membranes in the nasopharynx and olfactory routes^{Footnote 82}^{Footnote 83}^{Footnote 84}. HHV-6 (A and B) can also cause congenital infection via germline passage of chromosomally-integrated HHV-6 DNA and from transplacental passage of maternal HHV-6 infection^{Footnote 11}. Inherited-chromosomally-integrated HHV-6 (A and B) affects approximately 1% of infants and is the more common mode of in-utero transmission^{Footnote 71}^{Footnote 85}. A case of HHV-7 congenital infection via germline passage of chromosomally-integrated HHV-7 has been reported^{Footnote 9}. There have been rare cases of HHV-6 transmission through organ transplantation^{Footnote 86}.

Section III – Dissemination

Reservoir

Humans^{Footnote 5}.

Zoonosis

None.

Vectors

None.

Section IV – Stability and viability

Drug susceptibility/resistance

Ganciclovir (valganciclovir), foscarnet, and cidofovir inhibit replication of HHV-6 (A and B) and HHV-7^{Footnote 5}. Brincidofovir (CMX001) is a lipid-ester derivative effective against DNA viruses including HHV-6 (A and B) and HHV-7^{Footnote 5}. HHV-6 is naturally resistant to acyclovir because the high concentrations required for HHV-6 inhibition is only achievable in vitro and not in vivo^{Footnote 87}.

Susceptibility to disinfectants

Quaternary ammonium compounds, chlorhexidine (0.02%), rubbing alcohol (1:1 mixture), sodium hypochlorite (0.2%), alkaline glutaraldehyde (2%) are effective against herpesviruses^{Footnote 88}^{Footnote 89}^{Footnote 90}^{Footnote 91}^{Footnote 92}.

Physical inactivation

Herpesviruses are inactivated by heat (56°C for 10 minutes), pH less than 5 or greater than 11, and incubation under UV light (20 cm for 5 minutes)^{Footnote 90}^{Footnote 93}^{Footnote 94}.

Survival outside host

When dried on inanimate surfaces, herpesviruses generally remain infective for less than one day at room temperature with relative humidity greater than 55%^{Footnote 95}, but can persist for up to 8 weeks when relative humidity is low^{Footnote 96}. Herpesviruses can remain infective in water for up to 3 weeks under certain conditions^{Footnote 97}.

Section V – First aid/medical

Surveillance

HHV-6 (A and B) and HHV-7 nucleic acid can be detected in clinical specimens using PCR^{Footnote 98}^{Footnote 99}. However there is a need to distinguish between iciHHV-6/iciHHV-7, latent infection, and active infection (i.e., primary infection or reactivation) when viral nucleic acids are detected. To rule out iciHHV-6 or iciHHV-7, hair follicles or nails can be tested. Active HHV-6 infections usually have viral loads exceeding 1,000 DNA copies per mL of whole blood^{Footnote 5}^{Footnote 100}. Active HHV-6 or HHV-7 infection can also be shown by quantifying viral mRNA using reverse transcriptase PCR^{Footnote 38}. Primary HHV-6 or HHV-7 infections can be identified by measuring the increase in IgG antibody titer in serum at acute and convalescent phases of infection using immunofluorescent antibody assays^{Footnote 5}^{Footnote 33}^{Footnote 101}. Virus isolation in cell culture and antigen detection are other methods of directly detecting HHV-6 and HHV-7, however, these methods are not sensitive and are time-consuming^{Footnote 87}.

Note: The specific recommendations for surveillance in the laboratory should come from the medical surveillance program, which is based on a local risk assessment of the pathogens and activities being undertaken, as well as an overarching risk assessment of the biosafety program as a whole. More information on medical surveillance is available in the Canadian Biosafety Handbook.

First aid/treatment

Primary HHV-6 (A and B) and HHV-7 infections are usually self-limiting^{Footnote 5}^{Footnote 38}. HHV-6 or HHV-7 infections with complications, such as encephalitis, can be treated using antiviral drugs including ganciclovir, foscarnet, and/or cidofovir^{Footnote 5}^{Footnote 13}^{Footnote 38}. Virus-specific T cells have been used to treat HHV-6 infections in allogeneic hematopoietic stem cell transplant recipients^{Footnote 102}.

