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Journal articles on the topic 'Herpesvirus 6 humain'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

Gautheret-Dejean, Agnès. "Actualités sur la forme intégrée du génome du sixième herpesvirus humain au génome humain (iciHHV-6)." médecine/sciences 33, no. 8-9 (August 2017): 730–31. http://dx.doi.org/10.1051/medsci/20173308014.

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2

Bonnafous, P., S. Nguyen-Quoc, E. Frobert, N. Weiss, C. Henquell, A. Dewilde, C. Gaudy-Graffin, and A. Gautheret-Dejean. "Algorithme d’interprétation de la charge virale sanguine du sixième herpesvirus humain (HHV-6)." Médecine et Maladies Infectieuses 47, no. 4 (June 2017): S114. http://dx.doi.org/10.1016/j.medmal.2017.03.278.

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3

Yamanishi, Koichi. "New human herpesviruses; human herpesvirus 6 and 7." Clinical Biochemistry 28, no. 3 (June 1995): 348. http://dx.doi.org/10.1016/0009-9120(95)91425-3.

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4

Morris, DavidJ, Edward Littler, Debbie Jordan, JohnR Arrand, Martin Andre, and Bertfried Matz. "ANTIBODY RESPONSES TO HUMAN HERPESVIRUS 6 AND OTHER HERPESVIRUSES." Lancet 332, no. 8625 (December 1988): 1425–26. http://dx.doi.org/10.1016/s0140-6736(88)90618-6.

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5

Buchbinder, A., D. V. Ablashi, C. Saxinger, S. F. Josephs, S. Z. Salahuddin, R. C. Gallo, P. Biberfeld, and A. Linde. "HUMAN HERPESVIRUS-6 AND CROSS-REACTIVITY WITH OTHER HERPESVIRUSES." Lancet 333, no. 8631 (January 1989): 217. http://dx.doi.org/10.1016/s0140-6736(89)91228-2.

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6

Kaufer, Benedikt B., Keith W. Jarosinski, and Nikolaus Osterrieder. "Herpesvirus telomeric repeats facilitate genomic integration into host telomeres and mobilization of viral DNA during reactivation." Journal of Experimental Medicine 208, no. 3 (March 7, 2011): 605–15. http://dx.doi.org/10.1084/jem.20101402.

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Some herpesviruses, particularly lymphotropic viruses such as Marek’s disease virus (MDV) and human herpesvirus 6 (HHV-6), integrate their DNA into host chromosomes. MDV and HHV-6, among other herpesviruses, harbor telomeric repeats (TMRs) identical to host telomeres at either end of their linear genomes. Using MDV as a natural virus-host model, we show that herpesvirus TMRs facilitate viral genome integration into host telomeres and that integration is important for establishment of latency and lymphoma formation. Integration into host telomeres also aids in reactivation from the quiescent state of infection. Our results and the presence of TMRs in many herpesviruses suggest that integration mediated by viral TMRs is a conserved mechanism, which ensures faithful virus genome maintenance in host cells during cell division and allows efficient mobilization of dormant viral genomes. This finding is of particular importance as reactivation is critical for virus spread between susceptible individuals and is necessary for continued herpesvirus evolution and survival.

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7

Reynaud, Joséphine M., and Branka Horvat. "Human Herpesvirus 6 and Neuroinflammation." ISRN Virology 2013 (March 14, 2013): 1–11. http://dx.doi.org/10.5402/2013/834890.

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Human herpesvirus (HHV-) 6A and HHV-6B are two distinct β-herpesviruses which have been associated with various neurological diseases, including encephalitis, meningitis, epilepsy, and multiple sclerosis. Although the reactivation of both viruses is recognized as the cause of some neurological complications in conditions of immunosuppression, their involvement in neuroinflammatory diseases in immunocompetent people is still unclear, and the mechanisms involved have not been completely elucidated. Here, we review the available data providing evidence for the capacity of HHV-6A and -6B to infect the central nervous system and to induce proinflammatory responses by infected cells. We discuss the potential role of both viruses in neuroinflammatory pathologies and the mechanisms which could explain virus-induced neuropathogenesis.

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8

Lacoste, Vincent, Philippe Mauclere, Guy Dubreuil, John Lewis, Marie-Claude Georges-Courbot, Jacques Rigoulet, Thierry Petit, and Antoine Gessain. "Simian Homologues of Human Gamma-2 and Betaherpesviruses in Mandrill and Drill Monkeys." Journal of Virology 74, no. 24 (December 15, 2000): 11993–99. http://dx.doi.org/10.1128/jvi.74.24.11993-11999.2000.

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ABSTRACT Recent serological and molecular surveys of different primate species allowed the characterization of several Kaposi's sarcoma-associated herpesvirus (KSHV) homologues in macaques, African green monkeys, chimpanzees, and gorillas. Identification of these new primate rhadinoviruses revealed the existence of two distinct genogroups, called RV1 and RV2. Using a degenerate consensus primer PCR method for the herpesvirus DNA polymerase gene, the presence of KSHV homologues has been investigated in two semi-free-ranging colonies of eight drill (Mandrillus leucophaeus), five mandrill (Mandrillus sphinx), and two hybrid (Mandrillus leucophaeus-Mandrillus sphinx) monkeys, living in Cameroon and Gabon, Central Africa. This search revealed the existence of not only two distinct KSHV homologues, each one belonging to one of the two rhadinovirus genogroups, but also of two new betaherpesvirus sequences, one being close to cytomegaloviruses and the other being related to human herpesviruses 6 and 7 (HHV-6 and -7). The latter viruses are the first simian HHV-6 and -7 homologues identified to date. These data show that mandrill and drill monkeys are the hosts of at least four novel distinct herpesviruses. Moreover, mandrills, like macaques and African green monkeys, harbor also two distinct gamma-2 herpesviruses, thus strongly suggesting that a second gamma-2 herpesvirus, belonging to the RV2 genogroup, may exist in humans.

