Journal articles: 'Herpesvirus 4 Humano'

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Reina, J., J. Gascó, X. Bestard, and F. Ballesteros. "Aislamiento del herpesvirus humano tipo 6 en la sangre de pacientes receptores de trasplante renal." Revista Clínica Española 200, no. 11 (November 2000): 644–45. http://dx.doi.org/10.1016/s0014-2565(00)70032-4.

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Stevenson, P. G., J. P. Simas, and S. Efstathiou. "Immune control of mammalian gamma-herpesviruses: lessons from murid herpesvirus-4." Journal of General Virology 90, no. 10 (October 1, 2009): 2317–30. http://dx.doi.org/10.1099/vir.0.013300-0.

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Many acute viral infections can be controlled by vaccination; however, vaccinating against persistent infections remains problematic. Herpesviruses are a classic example. Here, we discuss their immune control, particularly that of gamma-herpesviruses, relating the animal model provided by murid herpesvirus-4 (MuHV-4) to human infections. The following points emerge: (i) CD8+ T-cell evasion by herpesviruses confers a prominent role in host defence on CD4+ T cells. CD4+ T cells inhibit MuHV-4 lytic gene expression via gamma-interferon (IFN-γ). By reducing the lytic secretion of immune evasion proteins, they may also help CD8+ T cells to control virus-driven lymphoproliferation in mixed lytic/latent lesions. Similarly, CD4+ T cells specific for Epstein–Barr virus lytic antigens could improve the impact of adoptively transferred, latent antigen-specific CD8+ T cells. (ii) In general, viral immune evasion necessitates multiple host effectors for optimal control. Thus, subunit vaccines, which tend to prime single effectors, have proved less successful than attenuated virus mutants, which prime multiple effectors. Latency-deficient mutants could make safe and effective gamma-herpesvirus vaccines. (iii) The antibody response to MuHV-4 infection helps to prevent disease but is suboptimal for neutralization. Vaccinating virus carriers with virion fusion complex components improves their neutralization titres. Reducing the infectivity of herpesvirus carriers in this way could be a useful adjunct to vaccinating naive individuals with attenuated mutants.

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Wright, Debbie E., Susanna Colaco, Camilo Colaco, and Philip G. Stevenson. "Antibody limits in vivo murid herpesvirus-4 replication by IgG Fc receptor-dependent functions." Journal of General Virology 90, no. 11 (November 1, 2009): 2592–603. http://dx.doi.org/10.1099/vir.0.014266-0.

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Antibody is an important antiviral defence. However, it is considered to do little against human gamma-herpesviruses, which establish predominantly latent infections regulated by T cells. One limitation on analysing these infections has been that latency is already well-established at clinical presentation; early infection may still be accessible to antibody. Here, using murid herpesvirus-4 (MuHV-4), we tested the impact of adoptively transferred antibody on early gamma-herpesvirus infection. Immune sera and neutralizing and non-neutralizing monoclonal antibodies (mAbs) all reduced acute lytic MuHV-4 replication. The reductions, even by neutralizing mAbs, were largely or completely dependent on host IgG Fc receptors. Therefore, passive antibody can blunt acute gamma-herpesvirus lytic infection, and does this principally by IgG Fc-dependent functions rather than by neutralization.

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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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Prichard, Mark N., Debra C. Quenelle, Caroll B. Hartline, Emma A. Harden, Geraldine Jefferson, Samuel L. Frederick, Shannon L. Daily, et al. "Inhibition of Herpesvirus Replication by 5-Substituted 4′-Thiopyrimidine Nucleosides." Antimicrobial Agents and Chemotherapy 53, no. 12 (September 21, 2009): 5251–58. http://dx.doi.org/10.1128/aac.00417-09.

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ABSTRACT A series of 4′-thionucleosides were synthesized and evaluated for activities against orthopoxviruses and herpesviruses. We reported previously that one analog, 5-iodo-4′-thio-2′-deoxyuridine (4′-thioIDU), exhibits good activity both in vitro and in vivo against two orthopoxviruses. This compound also has good activity in cell culture against many of the herpesviruses. It inhibited the replication of herpes simplex virus type 1 (HSV-1), HSV-2, and varicella-zoster virus with 50% effective concentrations (EC50s) of 0.1, 0.5, and 2 μM, respectively. It also inhibited the replication of human cytomegalovirus (HCMV) with an EC50 of 5.9 μM but did not selectively inhibit Epstein-Barr virus, human herpesvirus 6, or human herpesvirus 8. While acyclovir-resistant strains of HSV-1 and HSV-2 were comparatively resistant to 4′-thioIDU, it retained modest activity (EC50s of 4 to 12 μM) against these strains. Some ganciclovir-resistant strains of HCMV also exhibited reduced susceptibilities to the compound, which appeared to be related to the specific mutations in the DNA polymerase, consistent with the observed incorporation of the compound into viral DNA. The activity of 4′-thioIDU was also evaluated using mice infected intranasally with the MS strain of HSV-2. Although there was no decrease in final mortality rates, the mean length of survival after inoculation increased significantly (P < 0.05) for all animals receiving 4′-thioIDU. The findings from the studies presented here suggest that 4′-thioIDU is a good inhibitor of some herpesviruses, as well as orthopoxviruses, and this class of compounds warrants further study as a therapy for infections with these viruses.

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White, Douglas W., Catherine R. Keppel, Stephanie E. Schneider, James Coder, Tiffany A. Reese, Jacqueline E. Payton, Timothy J. Ley, Herbert W. Virgin, and Todd A. Fehniger. "Latent Murine Herpesvirus-4 Infection Arms NK Cells." Blood 114, no. 22 (November 20, 2009): 3678. http://dx.doi.org/10.1182/blood.v114.22.3678.3678.