Note: The specific recommendations for first aid/treatment in the laboratory should come from the post-exposure response plan, which is developed as part of the medical surveillance program. More information on the post-exposure response plan can be found in the Canadian Biosafety Handbook.

Immunization

There is no vaccine against HHV-6 or HHV-7.

Note: More information on the medical surveillance program can be found in the Canadian Biosafety Handbook, and by consulting the Canadian Immunization Guide.

Prophylaxis

None.

Note: More information on prophylaxis as part of the medical surveillance program can be found in the Canadian Biosafety Handbook.

Section VI – Laboratory hazard

Laboratory-acquired infections

None reported.

Note: Please consult the Canadian Biosafety Standard and Canadian Biosafety Handbook for additional details on requirements for reporting exposure incidents. A Canadian biosafety guideline describing notification and reporting procedures is also available.

Sources/specimens

Clinical specimens include saliva, blood/plasma, cerebrospinal fluid, bone marrow, biopsy samples (e.g., brain, lung, skin, liver), urine, female reproductive tissues and genital secretions^{Footnote 5}^{Footnote 23}^{Footnote 27}^{Footnote 38}^{Footnote 71}^{Footnote 103}.

Primary hazards

Inhalation of concentrated aerosolized infectious material, exposure of wounded skin or mucous membranes (e.g., eyes, nose, or mouth) to infectious material, and accidental autoinoculation with infectious material^{Footnote 82}^{Footnote 83}^{Footnote 84}.

Special hazards

None.

Section VII – Exposure controls/personal protection

Risk group classification

HHV-6 (A and B) and HHV-7 are Risk Group 2 Human Pathogens and Risk Group 1 Animal Pathogens^{Footnote 104}^{Footnote 105}.

Containment requirements

Containment Level 2 facilities, equipment, and operational practices outlined in the Canadian Biosafety Standard for work involving infectious or potentially infectious materials, animals, or cultures.

Protective clothing

The applicable Containment Level 2 requirements for personal protective equipment and clothing outlined in the Canadian Biosafety Standard are to be followed. The personal protective equipment could include the use of a labcoat and dedicated footwear (e.g., boots, shoes) or additional protective footwear (e.g., boot or shoe covers) where floors may be contaminated (e.g., animal cubicles, PM rooms), gloves when direct skin contact with infected materials or animals is unavoidable, and eye protection where there is a known or potential risk of exposure to splashes.

Note: A local risk assessment will identify the appropriate hand, foot, head, body, eye/face, and respiratory protection, and the personal protective equipment requirements for the containment zone and work activities must be documented.

Other precautions

A biological safety cabinet (BSC) or other primary containment devices to be used for activities with open vessels, based on the risks associated with the inherent characteristics of the regulated material, the potential to produce infectious aerosols or aerosolized toxins, the handling of high concentrations of regulated materials, or the handling of large volumes of regulated materials.

Use of needles and syringes to be strictly limited. Bending, shearing, re-capping, or removing needles from syringes to be avoided, and if necessary, performed only as specified in standard operating procedures (SOPs). Additional precautions are required with work involving animals or large-scale activities.

For diagnostic laboratories handling primary specimens that may contain HHV 6 (A and B) or HHV-7, the following resources may be consulted:

Section VIII – Handling and storage

Spills

Allow aerosols to settle. Wearing personal protective equipment, gently cover the spill with absorbent paper towel and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (Canadian Biosafety Handbook ).

Disposal

All materials/substances that have come in contact with the regulated materials should be completely decontaminated before they are removed from the containment zone or standard operating procedures (SOPs) to be in place to safely and securely move or transport waste out of the containment zone to a designated decontamination area / third party. This can be achieved by using decontamination technologies and processes that have been demonstrated to be effective against the regulated material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination (Canadian Biosafety Handbook ).

Storage

Containment Level 2: The applicable Containment Level 2 requirements for storage outlined in the Canadian Biosafety Standard are to be followed. Primary containers of regulated materials removed from the containment zone to be labelled, leakproof, impact resistant, and kept either in locked storage equipment or within an area with limited access.

Section IX – Regulatory and other information

Canadian regulatory information

Controlled activities with HHV-6 (A and B) and HHV-7 require a Human Pathogens and Toxins licence issued by the Public Health Agency of Canada.