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9

Nazaryan, R. S., Yu V. Fomenko, N. A. Scheblykina, T. A. Kolesova, N. V. Golik, and E. V. Sukhostavets. "Herpesviruses. Part 1." Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 5, no. 6 (December 12, 2020): 299–307. http://dx.doi.org/10.26693/jmbs05.06.299.

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One of the urgent problems of modern medicine is the high incidence of herpesvirus infections. The high prevalence of herpesviruses in the human population of the world allow us to consider herpes a common systemic disease of the whole organism. Doctors of any specialty are faced with the clinical manifestations of herpes infection in patients, and they themselves are a risk group of chronic herpes infections formation due to constant patient contacts and frequent professional psycho-emotional overload. Herpes infections are a group of infectious diseases caused by human herpesviruses. Now it is known 8 species of herpesvirus causing various human diseases that occur in the acute (during the initial contact with the infection) or chronic form. The herpesvirus family has a number of common properties that distinguish them from other human pathogenic viruses. There are three subfamilies in the Herpesviridae family. Alpha herpesviruses (Аlphaherpesvirinae) include the two serotypes of the herpes simplex virus (HSV-1 and HSV-2), and the varicella-zoster virus (herpes zoster). Beta herpesviruses (Betaherpesvirinae) include cytomegalovirus, human herpes viruses of types 6 and 7 (HHV-5, HHV-6, HHV-7). Gamma herpes viruses (Gammaherpesvirinae) include the Epstein-Barr virus, human herpesvirus type 8 (HHV-4, HHV-8). Clinical manifestations of herpes infection depend more on the immunity state of the infected organism than on the pathogenic properties of the pathogen itself, and develop only in conditions of immunodeficiency caused by various unfavorable factors. Herpesviruses are able to damage organs, weaken the body's immunity, creating conditions for the attachment of the other infections (fungal, bacterial), which in turn can cause organ damage. The herpesvirus ability to infect all organs and tissues of the body determines a significant clinical polymorphism of diseases, as well as the necessity to study various biological liquids. Herpesviruses can be transmitted from person to person by aerosol, contact, sexual and parenteral transmission, as well as from mother to fetus or newborn, they also can act as mutagens. The pathogenesis of herpesvirus infections is rather complex and not completely understood. For a proper understanding of the disease pathogenesis it is necessary to know the main stages of reproduction of human herpesviruses. Modern laboratory techniques are used for diagnosis of herpes infection and allow obtaining more complete information for an accurate diagnosis: virological method, electron microscopy method, the method of biological sample, the polymerase chain reaction methods for the detection of viral antigens, serological, immunological, cytological and histological methods. Conclusion. The high prevalence of diseases caused by herpes viruses, the complex, not fully understood pathogenesis and high contagiousness of diseases, as well as a variety of clinical manifestations of herpesvirus infections with the possibility of the formation of mixed forms with a blurred clinical picture dictate the need for a detailed study of herpes viruses and knowledge of methods for diagnosing herpes infections

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10

Prichard, Mark N., John D. Williams, Gloria Komazin-Meredith, Atiyya R. Khan, Nathan B. Price, Geraldine M. Jefferson, Emma A. Harden, Caroll B. Hartline, Norton P. Peet, and Terry L. Bowlin. "Synthesis and Antiviral Activities of Methylenecyclopropane Analogs with 6-Alkoxy and 6-Alkylthio Substitutions That Exhibit Broad-Spectrum Antiviral Activity against Human Herpesviruses." Antimicrobial Agents and Chemotherapy 57, no. 8 (May 13, 2013): 3518–27. http://dx.doi.org/10.1128/aac.00429-13.

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ABSTRACTMethylenecyclopropane nucleosides have been reported to be active against many of the human herpesviruses. The most active compound of this class is cyclopropavir (CPV), which exhibits good antiviral activity against human cytomegalovirus (HCMV), Epstein-Barr virus, both variants of human herpesvirus 6, and human herpesvirus 8. CPV has two hydroxymethyl groups on the methylenecyclopropane ring, but analogs with a single hydroxymethyl group, such as the prototypical (S)-synguanol, are also active and exhibit a broader spectrum of antiviral activity that also includes hepatitis B virus and human immunodeficiency virus. Here, a large set of monohydroxymethyl compounds with ether and thioether substituents at the 6 position of the purine was synthesized and evaluated for antiviral activity against a range of human herpesviruses. Some of these analogs had a broader spectrum of antiviral activity than CPV, in that they also inhibited the replication of herpes simplex viruses 1 and 2 and varicella-zoster virus. Interestingly, the antiviral activity of these compounds appeared to be dependent on the activity of the HCMV UL97 kinase but was relatively unaffected by the absence of thymidine kinase activity in HSV. These data taken together indicate that the mechanism of action of these analogs is distinct from that of CPV. They also suggest that they might be useful as broad-spectrum antiherpesvirus agents and may be effective in the treatment of resistant virus infections.