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Abstract Abstract 3678 Poster Board III-614 Natural killer (NK) cells are lymphocytes originally identified by their ability to kill target cells without prior sensitization. However, murine NK cells require an antecedent ‘arming’ event to translate cytotoxic effector proteins (perforin and granzymes) resulting in potent cytotoxic capacity. In contrast to mice, most NK cells (CD56dim) from the peripheral blood of healthy humans are armed with pre-formed perforin and granzyme B proteins and mediate killing of NK sensitive targets directly ex vivo. This suggests that NK cells from specific pathogen free (SPF) laboratory mice are lacking a critical arming event present in healthy humans, and provides an experimental system to elucidate the events that result in NK cell arming in vivo. Since latent herpesviruses are highly prevalent and alter multiple aspects of host immunity, we hypothesized that the immune environment created by a latent herpesvirus infection arms NK cells. NK cells from mice latently infected with Murid herpesvirus 4 (MuHV-4), a virus closely related to the human viruses Kaposi's sarcoma associated herpesvirus (KSHV) and Epstein-Barr virus (EBV), were armed as evidenced by increased granzyme B protein expression, cytotoxicity, and interferon-gamma production. Adoptive transfer experiments with naïve NK cells indicated that NK arming occurred rapidly (≤ 72 hours) in the latently infected host and did not require acute infection. In addition, experiments utilizing a genetic variant of MuHV-4 that acutely infects mice similar to wild-type MuHV-4, but does not establish latency, confirmed that acute infection was not responsible for this NK cell modulation. Finally, NK cells armed by latent infection protected the host against a lethal RMA-S lymphoma challenge. Thus, the immune environment created by a latent herpesvirus infection arms NK cell function in vivo. These results indicate that some of the differences between human and SPF laboratory-mouse NK cell function may reflect a disparity in immune activation induced by chronic virus infection, as opposed to an intrinsic difference in the NK cells themselves. Moreover, these findings indicate that the activation state of the innate immune system needs to be taken into account when using mice to model immune responses against pathogens and tumors. Disclosures: No relevant conflicts of interest to declare.

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Rincón-Amador, Rubén Alejandro, and Rodolfo Fragoso-Ríos. "Virus de Epstein-Barr y su relación con la estomatología pediátrica. Una revisión narrativa." Casos y Revisiones de Salud 3, no. 1 (July 1, 2021): 60–73. http://dx.doi.org/10.22201/fesz.26831422e.2021.3.1.7.

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Introducción. El Virus de Epstein-Barr (VEB) pertenece a la familia Herpesviridae y se clasifica como herpesvirus humano 4 (HVH-4). La prevalencia estimada a nivel mundial de infección por VEB rebasa el 95%. La mononucleosis infecciosa (MI), es una enfermedad sistémica producida en el 90% de ocasiones por el virus de VEB y que infecta al 95% de la población. Además, existe evidencia de que el VEB es un factor de riesgo para numerosas enfermedades inflamatorias orales como liquen plano oral (LPO), enfermedad periodontal y síndrome de Sjögren. La actualización del personal en este ámbito es fundamental para asegurar que las medidas se lleven a cabo correctamente. Objetivo. Presentar el estado del arte del conocimiento sobre el VEB y su relación con la estomatología pediátrica. Desarrollo. Se identificaron aquellos artículos que estudiaron las generalidades del VEB y de la MI en pacientes pediátricos a través de una revisión exhaustiva de la literatura. Se incluyeron artículos de investigación y revisión para la evaluación de esta relación. Conclusión. Debido a que la infección por VEB tiene una alta prevalencia, el estomatólogo general y pediatra deben tener conocimiento suficiente de los signos y síntomas de MI que se puedan presentar en la consulta debido a una infección sintomática por este virus, de esta manera podrá realizar un diagnóstico de la salud general del paciente y brindar una atención dental adecuada.

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Vider-Shalit, Tal, Vered Fishbain, Shai Raffaeli, and Yoram Louzoun. "Phase-Dependent Immune Evasion of Herpesviruses." Journal of Virology 81, no. 17 (July 3, 2007): 9536–45. http://dx.doi.org/10.1128/jvi.02636-06.

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ABSTRACT Viruses employ various modes to evade immune detection. Two possible evasion modes are a reduction of the number of epitopes presented and the mimicry of host epitopes. The immune evasion efforts are not uniform among viral proteins. The number of epitopes in a given viral protein and the similarity of the epitopes to host peptides can be used as a measure of the viral attempts to hide this protein. Using bioinformatics tools, we here present a genomic analysis of the attempts of four human herpesviruses (herpes simplex virus type 1-human herpesvirus 1, Epstein-Barr virus-human herpesvirus 4, human cytomegalovirus-human herpesvirus 5, and Kaposi's sarcoma-associated herpesvirus-human herpesvirus 8) and one murine herpesvirus (murine herpesvirus 68) to escape from immune detection. We determined the full repertoire of CD8 T-lymphocyte epitopes presented by each viral protein and show that herpesvirus proteins present many fewer epitopes than expected. Furthermore, the epitopes that are presented are more similar to host epitopes than are random viral epitopes, minimizing the immune response. We defined a score for the size of the immune repertoire (the SIR score) based on the number of epitopes in a protein. The numbers of epitopes in proteins expressed in the latent and early phases of infection were significantly smaller than those in proteins expressed in the lytic phase in all tested viruses. The latent and immediate-early epitopes were also more similar to host epitopes than were lytic epitopes. A clear trend emerged from the analysis. In general, herpesviruses demonstrated an effort to evade immune detection. However, within a given herpesvirus, proteins expressed in phases critical to the fate of infection (e.g., early lytic and latent) evaded immune detection more than all others. The application of the SIR score to specific proteins allows us to quantify the importance of immune evasion and to detect optimal targets for immunotherapy and vaccine development.

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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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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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Mätz-Rensing, K., K. D. Jentsch, S. Rensing, S. Langenhuyzen, E. Verschoor, H. Niphuis, and F. J. Kaup. "Fatal Herpes simplex Infection in a Group of Common Marmosets (Callithrix jacchus)." Veterinary Pathology 40, no. 4 (July 2003): 405–11. http://dx.doi.org/10.1354/vp.40-4-405.

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An outbreak of classical herpetic infection causing vesicoulcerative stomatitis in a family group (eight animals) of Callithrix jacchus is described. In all eight infected animals, human herpesvirus 1 (HHV-1) was identified as the causative agent. This was confirmed by histologic, immunohistologic, and molecular biologic investigations, as well as by virus isolation. The clinical picture, the macroscopic appearance, and the histologic results indicated a herpes infection as the cause of mortality. Alterations of the oral mucous membranes were erosive to ulcerative with typical intranuclear inclusions. Immunohistologic and molecular biologic techniques clearly identified the HHV-1 virus and excluded other possible primate herpesviruses such as B-virus, SA8, HVP-2, and Herpes tamarinus. The significance of this herpesvirus infection for colony management is discussed.

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Yuan, Wei-yuan, Xue Chen, Ning-ning Liu, Yi-ning Wen, Bei Yang, Graciela Andrei, Robert Snoeck, et al. "Synthesis, Anti-Varicella-Zoster Virus and Anti-Cytomegalovirus Activity of 4,5-Disubstituted 1,2,3-(1H)-Triazoles." Medicinal Chemistry 15, no. 7 (October 14, 2019): 801–12. http://dx.doi.org/10.2174/1573406414666181109095239.