The following is a non-exhaustive list of applicable designations, regulations, or legislations:

Last file update

September 2023

Prepared by

Centre for Biosecurity, Public Health Agency of Canada.

Disclaimer

The scientific information, opinions, and recommendations contained in this Pathogen Safety Data Sheet have been developed based on or compiled from trusted sources available at the time of publication. Newly discovered hazards are frequent and this information may not be completely up to date. The Government of Canada accepts no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information.

Persons in Canada are responsible for complying with the relevant laws, including regulations, directives and standards applicable to the import, transport, and use of pathogens and toxins in Canada set by relevant regulatory authorities, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment and Climate Change Canada, and Transport Canada. The risk classification and related regulatory requirements referenced in this Pathogen Safety Data Sheet, such as those found in the Canadian Biosafety Standard, may be incomplete and are specific to the Canadian context. Other jurisdictions will have their own requirements.

References

Footnotes

Footnote 1

Ablashi, D., H. Agut, R. Alvarez-Lafuente, D. A. Clark, S. Dewhurst, D. DiLuca, L. Flamand, N. Frenkel, R. Gallo, U. A. Gompels, P. Hollsberg, S. Jacobson, M. Luppi, P. Lusso, M. Malnati, P. Medveczky, Y. Mori, P. E. Pellett, J. C. Pritchett, K. Yamanishi, and T. Yoshikawa. 2014. Classification of HHV-6A and HHV-6B as distinct viruses. Arch. Virol. 159:863-870.

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Footnote 2

Salahuddin, S. Z., D. V. Ablashi, P. D. Markham, S. F. Josephs, S. Sturzenegger, M. Kaplan, G. Halligan, P. Biberfeld, F. Wong-Staal, and B. Kramarsky. 1986. Isolation of a new virus, HBLV, in patients with lymphoproliferative disorders. Science. 234:596-601.

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Footnote 3

Tanaka, K., T. Kondo, S. Torigoe, S. Okada, T. Mukai, and K. Yamanishi. 1994. Human herpesvirus 7: another causal agent for roseola (exanthem subitum). J. Pediatr. 125:1-5.

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Footnote 4

Asano, Y., T. Yoshikawa, S. Suga, I. Kobayashi, T. Nakashima, T. Yazaki, Y. Kajita, and T. Ozaki. 1994. Clinical features of infants with primary human herpesvirus 6 infection (exanthem subitum, roseola infantum). Pediatrics. 93:104-108.

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Footnote 5

Agut, H., P. Bonnafous, and A. Gautheret-Dejean. 2016. Human Herpesviruses 6A, 6B, and 7. Microbiol. Spectr. 4:10.1128/microbiolspec.DMIH2-0007-2015.

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Footnote 6

Close, W. L., A. N. Anderson, and P. E. Pellett. 2018. Betaherpesvirus Virion Assembly and Egress. Adv. Exp. Med. Biol. 1045:167-207.

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Footnote 7

Pantry, S. N., and P. G. Medveczky. 2017. Latency, Integration, and Reactivation of Human Herpesvirus-6. Viruses. 9:10.3390/v9070194.

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Footnote 8

Dominguez, G., T. R. Dambaugh, F. R. Stamey, S. Dewhurst, N. Inoue, and P. E. Pellett. 1999. Human herpesvirus 6B genome sequence: coding content and comparison with human herpesvirus 6A. J Virol 73:8040-52.

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Footnote 9

Prusty, B. K., N. Gulve, S. Rasa, M. Murovska, P. C. Hernandez, and D. V. Ablashi. 2017. Possible chromosomal and germline integration of human herpesvirus 7. J. Gen. Virol. 98:266-274.

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Footnote 10

Thomson, B. J., S. Dewhurst, and D. Gray. 1994. Structure and heterogeneity of the a sequences of human herpesvirus 6 strain variants U1102 and Z29 and identification of human telomeric repeat sequences at the genomic termini. J. Virol. 68:3007-3014.

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Footnote 11

Hall, C. B., M. T. Caserta, K. C. Schnabel, L. M. Shelley, J. A. Carnahan, A. S. Marino, C. Yoo, and G. K. Lofthus. 2010. Transplacental congenital human herpesvirus 6 infection caused by maternal chromosomally integrated virus. J. Infect. Dis. 201:505-507.