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11

Minjolle, Sophie, C. Michelet, I. Jusselin, M. Joannes, F. Cartier, and R. Colimon. "Amplification of the Six Major Human Herpesviruses from Cerebrospinal Fluid by a Single PCR." Journal of Clinical Microbiology 37, no. 4 (1999): 950–53. http://dx.doi.org/10.1128/jcm.37.4.950-953.1999.

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We used a novel type of primer system, a system that uses stair primers, in which the primer sequences are based on consensus sequences in the DNA polymerase gene of herpesvirus to detect herpesviruses by PCR. A single PCR in a single tube detected the six major herpesviruses that infect the central nervous system: herpes simplex virus type 1 (HSV-1), and type 2 (HSV-2), cytomegalovirus (CMV), Epstein-Barr virus (EBV), varicella-zoster virus (VZV), and human herpesvirus 6 (HHV-6). We used the technique to analyze 142 cerebrospinal fluid (CSF) samples that had been stored at −80°C and compared the results with those obtained previously for the same samples by standard, targeted PCR. Four hundred one targeted PCR tests had been run with the 142 samples to detect HSV-1, HSV-2, CMV, and VZV; screening for EBV and HHV-6 was not prescribed when the samples were initially taken. Eighteen CSF samples tested positive by classic targeted PCR. The herpesvirus consensus PCR detected herpesviruses in 37 samples, including 3 samples with coinfections and 17 viral isolates which were not targeted. Two samples identified as infected by the targeted PCR tested negative by the consensus PCR, and eight samples that tested positive by the consensus PCR were negative by the targeted PCR. One hundred three samples scored negative by both the targeted and the consensus PCRs. This preliminary study demonstrates the value of testing for six different herpesviruses simultaneously by a sensitive and straightforward technique rather than screening only for those viruses that are causing infections as suggested by clinical signs.

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12

Dockrell, David H., Thomas F. Smith, and Carlos V. Paya. "Human Herpesvirus 6." Mayo Clinic Proceedings 74, no. 2 (February 1999): 163–70. http://dx.doi.org/10.4065/74.2.163.

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13

Dewhurst, Stephen, David Skrincosky, and Nanette van Loon. "Human herpesvirus 6." Expert Reviews in Molecular Medicine 1, no. 1 (November 5, 1997): 1–17. http://dx.doi.org/10.1017/s146239949700001x.

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Human herpesvirus 6 (HHV-6) is a T-lymphotropic herpesvirus, which infects almost all children by the age of two years and persists lifelong. Two distinct variants of HHV-6, HHV-6A and HHV-6B, have been described, and the latter has been shown to be a common cause of acute febrile illnesses in young children, including exanthem subitum (roseola). HHV-6 has also been associated with a number of neurological disorders, including encephalitis and seizures, and the virus has been postulated to play a role in acquired immunodeficiency syndrome (AIDS), multiple sclerosis (MS) and chronic fatigue immunodeficiency syndrome (CFIDS). This review provides a critical summary of research conducted on HHV-6.

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14

Ongrádi, József, Valéria Kövesdi, and G. Péter Medveczky. "Human herpesvirus 6." Orvosi Hetilap 151, no. 13 (March 1, 2010): 523–32. http://dx.doi.org/10.1556/oh.2010.28848.

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Az 1986-ban felfedezett emberi 6-os herpeszvírus A és B változata molekuláris tulajdonságai alapján a legősibb emberi herpeszvírus. A B változat cseppfertőzéssel terjed a tünetmentes vírusürítő felnőttekről a két év alatti kisgyermekekre, akikben alkalmilag exanthema subitum jöhet létre. A vírus a CD4+ macrophagokat, lymphocytákat fertőzi, utóbbiakban élethossziglan lappangás, időnként a nyálmirigyekben vírustermeléssel járó perzisztencia alakul ki. Felnőttkorban ez a változat csontvelő- és szervátültetések kapcsán, immunszuppresszió talaján reaktiválódik, és akár halálos szövődményeket hoz létre. Sclerosis multiplex, idült fáradtság tünetegyüttes, Hodgkin- és nem Hodgkin-lymphomák kialakulásában kofaktor. A CD+-sejteket fertőző és bennük lappangó A változat közvetlen kórokozó képessége nem ismert. A HIV-fertőzést rendkívül erősen transzaktiváljain vitroés betegekben egyaránt. Papillomavírusok által okozott daganatokban is transzaktivátor. Mindkét vírusváltozat kórokozó képessége a megváltozott citokin- és kemokinegyensúlyon alapszik. A két változat elkülönítése szerológiailag nehézkes, erre a savóból vagy a fehérvérsejtekből végzett változatspecifikus PCR alkalmas. A súlyos komplikációk kezelésére, esetleg kemoprofilaxisára ganciclovir, esetleg foscarnet és cidofovir használható.

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15

Caserta, Mary T., David J. Mock, and Stephen Dewhurst. "Human Herpesvirus 6." Clinical Infectious Diseases 33, no. 6 (September 15, 2001): 829–33. http://dx.doi.org/10.1086/322691.