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Background: Clinical drugs for herpesvirus exhibit high toxicity and suffer from significant drug resistance. The development of new, effective, and safe anti-herpesvirus agents with different mechanisms of action is greatly required. Objective: Novel inhibitors against herpesvirus with different mechanisms of action from that of clinical drugs. Methods: A series of novel 5-(benzylamino)-1H-1,2,3-triazole-4-carboxamides were efficiently synthesized and EC50 values against Human Cytomegalovirus (HCMV), Varicella-Zoster Virus (VZV) and Herpes Simplex Virus (HSV) were evaluated in vitro. Results: Some compounds present antiviral activity. Compounds 5s and 5t are potent against both HCMV and VZV. Compounds 5m, 5n, 5s, and 5t show similar EC50 values against both TK+ and TK− VZV strains. Conclusion: 5-(Benzylamino)-1H-1, 2,3-triazole-4-carboxamides are active against herpesviruses and their activity is remarkably affected by the nature and the position of substituents in the benzene ring. The results indicate that these derivatives are independent of the viral thymidine kinase (TK) for activation, which is indispensable for current drugs. Their mechanisms of action may differ from those of the clinic anti-herpesvirus drugs.

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Andronova, V. L. "MODERN ETHIOTROPIC CHEMOTHERAPY OF HERPESVIRUS INFECTIONS: ADVANCES, NEW TRENDS AND PERSPECTIVES. ALPHAHERPESVIRUSES (PART II)." Problems of Virology, Russian journal 63, no. 4 (August 20, 2018): 149–59. http://dx.doi.org/10.18821/0507-4088-2018-63-4-149-159.

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A key role in the treatment of herpesviral infections is played by modified nucleosides and their predecessors - acyclovir, its L-valine ester (valaciclovir) and famciclovir (prodrug of penciclovir). The biological activity of compounds of this class is determined by their similarity to natural nucleosides. After phosphorylation by viral thymidine kinase and then cell enzymes to the triphosphate forms, acyclovir and penciclovir inhibit the activity of viral DNA polymerase and synthesis of viral DNA. The increasing role of herpesvirus infections in human infectious pathology, as well as the development of drug resistance in viruses, mainly in patients with immunodeficiencies of various origins, necessitate the search for new compounds possessing anti-herpesvirus activity, using as a biological target not DNA polymerase, but other viral proteins and enzymes, unique or different from cellular proteins, performing similar functions.

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Krown, Susan E., Dirk P. Dittmer, and Ethel Cesarman. "Pilot Study of Oral Valganciclovir Therapy in Patients With Classic Kaposi Sarcoma." Journal of Infectious Diseases 203, no. 8 (April 15, 2011): 1082–86. http://dx.doi.org/10.1093/infdis/jiq177.

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AbstractWe conducted a clinical trial of oral valganciclovir, a drug with in vitro activity against Kaposi sarcoma (KS)–associated herpesvirus (KSHV), in classic KS. Five human immunodeficiency virus–seronegative participants received valganciclovir for up to six 4-week cycles at doses used for cytomegalovirus infection. None of the study subjects showed an objective response; KS progressed in 4 subjects after 1–4 cycles and remained stable in 1 subject after 6 cycles. KS biopsies showed minimal lytic KSHV antigen and gene expression at baseline and no treatment-associated changes. Although valganciclovir was not active against KS in this setting, other appropriately targeted anti-herpesviral strategies may prove to be more effective.

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McGeoch, Duncan J. "Molecular evolution of the γ–Herpesvirinae." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 356, no. 1408 (April 29, 2001): 421–35. http://dx.doi.org/10.1098/rstb.2000.0775.

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Genomic sequences available for members of the γ– Herpesvirinae allow analysis of many aspects of the group's evolution. This paper examines four topics: (i) the phylogeny of the group; (ii) the histories of γ–herpesvirus–specific genes; (iii) genomic variation of human herpesvirus 8 (HHV–8); and (iv) the relationship between Epstein–Barr virus types 1 and 2 (EBV–1 and EBV–2). A phylogenetic tree based on eight conserved genes has been constructed for eight γ–herpesviruses and extended to 14 species with smaller gene sets. This gave a generally robust assignment of evolutionary relationships, with the exception of murine herpesvirus 4 (MHV–4), which could not be placed unambiguously on the tree and which has evidently experienced an unusually high rate of genomic change. The γ–herpesviruses possess a variable complement of genes with cellular homologues. In the clearest cases these virus genes were shown to have originated from host genome lineages in the distant past. HHV–8 possesses at its left genomic terminus a highly diverse gene ( K1 ) and at its right terminus a gene ( K15 ) having two diverged alleles. It was proposed that the high diversity of K1 results from a positive selection on K1 and a hitchhiking effect that reduces diversity elsewhere in the genome. EBV–1 and EBV–2 differ in their alleles of the EBNA–2 , EBNA–3A , EBNA–3B and EBNA–3C genes. It was suggested that EBV–1 and EBV–2 may recombine in mixed infections so that their sequences outside these genes remain homogeneous. Models for genesis of the types, by recombination between diverged parents or by local divergence from a single lineage, both present difficulties.

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Pashinyan, Albina G., L. I. Ilienko, A. N. Akopyan, and D. G. Dzhavaeva. "THE FEATURES OF THE CLINICAL MANIFESTATIONS OF THE VIRAL EXANTHEMA." Russian Journal of Skin and Venereal Diseases 20, no. 4 (September 15, 2017): 205–8. http://dx.doi.org/10.18821/1560-9588-2017-20-4-205-208.

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Currently there are about 200 different studied herpes viruses, only 8 types are pathogenic for humans. They all belong to the family Herpesviridae, which according to the structure of the virion and biological properties is divided into three subfamilies: α, β, and γ. Human herpesvirus 6B belongs to the subfamily of β-herpesvirus, genus Roseolovirus. The overview of current information on the etiology, epidemiology, clinical manifestations of infection caused by human herpesvirus 6B is presented. The diagnosis of the viral exanthema using modern laboratory technology is considered.

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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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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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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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Egyed, László. "Replication of Bovine Herpesvirus Type 4 in Human Cells In Vitro." Journal of Clinical Microbiology 36, no. 7 (1998): 2109–11. http://dx.doi.org/10.1128/jcm.36.7.2109-2111.1998.