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Footnote 12

Miyake, F., T. Yoshikawa, H. Sun, A. Kakimi, M. Ohashi, S. Akimoto, Y. Nishiyama, and Y. Asano. 2006. Latent infection of human herpesvirus 7 in CD4(+) T lymphocytes. J. Med. Virol. 78:112-116.

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Footnote 13

Zerr, D. M. 2018. Human Herpesvirus 6B in the Transplant Recipient: When to Worry, When to Act. J. Pediatric Infect. Dis. Soc. 7:S75-S78.

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Footnote 14

Chan, P. K., H. K. Ng, M. Hui, and A. F. Cheng. 2001. Prevalence and distribution of human herpesvirus 6 variants A and B in adult human brain. J. Med. Virol. 64:42-46.

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Footnote 15

Chapenko, S., S. Roga, S. Skuja, S. Rasa, M. Cistjakovs, S. Svirskis, Z. Zaserska, V. Groma, and M. Murovska. 2016. Detection frequency of human herpesviruses-6A, -6B, and -7 genomic sequences in central nervous system DNA samples from post-mortem individuals with unspecified encephalopathy. J. Neurovirol. 22:488-497.

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Footnote 16

Cohen, J. I., G. Fahle, M. A. Kemp, K. Apakupakul, and T. P. Margolis. 2010. Human herpesvirus 6-A, 6-B, and 7 in vitreous fluid samples. J. Med. Virol. 82:996-999.

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Footnote 17

Sugita, S., N. Shimizu, K. Watanabe, M. Ogawa, K. Maruyama, N. Usui, and M. Mochizuki. 2012. Virological analysis in patients with human herpes virus 6-associated ocular inflammatory disorders. Invest. Ophthalmol. Vis. Sci. 53:4692-4698.

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Footnote 18

Gautheret-Dejean, A., O. Dejean, L. Vastel, M. Kerboull, J. T. Aubin, M. Franti, and H. Agut. 2000. Human herpesvirus-6 and human herpesvirus-7 in the bone marrow from healthy subjects. Transplantation. 69:1722-1723.

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Footnote 19

Kempf, W., B. Muller, R. Maurer, V. Adams, and G. Campadelli Fiume. 2000. Increased expression of human herpesvirus 7 in lymphoid organs of AIDS patients. J. Clin. Virol. 16:193-201.

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Footnote 20

Roush, K. S., R. K. Domiati-Saad, L. R. Margraf, K. Krisher, R. H. Scheuermann, B. B. Rogers, and D. B. Dawson. 2001. Prevalence and cellular reservoir of latent human herpesvirus 6 in tonsillar lymphoid tissue. Am. J. Clin. Pathol. 116:648-654.

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Footnote 21

Aberle, S. W., C. W. Mandl, C. Kunz, and T. Popow-Kraupp. 1996. Presence of human herpesvirus 6 variants A and B in saliva and peripheral blood mononuclear cells of healthy adults. J. Clin. Microbiol. 34:3223-3225.

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Footnote 22

Magalhaes, I. M., R. V. Martins, J. J. Cossatis, R. M. Cavaliere, L. A. Afonso, N. Moyses, S. A. Oliveira, and S. M. Cavalcanti. 2010. Detection of human herpesvirus 6 and 7 DNA in saliva from healthy adults from Rio de Janeiro, Brazil. Mem. Inst. Oswaldo Cruz. 105:925-927.

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Footnote 23

Cone, R. W., M. L. Huang, R. C. Hackman, and L. Corey. 1996. Coinfection with human herpesvirus 6 variants A and B in lung tissue. J. Clin. Microbiol. 34:877-881.

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Footnote 24

Yamamoto, K., T. Yoshikawa, S. Okamoto, K. Yamaki, K. Shimokata, and Y. Nishiyama. 2005. HHV-6 and 7 DNA loads in lung tissues collected from patients with interstitial pneumonia. J. Med. Virol. 75:70-75.

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Footnote 25

Sasaki, M., N. Shimizu, Y. Zushi, T. Saito, H. Tsunemine, K. Itoh, Y. Aoyama, Y. Goto, T. Kodaka, G. Tsuji, E. Senda, T. Fujimori, T. Itoh, and T. Takahashi. 2018. Analysis of gastrointestinal virus infection in immunocompromised hosts by multiplex virus PCR assay. AIMS Microbiol. 4:225-239.