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16

RATHORE, MOBEEN H. "Human Herpesvirus 6." Southern Medical Journal 86, no. 11 (November 1993): 1197–201. http://dx.doi.org/10.1097/00007611-199311000-00001.

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17

Caserta, M. T., and C. B. Hall. "Human Herpesvirus-6." Annual Review of Medicine 44, no. 1 (February 1993): 377–83. http://dx.doi.org/10.1146/annurev.me.44.020193.002113.

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18

Clark, Duncan A. "Human herpesvirus 6." Reviews in Medical Virology 10, no. 3 (May 2000): 155–73. http://dx.doi.org/10.1002/(sici)1099-1654(200005/06)10:3<155::aid-rmv277>3.0.co;2-6.

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19

Enlander, D. "Human herpesvirus 6." Cleveland Clinic Journal of Medicine 69, no. 1 (January 1, 2002): 92. http://dx.doi.org/10.3949/ccjm.69.1.92.

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20

Braun, D. K., G. Dominguez, and P. E. Pellett. "Human herpesvirus 6." Clinical Microbiology Reviews 10, no. 3 (July 1997): 521–67. http://dx.doi.org/10.1128/cmr.10.3.521.

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Human herpesvirus 6 variant A (HHV-6A) and human herpesvirus 6 variant B (HHV-6B) are two closely related yet distinct viruses. These visuses belong to the Roseolovirus genus of the betaherpesvirus subfamily; they are most closely related to human herpesvirus 7 and then to human cytomegalovirus. Over 95% of people older than 2 years of age are seropositive for either or both HHV-6 variants, and current serologic methods are incapable of discriminating infection with one variant from infection with the other. HHV-6A has not been etiologically linked to any human disease, but such an association will probably be found soon. HHV-6B is the etiologic agent of the common childhood illness exanthem subitum (roseola infantum or sixth disease) and related febrile illnesses. These viruses are frequently active and associated with illness in immunocompromised patients and may play a role in the etiology of Hodgkin's disease and other malignancies. HHV-6 is a commensal inhabitant of brains; various neurologic manifestations, including convulsions and encephalitis, can occur during primary HHV-6 infection or in immunocompromised patients. HHV-6 and distribution in the central nervous system are altered in patients with multiple sclerosis; the significance of this is under investigation.

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21

Braun, D. K., G. Dominguez, and P. E. Pellett. "Human herpesvirus 6." Clinical microbiology reviews 10, no. 3 (1997): 521–67. http://dx.doi.org/10.1128/cmr.10.3.521-567.1997.

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22

IRVING, W. L. "Human herpesvirus-6." Journal of Medical Microbiology 36, no. 4 (April 1, 1992): 221–22. http://dx.doi.org/10.1099/00222615-36-4-221.

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23

Yamanishi, Koichi. "Human Herpesvirus 6." Microbiology and Immunology 36, no. 6 (June 1992): 551–61. http://dx.doi.org/10.1111/j.1348-0421.1992.tb02055.x.

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24

Holt, Douglas A., Jose Prieto, and John T. Sinnott. "Human herpesvirus 6." Infectious Diseases Newsletter 9, no. 3 (March 1990): 17–18. http://dx.doi.org/10.1016/0278-2316(90)90053-i.

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25

Kirchesch, Herbert, Thomas Mertens, Ulrich Burkhardt, JohannesP Kruppenbacher, Aniane Höffken, and HansJ Eggers. "SEROCONVERSION AGAINST HUMAN HERPESVIRUS-6 (AND OTHER HERPESVIRUSES) AND CLINICAL ILLNESS." Lancet 332, no. 8605 (July 1988): 273–74. http://dx.doi.org/10.1016/s0140-6736(88)92557-3.

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26

Boivin, Guy. "Recent Developments in Viral Load Measurements in Human Herpesviruses." Canadian Journal of Infectious Diseases 10, suppl c (1999): 33C—40C. http://dx.doi.org/10.1155/1999/965245.

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Recent developments in molecular biology have allowed precise quantitative analysis of herpesvirus DNA in many biological fluids. Th is paper reviews the clinical utility of performing quantitative polymerase chain reaction testing for herpesviruses. In particular, the assessment of the cytomegalovirus (CMV) DNA load in blood with regard to the development of CMV disease in immunocompromised patients is discussed in greater detail. Relevant information exists to support measuring the CMV burden in the blood of AIDS and transplant patients for diagnostic and treatment monitoring purposes, and, to a lesser extent, to envision the monitoring of the circulating Epstein-Barr virus load for the prevention of pose-transplant lymphoproliferative disorders. On the ocher hand, there are controversial data on the clinical utility of measuring the herpes simplex virus (HSV) load in cerebrospinal fluid of patients with HSV encephalitis and on the relationship between the human herpesvirus 8 DNA load in diverse biological fluids and the presence of Kaposi's sarcoma. There is a paucity of information about the clinical impact of quantifying the other human herpesviruses (varicella-zoster virus, and human herpesviruses 6 and 7).

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27

Pitkäranta, A., H. Piiparinen, L. Mannonen, M. Vesaluoma, and A. Vaheri. "Detection of Human Herpesvirus 6 and Varicella-Zoster Virus in Tear Fluid of Patients with Bell's Palsy by PCR." Journal of Clinical Microbiology 38, no. 7 (2000): 2753–55. http://dx.doi.org/10.1128/jcm.38.7.2753-2755.2000.