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A reference strain (Movár 33/63) of bovine herpesvirus type 4 (BHV-4) was inoculated into 14 different human cell lines and five primary cell cultures representing various human tissues. BHV-4 replicated in two embryonic lung cell lines, MRC-5 and Wistar-38, and in a giant-cell glioblastoma cell culture. Cytopathic effect and intranuclear inclusion bodies were observed in these cells. PCR detected a 10,000-times-higher level of BHV-4 DNA. Titration of the supernatant indicated a 100-fold increase of infectious particles. Since this is the first bovine (human herpesvirus 8 and Epstein-Barr virus related) herpesvirus which replicates on human cells in vitro, the danger of possible human BHV-4 infection should not be ignored.

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Thomsen, Darrell R., Nancee L. Oien, Todd A. Hopkins, Mary L. Knechtel, Roger J. Brideau, Michael W. Wathen, and Fred L. Homa. "Amino Acid Changes within Conserved Region III of the Herpes Simplex Virus and Human Cytomegalovirus DNA Polymerases Confer Resistance to 4-Oxo-Dihydroquinolines, a Novel Class of Herpesvirus Antiviral Agents." Journal of Virology 77, no. 3 (February 1, 2003): 1868–76. http://dx.doi.org/10.1128/jvi.77.3.1868-1876.2003.

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ABSTRACT The 4-oxo-dihydroquinolines (PNU-182171 and PNU-183792) are nonnucleoside inhibitors of herpesvirus polymerases (R. J. Brideau et al., Antiviral Res. 54:19-28, 2002; N. L. Oien et al., Antimicrob. Agents Chemother. 46:724-730, 2002). In cell culture these compounds inhibit herpes simplex virus type 1 (HSV-1), HSV-2, human cytomegalovirus (HCMV), varicella-zoster virus (VZV), and human herpesvirus 8 (HHV-8) replication. HSV-1 and HSV-2 mutants resistant to these drugs were isolated and the resistance mutation was mapped to the DNA polymerase gene. Drug resistance correlated with a point mutation in conserved domain III that resulted in a V823A change in the HSV-1 or the equivalent amino acid in the HSV-2 DNA polymerase. Resistance of HCMV was also found to correlate with amino acid changes in conserved domain III (V823A+V824L). V823 is conserved in the DNA polymerases of six (HSV-1, HSV-2, HCMV, VZV, Epstein-Barr virus, and HHV-8) of the eight human herpesviruses; the HHV-6 and HHV-7 polymerases contain an alanine at this amino acid. In vitro polymerase assays demonstrated that HSV-1, HSV-2, HCMV, VZV, and HHV-8 polymerases were inhibited by PNU-183792, whereas the HHV-6 polymerase was not. Changing this amino acid from valine to alanine in the HSV-1, HCMV, and HHV-8 polymerases alters the polymerase activity so that it is less sensitive to drug inhibition. In contrast, changing the equivalent amino acid in the HHV-6 polymerase from alanine to valine alters polymerase activity so that PNU-183792 inhibits this enzyme. The HSV-1, HSV-2, and HCMV drug-resistant mutants were not altered in their susceptibilities to nucleoside analogs; in fact, some of the mutants were hypersensitive to several of the drugs. These results support a mechanism where PNU-183792 inhibits herpesviruses by interacting with a binding determinant on the viral DNA polymerase that is less important for the binding of nucleoside analogs and deoxynucleoside triphosphates.

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Xue, Tianjiao, Huan Ye, Fang Li, Chengyu Luo, Shumei Liu, Jing Luo, and Yanguo Tan. "A case of abdominal-pelvic infiltrative lesion of chronic active Epstein–Barr virus infection." European Journal of Inflammation 18 (January 2020): 205873922093688. http://dx.doi.org/10.1177/2058739220936889.

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Epstein–Barr virus (EBV) belongs to a subfamily of herpesviruses, also known as human herpesvirus type 4. EBV is widely distributed in the population, with a high infection rate of 90%. EBV infects mainly B lymphocytes, stimulates cell proliferation and transformation and even causes cancer. In recent years, it has been found that it can also infect T lymphocytes, epithelial cells and natural killer (NK) cells and can cause related diseases. EBV infection can cause a variety of clinical symptoms and clinical manifestations, which brings some confusion to clinical diagnosis and easily leads to missed diagnosis and misdiagnosis. In this article, we report a case of EBV-induced severe abdominal and pelvic infection, which eventually led to death.

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Latif, Muhammad Bilal, Bénédicte Machiels, Xue Xiao, Jan Mast, Alain Vanderplasschen, and Laurent Gillet. "Deletion of Murid Herpesvirus 4 ORF63 Affects the Trafficking of Incoming Capsids toward the Nucleus." Journal of Virology 90, no. 5 (December 16, 2015): 2455–72. http://dx.doi.org/10.1128/jvi.02942-15.

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ABSTRACTGammaherpesviruses are important human and animal pathogens. Despite the fact that they display the classical architecture of herpesviruses, the function of most of their structural proteins is still poorly defined. This is especially true for tegument proteins. Interestingly, a potential role in immune evasion has recently been proposed for the tegument protein encoded by Kaposi's sarcoma-associated herpesvirus open reading frame 63 (ORF63). To gain insight about the roles of ORF63 in the life cycle of a gammaherpesvirus, we generated null mutations in the ORF63 gene of murid herpesvirus 4 (MuHV-4). We showed that disruption of ORF63 was associated with a severe MuHV-4 growth deficit bothin vitroandin vivo. The latter deficit was mainly associated with a defect of replication in the lung but did not affect the establishment of latency in the spleen. From a functional point of view, inhibition of caspase-1 or the inflammasome did not restore the growth of the ORF63-deficient mutant, suggesting that the observed deficit was not associated with the immune evasion mechanism identified previously. Moreover, this growth deficit was also not associated with a defect in virion egress from the infected cells. In contrast, it appeared that MuHV-4 ORF63-deficient mutants failed to address most of their capsids to the nucleus during entry into the host cell, suggesting that ORF63 plays a role in capsid movement. In the future, ORF63 could therefore be considered a target to block gammaherpesvirus infection at a very early stage of the infection.IMPORTANCEThe important diseases caused by gammaherpesviruses in human and animal populations justify a better understanding of their life cycle. In particular, the role of most of their tegument proteins is still largely unknown. In this study, we used murid herpesvirus 4, a gammaherpesvirus infecting mice, to decipher the role of the protein encoded by the viral ORF63 gene. We showed that the absence of this protein is associated with a severe growth deficit bothin vitroandin vivothat was mainly due to impaired migration of viral capsids toward the nucleus during entry. Together, our results provide new insights about the life cycle of gammaherpesviruses and could allow the development of new antiviral strategies aimed at blocking gammaherpesvirus infection at the very early stages.