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Footnote 26

Lempinen, M., L. Halme, J. Arola, E. Honkanen, K. Salmela, and I. Lautenschlager. 2012. HHV-6B is frequently found in the gastrointestinal tract in kidney transplantation patients. Transpl. Int. 25:776-782.

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Footnote 27

Ozaki, Y., H. Tajiri, K. Tanaka-Taya, S. Mushiake, A. Kimoto, K. Yamanishi, and S. Okada. 2001. Frequent detection of the human herpesvirus 6-specific genomes in the livers of children with various liver diseases. J. Clin. Microbiol. 39:2173-2177.

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Footnote 28

Rauber, C., K. Bartelheimer, T. Zhou, C. Rupp, P. Schnitzler, P. Schemmer, P. Sauer, K. H. Weiss, and D. N. Gotthardt. 2019. Prevalence of human herpesviruses in biliary fluid and their association with biliary complications after liver transplantation. BMC Gastroenterol. 19:110-019-1033-x.

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Footnote 29

Bates, M., M. Monze, H. Bima, M. Kapambwe, D. Clark, F. C. Kasolo, and U. A. Gompels. 2009. Predominant human herpesvirus 6 variant A infant infections in an HIV-1 endemic region of Sub-Saharan Africa. J. Med. Virol. 81:779-789.

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Footnote 30

Caserta, M. T., C. B. Hall, K. Schnabel, C. E. Long, and N. D'Heron. 1998. Primary human herpesvirus 7 infection: a comparison of human herpesvirus 7 and human herpesvirus 6 infections in children. J. Pediatr. 133:386-389.

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Footnote 31

Tesini, B. L., L. G. Epstein, and M. T. Caserta. 2014. Clinical impact of primary infection with roseoloviruses. Curr. Opin. Virol. 9:91-96.

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Footnote 32

Hall, C. B., M. T. Caserta, K. C. Schnabel, M. P. McDermott, G. K. Lofthus, J. A. Carnahan, L. M. Gilbert, and S. Dewhurst. 2006. Characteristics and acquisition of human herpesvirus (HHV) 7 infections in relation to infection with HHV-6. J. Infect. Dis. 193:1063-1069.

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Footnote 33

Ward, K. N., N. J. Andrews, C. M. Verity, E. Miller, and E. M. Ross. 2005. Human herpesviruses-6 and -7 each cause significant neurological morbidity in Britain and Ireland. Arch. Dis. Child. 90:619-623.

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Footnote 34

Laina, I., V. P. Syriopoulou, G. L. Daikos, E. S. Roma, F. Papageorgiou, T. Kakourou, and M. Theodoridou. 2010. Febrile seizures and primary human herpesvirus 6 infection. Pediatr. Neurol. 42:28-31.

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Footnote 35

Zerr, D. M., A. S. Meier, S. S. Selke, L. M. Frenkel, M. L. Huang, A. Wald, M. P. Rhoads, L. Nguy, R. Bornemann, R. A. Morrow, and L. Corey. 2005. A population-based study of primary human herpesvirus 6 infection. N. Engl. J. Med. 352:768-776.

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Footnote 36

De Bolle, L., L. Naesens, and E. De Clercq. 2005. Update on human herpesvirus 6 biology, clinical features, and therapy. Clin. Microbiol. Rev. 18:217-245.

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Footnote 37

Torigoe, S., T. Kumamoto, W. Koide, K. Taya, and K. Yamanishi. 1995. Clinical manifestations associated with human herpesvirus 7 infection. Arch. Dis. Child. 72:518-519.

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Footnote 38

Ongradi, J., D. V. Ablashi, T. Yoshikawa, B. Stercz, and M. Ogata. 2017. Roseolovirus-associated encephalitis in immunocompetent and immunocompromised individuals. J. Neurovirol. 23:1-19.

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Footnote 39

Ishiguro, N., S. Yamada, T. Takahashi, Y. Takahashi, T. Togashi, T. Okuno, and K. Yamanishi. 1990. Meningo-encephalitis associated with HHV-6 related exanthem subitum. Acta Paediatr. Scand. 79:987-989.

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Footnote 40

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