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Human herpesvirus 6 DNA was detected by PCR in the tear fluid of 7 (35%) of 20 patients with Bell's palsy and of 1 (5%) of 20 healthy controls. Varicella-zoster virus was detected by PCR in the tear fluid of 2 of 20 Bell's palsy patients but in none of the tear fluids from 20 healthy controls. These findings suggest an association between human herpesviruses and Bell's palsy.

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28

Lusso, Paolo. "Human herpesvirus 6 (HHV-6)." Antiviral Research 31, no. 1-2 (June 1996): 1–21. http://dx.doi.org/10.1016/0166-3542(96)00949-7.

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29

Jenson, Hal B., Yasmin Ench, Yanjin Zhang, Shou-Jiang Gao, John R. Arrand, and Michael Mackett. "Characterization of an Epstein–Barr virus-related gammaherpesvirus from common marmoset (Callithrix jacchus)." Journal of General Virology 83, no. 7 (July 1, 2002): 1621–33. http://dx.doi.org/10.1099/0022-1317-83-7-1621.

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A gammaherpesvirus related to Epstein–Barr virus (EBV; Human herpesvirus 4) infects otherwise healthy common marmosets (Callithrix jacchus). Long-term culture of common marmoset peripheral blood lymphocytes resulted in outgrowth of spontaneously immortalized lymphoblastoid cell lines, primarily of B cell lineage. Electron microscopy of cells and supernatants showed herpesvirus particles. There were high rates of serological cross-reactivity to other herpesviruses (68–86%), but with very low geometric mean antibody titres [1:12 to human herpesvirus 6 and 1:14 to Herpesvirus papio (Cercopithecine herpesvirus 12)]. Sequence analysis of the conserved herpesvirus DNA polymerase gene showed that the virus is a member of the lymphocryptovirus subgroup and is most closely related to a lymphocryptovirus from rhesus macaques and is closely related to EBV and Herpesvirus papio. High seroprevalence (79%, with geometric mean antibody titre of 1:110) among 28 common marmosets from two geographically distinct colonies indicated that the virus is likely present in many common marmosets in captivity. A New World primate harbouring a lymphocryptovirus suggests that this subgroup arose much earlier than previously thought.

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30

TANG, Huamin, Tomohiko SADAOKA, and Yasuko MORI. "Human herpesvirus-6 and human herpesvirus-7 (HHV-6, HHV-7)." Uirusu 60, no. 2 (2010): 221–36. http://dx.doi.org/10.2222/jsv.60.221.

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31

Virtanen, JO, J. Wohler, K. Fenton, DS Reich, and S. Jacobson. "Oligoclonal bands in multiple sclerosis reactive against two herpesviruses and association with magnetic resonance imaging findings." Multiple Sclerosis Journal 20, no. 1 (May 30, 2013): 27–34. http://dx.doi.org/10.1177/1352458513490545.

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Background: Two human herpesviruses, human herpesvirus 6 (HHV-6), and Epstein-Barr virus (EBV), have been repeatedly linked to multiple sclerosis (MS). Objective: The aim of this study was to investigate HHV-6 and EBV reactive oligoclonal bands (OCBs), and viral DNA in the intrathecal compartment in MS. Methods: The reactivity of OCBs in cerebrospinal fluid (CSF) for EBV and HHV-6 antigens and stability of virus reactive OCBs over time were studied in a well-characterized MS patient cohort. Associations between virus reactive OCBs and viral DNA in CSF (and any clinical and/or radiological findings) were investigated. Results: Of patients with MS, 38% had OCBs reactive to either one of the viruses studied, compared to none in the patients with other inflammatory neurological diseases ( p=0.005). The banding pattern of virus reactive OCBs remained the same over time. Furthermore, MS patients with viral DNA in CSF had more contrast enhancing lesions (CELs). Conclusion: The stable presence of herpesvirus reactive OCBs in CSF further strengthens the association of MS with these viruses. The finding that herpesviruses might be linked to the appearance of active lesions warrants investigation of new therapeutic strategies to treat these viruses in MS.

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32

Lusso, Paolo, and Robert C. Gallo. "9 Human herpesvirus 6." Baillière's Clinical Haematology 8, no. 1 (March 1995): 201–23. http://dx.doi.org/10.1016/s0950-3536(05)80238-0.

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33

Horwitz, Charles A., and Janet Beneke. "Human Herpesvirus-6 Revisited." American Journal of Clinical Pathology 99, no. 5 (May 1, 1993): 533–35. http://dx.doi.org/10.1093/ajcp/99.5.533.

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34

Soto-Hernandez, Jose Luis. "Human Herpesvirus 6 Encephalomyelitis." Emerging Infectious Diseases 10, no. 9 (September 2004): 1700–1702. http://dx.doi.org/10.3201/eid1009.040365.

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35

Denes, Eric, and Sylvie Ranger-Rogez. "Human Herpesvirus 6 Encephalomyelitis." Emerging Infectious Diseases 10, no. 9 (September 2004): 1701–2. http://dx.doi.org/10.3201/eid1009.040522.

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36

Jones, C. A., and D. Isaacs. "Human herpesvirus-6 infections." Archives of Disease in Childhood 74, no. 2 (February 1, 1996): 98–100. http://dx.doi.org/10.1136/adc.74.2.98.