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Ongrádi, József, Valéria Kövesdi, and Enikő Kováts. "Human herpesvirus 7." Orvosi Hetilap 151, no. 16 (April 1, 2010): 645–51. http://dx.doi.org/10.1556/oh.2010.28856.

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Az emberi 7-es herpeszvírus 1990 óta ismert, közeli rokonságban áll a 6-os herpeszvírussal, annak B változatával. Csak emberi sejtekben szaporodik, receptora a CD4 molekula. A fertőzött sejtek egy részében élethossziglan lappang, gyakran reaktiválódik és a nyálban tünetmentesen ürül. Gyermekek egy része 3–4 éves korára tünetmentesen fertőződik, de minden életkorban találhatók szeronegatív egyének, akik fogékonyak a fertőzés iránt. Gyermekekben ritkán exanthema subitum, múló lázas-görcsös állapotok, fiatal felnőttekben rózsahámlás, immunszuppresszált egyénekben a reaktiválódott 6-os B herpeszvírussal és cytomegalovirussal egyetemben halálos szövődmények alakulhatnak ki. Egyéb vírusokat is aktiválhat más kórképekben. A vírus patogenezisében a legfontosabb, hogy megváltozik a fertőzött lymphocytákból kiáramló citokinek és növekedési faktorok egyensúlya, amely láncreakcióként hat az immunrendszer és egyéb szervek sejtjeire. A vírusellenes antitestek kimutatása kereskedelmi forgalomban kapható készletekkel (immunfluoreszcencia, ELISA, immunoblot), a nukleinsav kimutatása fészkes polimeráz láncreakcióval lehetséges. A fertőzés következtében kialakult betegségek legtöbbje nem igényel kezelést, de súlyos szövődmények esetén ganciclovir és származékai, valamint foscarnet és cidofovir alkalmazható.

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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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Dęborska, D., M. Durlik, A. Sadowska, B. Matłosz, T. Bączkowska, L. Pączek, J. Szmidt, W. Rowiński, and M. Lao. "Human herpesvirus-6 and human herpesvirus-8 seroprevalence in kidney transplant recipients." Transplantation Proceedings 34, no. 2 (March 2002): 673–74. http://dx.doi.org/10.1016/s0041-1345(01)02883-4.

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Vikulov, G. Kh, E. A. Domonova, E. V. Melekhina, О. Yu Silveystrova, and К. V. Кuleshov. "Inherited chromosomally integrated Human herpesvirus 6B in a woman with herpesvirus infection and secondary immune deficiency." Infekcionnye bolezni 18, no. 4 (2020): 182–88. http://dx.doi.org/10.20953/1729-9225-2020-4-182-188.

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In this article, we discuss some aspects of investigating characteristics of infections caused by Human betaherpesvirus 6A/B (HHV-6A/B) and report a case of laboratory confirmed chromosomally integrated HHV-6B (iciHHV-6B) in a 35-year-old woman with herpesvirus infection and secondary immunodeficiency of unknown origin. We have also described an algorithm for the diagnosis and management of patients with positive iciHHV-6A/B status. Key words: HHV-6-infection, diagnostics, human betaherpesvirus 6B, human herpesvirus 6B, chromosomal integration, inheritance, iciHHV-6B, algorithm

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Black, Jodi B., and Philip E. Pellett. "Human herpesvirus 7." Reviews in Medical Virology 9, no. 4 (October 1999): 245–62. http://dx.doi.org/10.1002/(sici)1099-1654(199910/12)9:4<245::aid-rmv253>3.0.co;2-i.

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Balabanova, R. M. "Rheumatic diseases and viral infection: is there an association?" Modern Rheumatology Journal 14, no. 4 (November 25, 2020): 98–102. http://dx.doi.org/10.14412/1996-7012-2020-4-98-102.

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Viral infections, hepatitis B and C and herpesvirus-induced infections in particular, are widespread in the population. Recent years have seen the emergence of new viral infections that were previously endemic. Understanding the role of viruses in the pathogenesis of rheumatic diseases (RDs) is of great importance. First, they cause the clinical manifestations characteristic of many RDs (systemic lupus erythematosus, rheumatoid arthritis, polymyositis, and Sjö gren's disease). The author discusses several possible mechanisms of the involvement of viruses in the development of autoimmune disorders: molecular mimicry; polyclonal B cell activation with overproduction of antibodies and immune complexes; T cell activation with cytokine overproduction. Secondly, viral infection can be reactivated during immunosuppressive therapy (also using biological agents), which is widely used to treat RDs. The review presents data on both the most common viruses (hepatitis B and C viruses, HIV, and human herpesviruses types 1–6) and more rare ones (chikungunya virus and polyomavirus) in the Russian population.

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Davison, Andrew J., Benes L. Trus, Naiqian Cheng, Alasdair C. Steven, Moira S. Watson, Charles Cunningham, Rose-Marie Le Deuff, and Tristan Renault. "A novel class of herpesvirus with bivalve hosts." Journal of General Virology 86, no. 1 (January 1, 2005): 41–53. http://dx.doi.org/10.1099/vir.0.80382-0.

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Ostreid herpesvirus 1 (OsHV-1) is the only member of the Herpesviridae that has an invertebrate host and is associated with sporadic mortality in the Pacific oyster (Crassostrea gigas) and other bivalve species. Cryo-electron microscopy of purified capsids revealed the distinctive T=16 icosahedral structure characteristic of herpesviruses, although the preparations examined lacked pentons. The gross genome organization of OsHV-1 was similar to that of certain mammalian herpesviruses (including herpes simplex virus and human cytomegalovirus), consisting of two invertible unique regions (UL, 167·8 kbp; US, 3·4 kbp) each flanked by inverted repeats (TRL/IRL, 7·6 kbp; TRS/IRS, 9·8 kbp), with an additional unique sequence (X, 1·5 kbp) between IRL and IRS. Of the 124 unique genes predicted from the 207 439 bp genome sequence, 38 were members of 12 families of related genes and encoded products related to helicases, inhibitors of apoptosis, deoxyuridine triphosphatase and RING-finger proteins, in addition to membrane-associated proteins. Eight genes in three of the families appeared to be fragmented. Other genes that did not belong to the families were predicted to encode DNA polymerase, the two subunits of ribonucleotide reductase, a helicase, a primase, the ATPase subunit of terminase, a RecB-like protein, additional RING-like proteins, an ion channel and several other membrane-associated proteins. Sequence comparisons showed that OsHV-1 is at best tenuously related to the two classes of vertebrate herpesviruses (those associated with mammals, birds and reptiles, and those associated with bony fish and amphibians). OsHV-1 thus represents a third major class of the herpesviruses.

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Alexandrova, L. A., D. G. Semizarov, A. A. Krayevsky, and R. T. Walker. "4′-Thio-5-Ethyl-2′-Deoxyuridine5′-Triphosphate (TEDUTP): Synthesis and Substrate Properties in DNA-Synthesizing Systems." Antiviral Chemistry and Chemotherapy 7, no. 5 (October 1996): 237–42. http://dx.doi.org/10.1177/095632029600700503.

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An efficient synthesis of the 5′-phosphate and 5′-triphosphate of a 4′-thio-2′-deoxynucleoside is described for the first time. The 5′-triphosphate of the antiherpesvirus agent 4′-thio-5-ethyl-2′-deoxyuridine (TEDU) has been shown to be a good substrate for human placental DNA polymerase α, calf thymus terminal deoxynucleotidyl transferase, and the reverse transcriptases of human immunodeficiency virus and avian myeloblastosis virus. As it is known that TEDU is a substrate only for herpesvirus-encoded thymidine kinases and not the cellular kinases, it is likely that the utilization of TEDUTP by DNA-synthesizing enzymes results in the selective toxicity seen in vitro in herpesvirus-infected cells.

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Revankar, GR, JO Ojwang, SD Mustain, RF Rando, E. De Clercq, JH Huffman, JC Drach, J.-P. Sommadossi, and AF Lewis. "Thiazolo[4,5-d]Pyrimidines. Part II. Synthesis and Anti-Human Cytomegalovirus Activity in Vitro of Certain Acyclonucleosides and Acyclonucleotides Derived from the Guanine Analogue 5-Aminothiazolo[4,5-d]Pyrimidine-2,7(3H,6H)-Dione." Antiviral Chemistry and Chemotherapy 9, no. 1 (February 1998): 53–63. http://dx.doi.org/10.1177/095632029800900102.

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The synthesis and in vitro antiviral activity of certain hydroxyalkoxymethyl, hydroxyalkyl, hydroxyalkenyl and phosphonoalkenyl derivatives of the guanine congener 5-aminothiazolo-[4,5- d]pyrimidine-2,7(3 H,6 H)-dione are reported. The compounds of this study were selected for their structural similarity to acyclonucleosides with known anti-herpesvirus activity. 5-Amino-3-[(Z)-4-hydroxy-2-buten-1-yl]thiazolo[4,5- d]pyrimidine-2,7(3 H,6 H)-dione was the only member of the series to display significant in vitro activity against human cytomegalovirus (HCMV); however, this compound did not inhibit other herpesviruses, human immunodeficiency virustype 1 or murine cytomegalovirus. It was found to have a cytotoxicity profile similar to that of ganciclovir (DHPG). The antiviral effect was found to be sensitive to the initial viral input and the time of addition during the virus replication cycle. Significantly, the compound was found to have equal anti-HCMV activity, against standard virus strains, to DHPG, but also showed potent activity against DHPG-resistant virus strains, except for a strain mutated in the UL97 (phosphotransferase) gene.

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Krueger, GerhardR F. "HUMAN HERPESVIRUS-6 INFECTION AND DISEASE." Lancet 332, no. 8609 (August 1988): 518. http://dx.doi.org/10.1016/s0140-6736(88)90175-4.

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Asano, Yoshizo, Tetsushi Yoshikawa, Sadao Suga, Takehiko Yazaki, Satoshi Hirabayashi, Yoshinari Ono, Kazuo Tsuzuki, and Shinichi Oshima. "HUMAN HERPESVIRUS 6 HARBOURING IN KIDNEY." Lancet 334, no. 8676 (December 1989): 1391. http://dx.doi.org/10.1016/s0140-6736(89)91993-4.

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Messick, Troy E., Lois Tolvinski, Edward R. Zartler, Anna Moberg, Åsa Frostell, Garry R. Smith, Allen B. Reitz, and Paul M. Lieberman. "Biophysical Screens Identify Fragments That Bind to the Viral DNA-Binding Proteins EBNA1 and LANA." Molecules 25, no. 7 (April 10, 2020): 1760. http://dx.doi.org/10.3390/molecules25071760.

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The human gamma-herpesviruses Epstein–Barr virus (EBV) (HHV-4) and Kaposi’s sarcoma-associated herpesvirus (KSHV) (HHV-8) are responsible for a number of diseases, including various types of cancer. Epstein–Barr nuclear antigen 1 (EBNA1) from EBV and latency-associated nuclear antigen (LANA) from KSHV are viral-encoded DNA-binding proteins that are essential for the replication and maintenance of their respective viral genomes during latent, oncogenic infection. As such, EBNA1 and LANA are attractive targets for the development of small-molecule inhibitors. To this end, we performed a biophysical screen of EBNA1 and LANA using a fragment library by saturation transfer difference (STD)–NMR spectroscopy and surface plasmon resonance (SPR). We identified and validated a number of unique fragment hits that bind to EBNA1 or LANA. We also determined the high-resolution crystal structure of one fragment bound to EBNA1. Results from this screening cascade provide new chemical starting points for the further development of potent inhibitors for this class of viral proteins.

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Goldsmith, C. S., D. Burns, P. E. Pellett, S. R. Zaki, and J. B. Black. "Ultrastructure of human herpesvirus 7." Proceedings, annual meeting, Electron Microscopy Society of America 53 (August 13, 1995): 1032–33. http://dx.doi.org/10.1017/s0424820100141536.

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Human herpesvirus 7 (HHV-7) was originally isolated in 1989 from the peripheral blood lymphocytes of a healthy individual. Most children between 2 and 5 years of age develop antibodies against HHV-7, and the virus has recently been implicated as the causative agent in secondary episodes of the childhood disease roseola infantum. Approximately 90% of the general population is seropositive, and virus can be isolated from the saliva of up to 75% of healthy adults. This study describes the ultrastructural growth properties of an HHV-7 isolate obtained from a saliva specimen.Cord blood lymphocytes (CBLs) were inoculated with cell-free virus and harvested at days 1, 3, 4, 5, and 7. The growth curve for HHV-7 was determined by examining the ultrastructure of the cells for signs of viral production and by monitoring the cells with an anti-complement immunofluorescence assay for the presence of viral proteins.The nuclei of HHV-7-infected CBLs typically had viral nucleocapsids scattered throughout, although the capsids would occasionally converge into organized structures (Fig. 1).