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37

Stevenson, Linda, and Dawn Sabrina Brooke. "Roseola (human herpesvirus 6)." Journal of Pediatric Health Care 8, no. 6 (November 1994): 283. http://dx.doi.org/10.1016/0891-5245(94)90012-4.

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38

Gewurz, Benjamin E., Francisco M. Marty, Lindsey R. Baden, and Joel T. Katz. "Human herpesvirus 6 encephalitis." Current Infectious Disease Reports 10, no. 4 (July 2008): 292–99. http://dx.doi.org/10.1007/s11908-008-0048-1.

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Kleshcheva, E. A., S. A. Kochergin, and Yu B. Slonimskiy. "Features of Diagnostics and Complex Approach to Therapy of Herpetic Keratitis." Ophthalmology in Russia 16, no. 2 (June 30, 2019): 252–58. http://dx.doi.org/10.18008/1816-5095-2019-2-252-258.

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Objective. To determine the characteristics of drug therapy in patients with herpetic keratitis (HK), based on laboratory diagnosis.Material and methods. 49 patients with clinical symptoms of HK were included in the study. The conjunctival cells were used as a material for laboratory diagnosis of adenovirus and enterovirus infection by polymerase chain reaction (PCR) and for microbiological examination. Herpesvirus DNA in tears, saliva, urine and blood was determined using PCR (for varicella-zoster virus (VZV) and human herpesvirus type 7 (HHV-7)) and real-time PCR (for herpes simplex virus types 1 and 2 (HSV-1,2), Epstein-Barr virus (VEB), cytomegalovirus (CMV) and human herpesvirus type 6 (HHV-6). Tear and urine were examined for the presence of DNA of obligate intracellular parasites (chlamydia, ureaplasma, and mycoplasma) by PCR.Results. Сlinical picture of HK was presented by superficial (57.1 %, n = 28) and deep forms of corneal inflammation (42.9 %, n = 21). The results of laboratory diagnostics of herpetic infection had showed replication of herpesviruses in all examined patients. Genetic material of herpesviruses in lacrimal fluid was found in half of the examined patients (51 %), in saliva — in 67,3 % of cases. Viruria was observed in 21 patients (42.9 %), viraemia in 6 (12.2 %). DNA of intracellular parasites in lacrimal fluid was detected in 18.4 % of patients and in urine — in 12.2 % of patients. Bacteriological sowing of the conjunctiva scrape was positive in 75.5 % of cases.Conclusion. Instrumental diagnostics (visometry, biomicroscopy) of HK should be supplemented with laboratory research of activity of not only herpesvirus infection, but also bacterial pathogens. Positive results of microbiological sowing of conjunctival scrapers allow to approach reasonably the prescription of antimicrobial drugs in patients with HK.

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Johnson, Grant, Susan Nelson, Martin Petric, and Raymond Tellier. "Comprehensive PCR-Based Assay for Detection and Species Identification of Human Herpesviruses." Journal of Clinical Microbiology 38, no. 9 (2000): 3274–79. http://dx.doi.org/10.1128/jcm.38.9.3274-3279.2000.

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The description and evaluation of a PCR-based assay for the detection and species identification of the eight known human herpesviruses are presented. Two primer pairs targeting well-conserved regions of the genome allowed the amplification of the DNAs of all known human herpesviruses at a high level of sensitivity (10 to 100 genome copies for most viruses). Identification of the virus species was achieved through restriction enzyme digestion withBamHI and BstUI, which yielded fragment sizes that were characteristic for each herpesvirus. Furthermore, it was demonstrated that this restriction enzyme panel allowed the discrimination between human herpesvirus 6 variant A and variant B. This assay format was validated over the course of 1 year in a clinical virology laboratory setting, where it was shown that it readily detected human herpesviruses, including occasional multiple infections, in a variety of clinical samples. The PCR assay was compared to isolation and electron microscopy for the detection of herpes simplex (HSV) and varicella-zoster virus (VZV) in clinical samples. All specimens positive by conventional methods were also positive by PCR. However, in a number of clinical specimens in which HSV or VZV could not be detected by conventional methods, PCR was able to demonstrate the presence of the virus.

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Marques Filho, Jaime S., Jorge Gobara, Gustavo Vargas da Silva Salomao, Laura M. Sumita, Jamil A. Shibli, Renato G. Viana, Humberto O. Schwartz Filho, Claudio Sergio Pannuti, Paulo Henrique Braz-Silva, and Debora Pallos. "Cytokine Levels and Human Herpesviruses in Saliva from Clinical Periodontal Healthy Subjects with Peri-Implantitis: A Case-Control Study." Mediators of Inflammation 2018 (August 6, 2018): 1–7. http://dx.doi.org/10.1155/2018/6020625.

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This study evaluated the presence of cytokines (IL-1β, IL-2, IL-4, IL-6, MCP-1, MIP-1α, MIP-1β, and TNF-α) and human herpesvirus (HSV1, HSV2, EBV, CMV, VZV, HHV6, HHV7, and HHV8) in saliva samples taken from subjects with and without peri-implantitis. Forty-two periodontally healthy subjects were divided according to peri-implant condition: healthy and peri-implantitis groups. The clinical parameters as probing depth, clinical attachment level, plaque index, gingival bleeding, bleeding on probing, and suppuration were evaluated. For cytokine detection, multiplex analysis was performed, and PCR assay was used to identify herpesviruses. No significant differences were found in cytokine levels between groups (p>0.05). The presence of herpesvirus was 1.97-fold higher in patients with peri-implantitis (odds ratio, CI 0.52–7.49). The association of the presence or absence of herpesvirus with the salivary markers was statistically significant for MIP-1β(p=0.0087) and TNF-α(p=0.0437) only in the peri-implantitis group. The presence of herpesviruses in patients with peri-implantitis suggests the development of a proinflammatory environment, which is characterized by increased expression of MIP-1βand TNF-αin saliva.