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Kovalyk, V. P., M. A. Gomberg, E. E. Bragina, K. I. Yurlov, and A. A. Kushch. "Herpesvirus role in male infertility." Russian Medical Inquiry 5, no. 3 (2021): 123–29. http://dx.doi.org/10.32364/2587-6821-2021-5-3-123-129.

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Nowadays, the search for etiopathogenetic factors of infertility is an urgent medical and social task. 23 men with chronic abacterial prostatitis in a barren marriage underwent the follow-up. Herpesviruses of types IV–VI were detected in urogenital samples (urethra, ejaculate, prostate secretions) in 8 of 23 men who were treated with valacyclovir (500 mg 2 times a day for 3 months) and interferon α-2b in combination with antioxidants — vitamins E and C (rectal suppositories). Based on the personal experience of the authors, the patients were prescribed the following drug use regimen: 3 million IU twice a day — 10 days, then 3 million IU twice a day — 3 times per week for the next 3 weeks. The remaining 15 patients without any detected viruses were prescribed the following: levofloxacin 500 mg — 30 days, tamsulosin 0.4 mg — 90 days, diclofenac 50 mg — 10 days. By the end of therapy, electron microscopy and virology showed a decrease in the concentration and number of virus-positive urogenital samples, as well as a decrease in the number of spermatozoa with viral capsids. Within 6 months from the therapy initiation, the onset of pregnancy was observed in the married couples of 6 out of 8 men with herpesviruses vs. in 4 out of 11 without viruses (p=0.026). Thus, we obtained the data on the role of herpesviruses of types IV–VI in male infertility. A good reproductive effect was achieved with valacyclovir and interferon α-2b in combination with antioxidants in most patients. KEYWORDS: herpesviruses, Epstein-Barr virus, cytomegalovirus, human herpes virus type VI, male infertility. FOR CITATION: Kovalyk V.P., Gomberg M.A., Bragina E.E. et al. Herpesvirus role in male infertility. Russian Medical Inquiry. 2021;5(3):123– 129. DOI: 10.32364/2587-6821-2021-5-3-123-129.

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Ashshi, A. "Detection of human cytomegalovirus, human herpesvirus type 6 and human herpesvirus type 7 in urine specimens by multiplex PCR." Journal of Infection 47, no. 1 (July 2003): 59–64. http://dx.doi.org/10.1016/s0163-4453(03)00057-4.

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Asada, Hideo, Vera Klaus-Kovtun, Hana Golding, Stephen I. Katz, and Andrew Blauvelt. "Human Herpesvirus 6 Infects Dendritic Cells and Suppresses Human Immunodeficiency Virus Type 1 Replication in Coinfected Cultures." Journal of Virology 73, no. 5 (May 1, 1999): 4019–28. http://dx.doi.org/10.1128/jvi.73.5.4019-4028.1999.

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ABSTRACT Human herpesvirus 6 (HHV-6) has been implicated as a cofactor in the progressive loss of CD4+ T cells observed in AIDS patients. Because dendritic cells (DC) play an important role in the immunopathogenesis of human immunodeficiency virus (HIV) disease, we studied the infection of DC by HHV-6 and coinfection of DC by HHV-6 and HIV. Purified immature DC (derived from adherent peripheral blood mononuclear cells in the presence of granulocyte-macrophage colony-stimulating factor and interleukin-4) could be infected with HHV-6, as determined by PCR analyses, intracellular monoclonal antibody staining, and presence of virus in culture supernatants. However, HHV-6-infected DC demonstrated neither cytopathic changes nor functional defects. Interestingly, HHV-6 markedly suppressed HIV replication and syncytium formation in coinfected DC cultures. This HHV-6-mediated anti-HIV effect was DC specific, occurred when HHV-6 was added either before or after HIV, and was not due to decreased surface expression or function of CD4, CXCR4, or CCR5. Conversely, HIV had no demonstrable effect on HHV-6 replication. These findings suggest that HHV-6 may protect DC from HIV-induced cytopathicity in AIDS patients. We also demonstrate that interactions between HIV and herpesviruses are complex and that the observable outcome of dual infection is dependent on the target cell type.

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Millichap, J. Gordon. "Human Herpesvirus-6 and Roseola Infantum Meningitis." Pediatric Neurology Briefs 6, no. 4 (April 1, 1992): 26. http://dx.doi.org/10.15844/pedneurbriefs-6-4-2.

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Zimmermann, Wolfgang, Hermann Broll, Bernhard Ehlers, Hans-Jörg Buhk, André Rosenthal, and Michael Goltz. "Genome Sequence of Bovine Herpesvirus 4, a Bovine Rhadinovirus, and Identification of an Origin of DNA Replication." Journal of Virology 75, no. 3 (February 1, 2001): 1186–94. http://dx.doi.org/10.1128/jvi.75.3.1186-1194.2001.

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ABSTRACT Bovine herpesvirus 4 (BoHV-4) is a gammaherpesvirus of cattle. The complete long unique coding region (LUR) of BoHV-4 strain 66-p-347 was determined by a shotgun approach. Together with the previously published noncoding terminal repeats, the entire genome sequence of BoHV-4 is now available. The LUR consists of 108,873 bp with an overall G+C content of 41.4%. At least 79 open reading frames (ORFs) are present in this coding region, 17 of them unique to BoHV-4. In contrast to herpesvirus saimiri and human herpesvirus 8, BoHV-4 has a reduced set of ORFs homologous to cellular genes. Gene arrangement as well as phylogenetic analysis confirmed that BoHV-4 is a member of the genusRhadinovirus. In addition, an origin of replication (ori) in the genome of BoHV-4 was identified byDpnI assays. A minimum of 1.69 kbp located between ORFs 69 and 71 was sufficient to act as a cis signal for replication.

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Maeki, Takahiro, and Yasuko Mori. "Features of Human Herpesvirus-6A and -6B Entry." Advances in Virology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/384069.

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Human herpesvirus-6 (HHV-6) is a T lymphotropic herpesvirus belonging to theBetaherpesvirinaesubfamily. HHV-6 was long classified into variants A and B (HHV-6A and HHV-6B); however, recently, HHV-6A and HHV-6B were reclassified as different species. The process of herpesvirus entry into target cells is complicated, and in the case of HHV-6A and HHV-6B, the detailed mechanism remains to be elucidated, although both viruses are known to enter cells via endocytosis. In this paper, (1) findings about the cellular receptor and its ligand for HHV-6A and HHV-6B are summarized, and (2) a schematic model of HHV-6A’s replication cycle, including its entry, is presented. In addition, (3) reports showing the importance of lipids in both the HHV-6A envelope and target-cell membrane for viral entry are reviewed, and (4) glycoproteins involved in cell fusion are discussed.

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Taras, T. M., E. R. Luchkevich, V. I. Shupeniuk, O. P. Sabadakh, L. D. Bolibrukh, and L. R. Zhurakhivska. "Synthesis and predicted antiviral activity of 4-substituted 9,10-anthraquinone derivatives." Chemistry, Technology and Application of Substances 3, no. 2 (November 1, 2020): 67–72. http://dx.doi.org/10.23939/ctas2020.02.067.

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Antiviral activity was predicted by using data from program PASS Online for synthesized compounds against picornavirus, the influenza and the rhinovirus, what fits in today's strategy of creating of the anthraquinone-based anticancer drugs and with antibacterial effect. There are several current methods to synthesize 9,10-anthraquinone, which contain the biogenic amines in the 4-position. Antiviral activity was predicted by using program AVCpred in a percentage of inhibition against deadly viruses like Human immunodeficiency virus (HIV), Hepatitis C virus (HCV), Hepatitis B virus (HBV), Human herpesvirus (HHV)

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Roa-Linares, Vicky, Yaneth Miranda-Brand, Verónica Tangarife-Castaño, Rodrigo Ochoa, Pablo García, Mª Castro, Liliana Betancur-Galvis, and Arturo San Feliciano. "Anti-Herpetic, Anti-Dengue and Antineoplastic Activities of Simple and Heterocycle-Fused Derivatives of Terpenyl-1,4-Naphthoquinone and 1,4-Anthraquinone." Molecules 24, no. 7 (April 2, 2019): 1279. http://dx.doi.org/10.3390/molecules24071279.

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Quinones are secondary metabolites of higher plants associated with many biological activities, including antiviral effects and cytotoxicity. In this study, the anti-herpetic and anti-dengue evaluation of 27 terpenyl-1,4-naphthoquinone (NQ), 1,4-anthraquinone (AQ) and heterocycle-fused quinone (HetQ) derivatives was done in vitro against Human Herpesvirus (HHV) type 1 and 2, and Dengue virus serotype 2 (DENV-2). The cytotoxicity on HeLa and Jurkat tumor cell lines was also tested. Using plaque forming unit assays, cell viability assays and molecular docking, we found that NQ 4 was the best antiviral compound, while AQ 11 was the most active and selective molecule on the tested tumor cells. NQ 4 showed a fair antiviral activity against Herpesviruses (EC50: <0.4 µg/mL, <1.28 µM) and DENV-2 (1.6 µg/mL, 5.1 µM) on pre-infective stages. Additionally, NQ 4 disrupted the viral attachment of HHV-1 to Vero cells (EC50: 0.12 µg/mL, 0.38 µM) with a very high selectivity index (SI = 1728). The in silico analysis predicted that this quinone could bind to the prefusion form of the E glycoprotein of DENV-2. These findings demonstrate that NQ 4 is a potent and highly selective antiviral compound, while suggesting its ability to prevent Herpes and Dengue infections. Additionally, AQ 11 can be considered of interest as a leader for the design of new anticancer agents.

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Brown, NathanielA, CiroV Sumaya, Chun-Ren Liu, Yasmin Ench, Andrea Kovacs, Maria Coronesi, and MarkH Kaplan. "FALL IN HUMAN HERPESVIRUS 6 SEROPOSITIVITY WITH AGE." Lancet 332, no. 8607 (August 1988): 396. http://dx.doi.org/10.1016/s0140-6736(88)92864-4.

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Huang, Li-Min, Chin-Yun Lee, Kai-Hsin Lin, Wen-Min Chuu, Ping-Ing Lee, Rong-Long Chen, Jong-Ming Chen, and Dong-Tsamn Lin. "Human herpesvirus-6 associated with fatal haemophagocytic syndrome." Lancet 336, no. 8706 (July 1990): 60–61. http://dx.doi.org/10.1016/0140-6736(90)91580-4.

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Neyts, J., and E. De Clercq. "Antiviral drug susceptibility of human herpesvirus 8." Antimicrobial Agents and Chemotherapy 41, no. 12 (December 1997): 2754–56. http://dx.doi.org/10.1128/aac.41.12.2754.

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We studied the susceptibility of human herpesvirus 8 (HHV-8) to a number of antiherpesvirus agents. The acyclic nucleoside phosphonate (ANP) analogs cidofovir and HPMPA [(S)-1-(3-hydroxy-2-phosphonylmethoxypropyl)adenine] effected potent inhibition of HHV-8 DNA synthesis, with 50% effective concentrations (EC50) of 6.3 and 0.6 microM, respectively. Adefovir, an ANP with both antiretrovirus and antiherpesvirus activity, blocked HHV-8 DNA replication at a fourfold-lower concentration than did foscarnet (EC50 of 39 and 177 microM, respectively). The most potent inhibitory effect was obtained with the N-7-substituted nucleoside analog S2242 (EC50, 0.11 microM). The nucleoside analogs acyclovir, penciclovir, H2G ((R)-9-[4-hydroxy-2-(hydroxymethyl) butyl]guanine), and brivudine had weak to moderate effects (EC50 of > or =75, 43, 42, and 24 microM, respectively, and EC90 of > or =75 microM), whereas ganciclovir elicited pronounced anti-HHV-8 activity (EC50, 8.9 microM).

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Cloutier, N., O. van Eyll, M. E. Janelle, S. Lefort, S. J. Gao, and L. Flamand. "Increased tumorigenicity of cells carrying recombinant human herpesvirus 8." Archives of Virology 153, no. 1 (October 18, 2007): 93–103. http://dx.doi.org/10.1007/s00705-007-1072-4.

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Machiels, Bénédicte, Laurent Gillet, Sieberth Do Nascimento Brito, Pierre Drion, Cédric Delforge, Yannick Nizet, Pierre Gianello, et al. "Natural antibody–complement dependent neutralization of bovine herpesvirus 4 by human serum." Microbes and Infection 9, no. 14-15 (November 2007): 1530–37. http://dx.doi.org/10.1016/j.micinf.2007.08.007.

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Isaacson, E., C. A. Glaser, B. Forghani, Z. Amad, M. Wallace, R. W. Armstrong, M. M. Exner, and S. Schmid. "Evidence of Human Herpesvirus 6 Infection in 4 Immunocompetent Patients with Encephalitis." Clinical Infectious Diseases 40, no. 6 (March 15, 2005): 890–93. http://dx.doi.org/10.1086/427944.

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Journal articles on the topic 'Herpesvirus 4 Humano'

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