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Kawabata, Akiko, Satoshi Serada, Tetsuji Naka, and Yasuko Mori. "Human herpesvirus 6 gM/gN complex interacts with v-SNARE in infected cells." Journal of General Virology 95, no. 12 (December 1, 2014): 2769–77. http://dx.doi.org/10.1099/vir.0.069336-0.

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Human herpesvirus 6 (HHV-6) glycoprotein M (gM) is an envelope glycoprotein that associates with glycoprotein N (gN), forming the gM/gN protein complex, in a similar manner to the other herpesviruses. Liquid chromatography-MS/MS analysis showed that the HHV-6 gM/gN complex interacts with the v-SNARE protein, vesicle-associated membrane protein 3 (VAMP3). VAMP3 colocalized with the gM/gN complex at the trans-Golgi network and other compartments, possibly the late endosome in HHV-6-infected cells, and its expression gradually increased during the late phase of virus infection. Finally, VAMP3 was incorporated into mature virions and may be transported with the gM/gN complex.

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Caselli, Elisabetta, Maria D’Accolti, Francesca Caccuri, Irene Soffritti, Valentina Gentili, Daria Bortolotti, Antonella Rotola, et al. "The U94 Gene of Human Herpesvirus 6: A Narrative Review of Its Role and Potential Functions." Cells 9, no. 12 (December 4, 2020): 2608. http://dx.doi.org/10.3390/cells9122608.

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Human herpesvirus 6 (HHV-6) is a β-herpesvirus that is highly prevalent in the human population. HHV-6 comprises two recognized species (HHV-6A and HHV-6B). Despite different cell tropism and disease association, HHV-6A/B show high genome homology and harbor the conserved U94 gene, which is limited to HHV-6 and absent in all the other human herpesviruses. U94 has key functions in the virus life cycle and associated diseases, having demonstrated or putative roles in virus replication, integration, and reactivation. During natural infection, U94 elicits an immune response, and the prevalence and extent of the anti-U94 response are associated with specific diseases. Notably, U94 can entirely reproduce some virus effects at the cell level, including inhibition of cell migration, induction of cytokines and HLA-G expression, and angiogenesis inhibition, supporting a direct U94 role in the development of HHV-6-associated diseases. Moreover, specific U94 properties, such as the ability to modulate angiogenesis pathways, have been exploited to counteract cancer development. Here, we review the information available on this key HHV-6 gene, highlighting its potential uses.

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Enbom, Malin, Fu-Zhang Wang, Sten Fredrikson, Claes Martin, Helena Dahl, and Annika Linde. "Similar Humoral and Cellular Immunological Reactivities to Human Herpesvirus 6 in Patients with Multiple Sclerosis and Controls." Clinical Diagnostic Laboratory Immunology 6, no. 4 (July 1, 1999): 545–49. http://dx.doi.org/10.1128/cdli.6.4.545-549.1999.

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ABSTRACT Several studies have suggested an association between human herpesvirus 6 (HHV-6) and multiple sclerosis (MS). We have previously studied intrathecal production of antibody to lymphotropic herpesviruses in MS patients and the presence of human herpesvirus 1 to 7 DNAs in cerebrospinal fluid (CSF). In the present study anti-HHV-6 immunoglobulin M (IgM) in serum and anti-HHV-6 IgG subclasses in serum and CSF were examined and the lymphoproliferative response to HHV-6 was analyzed. The PCR examination was refined by purifying DNA from CSF and retesting the samples for HHV-6 DNA. There were no statistically significant differences between the groups concerning IgM positivity, distribution of IgG subclasses, or lymphoproliferative response to HHV-6. The purification of DNA increased the number of PCR-positive samples from 0 of 71 to 4 of 68. The study does not give additional support to the possibility that HHV-6 is a common cause of MS, but a role for the virus in a subset of patients cannot be excluded.

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Denner, Joachim, Rudolph Tanzi, and Steve Jacobson. "Animal Models of Alzheimer’s Disease Should Be Controlled for Roseolovirus." Journal of Alzheimer's Disease 77, no. 2 (September 15, 2020): 543–45. http://dx.doi.org/10.3233/jad-200591.

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Animal models to study Alzheimer’s disease (AD) pathogenesis are under development. Since herpesviruses have been postulated to be capable of triggering the pathogenic process, AD animal models (mouse, pig, and non-human primates) should be controlled for the presence of these viruses. Only virus-free models allow studying the genetic factors and the effect of adding viruses. Roseoloviruses such as human herpesvirus 6 and the related viruses in the animals are the main topic of this commentary.

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Kondo, Kazuhiro. ".BETA.-herpesvirus(human cytomegalovirus and human herpesvirus 6) latent infection." Uirusu 46, no. 2 (1996): 161–68. http://dx.doi.org/10.2222/jsv.46.161.

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Rybalkina, T. N., N. V. Karazhas, M. Y. Lysenkova, R. E. Boshyan, P. A. Veselovskiy, M. N. Kornienko, V. V. Kosenchuk, and M. S. Savenkova. "Formation of foci of herpesvirus infections in families." Infekcionnye bolezni 18, no. 3 (2020): 119–25. http://dx.doi.org/10.20953/1729-9225-2020-3-119-125.

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Objective. To analyze circulation of herpes simplex virus (HSV), Epstein–Barr virus (EBV), cytomegalovirus (CMV), and human herpes virus type six (HHV-6) within families, to evaluate the conditions of formation of family foci, and to identify possible sources of infection. Patients and methods. We examined 124 families, including 11 two-parent families (mother, father, and child) and 108 oneparent families (mother and child). Five families had a mother and two children. Antibodies of various classes against herpesviruses were detected using enzyme-linked immunosorbent assay (ELISA). Herpesvirus antigens were detected using indirect immunofluorescence assay; early antigens and herpesvirus reproduction were evaluated using culture method; viral DNA was identified using polymerase chain reaction. Results. We have revealed a high rate of infection with herpesviruses in both adults and children. Markers of infections caused by HSV and EBV were detected in the majority of mothers (96.0% and 90.3%; 119 and 112), while children had these infections less frequently (66.7% in each group (86)). Detection of active forms of infection and convalescents, both among children and adults, indicates an intensive circulation of herpesviruses within families and leads to the formation of family foci of infection. Active infections were primarily caused by CMV (20.2% of children, 17.8% of mothers, and 15.4% of fathers) and EBV (16.3% of children, 11.3% of mothers, and 9.1% of fathers). Out of 266 participants examined (mothers, fathers, and children), cases of acute mixed infection were observed in children only (4 of 129) and were caused by HHV-6 in combination with HSV (2 cases) or CMV (2 cases). Conclusion. Continuous and intensive circulation of herpesviruses in families leads to the formation of family foci of infection. To stop intra-family transmission of viruses, it is important to identify possible sources of infection and perform antiepidemic measures. This transmission is most likely to occur in families where the mother has markers of active or recent infection, while the child does not have them at all. Such combination was detected in 16 patients with EBV (12.4%), 10 patients with HHV-6 (7.8%), 6 patients with HSV (4.7%), and 5 patients with CMV (3.9%). It is crucial to identify the role of the child as a source of herpesvirus infection. Key words: herpesvirus infections, infection markers, family foci, cytomegalovirus infection.

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Lin, Liang-Yu, Ketaki Bhate, Harriet Forbes, Liam Smeeth, Charlotte Warren-Gash, and Sinéad Langan. "Vitamin D deficiency or supplementation and the risk of human herpesvirus infections or reactivation: a systematic review protocol." BMJ Open 9, no. 10 (October 2019): e031867. http://dx.doi.org/10.1136/bmjopen-2019-031867.

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IntroductionHuman herpesviruses induce lifelong latent infections and may reactivate as the immune system deteriorates. Recent studies have suggested that vitamin D, an essential element of bone health, may have some effect of protecting against infections, but investigations of its potential to prevent herpesvirus infection or reactivation are limited. We will review the current literature examining vitamin D and the risk of herpesvirus infections or reactivation.Methods and analysisOur systematic review will address two research questions: (1) Do deficient/insufficient serum vitamin D levels increase the risk of herpesvirus infections and (2) Does vitamin D supplementation protect against herpesvirus infections? We will include only intervention studies with control groups, cohort studies and case-control studies. We will use subject headings and keywords to search for synonyms of ‘vitamin D’ and ‘herpesviruses’ (including herpes simplex virus type 1 and 2, varicella-zoster virus, cytomegalovirus, Epstein-Barr virus and human herpesviruses type 6, 7 and 8) in Medline, Embase, Global Health, Web of Science, Scopus and Cochrane Central Register of Controlled Trials, and the grey literature databases Open Grey, EThOS and BASE from inception to 31 August 2019. References to the included articles and relevant systematic reviews will also be examined. Two reviewers will independently screen the study titles and abstracts, and examine the full texts to decide the final eligibility. They will independently extract data from the studies and assess bias using the Cochrane Collaboration approach. A third researcher will solve any discrepancies. The results will be narratively synthesised; if an adequate number of studies is included and the homogeneity between studies is acceptable, a meta-analysis will be performed. We will assess the quality of evidence using the Grading of Recommendations, Assessment, Development and Evaluation framework, and display the results in a summary of findings table.Ethics and disseminationEthical review is not required for a systematic review. We will publish the results in a peer-review journal. Any amendments to the protocol will be recorded in the supplementary section.PROSPERO registration numberCRD42019130153.

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Cone, Richard W., Meei-Li Wu Huang, and Robert C. Hackman. "Human Herpesvirus 6 and Pneumonia." Leukemia & Lymphoma 15, no. 3-4 (January 1994): 235–41. http://dx.doi.org/10.3109/10428199409049719.

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Nikolskiy, M. A., and V. S. Golubcova. "СHROMOSOMALLY INTEGRATED HUMAN HERPESVIRUS 6." Russian Journal of Infection and Immunity 5, no. 1 (April 21, 2015): 7. http://dx.doi.org/10.15789/2220-7619-2015-1-7-14.

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