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Herpesvirus: History
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Please note this is an old version of this entry, which may differ significantly from the current revision.
Contributor: Abel A. Soto ,
Gerardo Ortiz
,
Sofía Contreras
, Ricardo Soto-Rifo , Pablo A. González

Herpesviruses are double-stranded DNA viruses occurring at a high prevalence in the human population and are responsible for a wide array of clinical manifestations and diseases, from mild to severe. These viruses are classified in three subfamilies (Alpha-, Beta- and Gammaherpesvirinae), with eight members known to infect humans.

  • herpesvirus
  • latency
  • RNA modifications
  • herpes simplex virus
  • varicella virus
  • Epstein-Barr virus
  • cytomegalovirus
  • HHV-6
  • HHV-7
  • Kaposi's sarcoma virus
  • HSV-1
  • HSV-2
  • VZV
  • EBV
  • CMV
  • KSHV
  • prevalence
  • epigenetic modifications
  • DNA modifications

1. Introduction

Herpesviruses are double-stranded DNA viruses with genomes that range between 152–172 kbp in length. These viruses are members of the Herpesviridae family, which encompasses at least 100 different viruses [1]. From these, eight herpesviruses have been shown to affect humans, which are distributed within three subfamilies: Alpha-, Beta- and Gammaherpesvirinae [2]. While herpes simplex viruses type 1 and 2 (HSV-1 and HSV-2, respectively) and the varicella-zoster virus (VZV) are classified within the Alphaherpesvirinae subfamily, cytomegalovirus (CMV) and the human herpesviruses 6 and 7 (HHV-6, HHV-7) belong to the Betaherpesvirinae subfamily, and Epstein Barr virus (EBV) and the Kaposi’s sarcoma-associated herpesvirus (KSHV) are members of the Gammaherpesvirinae subfamily [2]. All these viruses can infect humans asymptomatically or symptomatically with a variety of symptoms and clinical manifestations, leading in some circumstances to mild up to severe diseases. Other commonly studied herpesviruses that affect animals are pseudorabies virus (PRV) and Marek’s disease virus (MDV), both belonging to the Alphaherpesvirinae subfamily [3][4].

2. Herpesviruses: Epidemiology and Illnesses

Human viruses of the Alphaherpesvirinae subfamily, such as HSV-1 and HSV-2, are highly prevalent worldwide with a prevalence estimated at 66.6% and 13.2%, respectively [5]. Data gathered in Asia indicate that these viruses have a frequency of 50% in children and 76.5% in adults [6], while in other countries lower values have been reported, such as 47.1% for HSV-1 and 12.1% for HSV-2 in the USA [7]. Diseases generated by HSV-1 and HSV-2 are usually mucocutaneous or affect the central nervous system [8]. The main transmission route of HSVs is through oral, oro-sexual, or sexual contact [8]. During early stages of infection, viral glycoproteins interact with their ligands on the cell surface for viral binding. HSV virions are overall composed by a lipid bilayer envelope decorated with numerous proteins and glycoproteins on the outer surface. Beneath the viral envelope, there are approximately 20 viral proteins, in a zone called the tegument, which harbors several viral proteins that play essential roles over the host antiviral response early on after infection [9]. Below the tegument is the viral capsid which harbors the viral genome in a lineal form [9]. A similar structure is found in other herpesviruses, although with particularities for each of them. At least five glycoproteins are critical for HSV-1 entry and four for HSV-2 [10]. Glycoprotein B (gB) is key for virus attachment to the heparan sulfates on the host cell for both HSVs, while gC is also important for HSV-1, but not for HSV-2 [11]. gD is also present on the virion surface, and binds to any of the receptors mentioned above, namely nectin-1, nectin-2, the herpes virus entry mediator (HVEM), or 3-OS heparan sulfates [10][12]. Upon binding to one of its ligands gD activates two other essential glycoproteins on the virion surface, gH and gL, which act as a complex (gH/gL) that in turn activates the fusogenic properties of gB [10]. Once these interactions are established, HSV entry into the cytoplasm is mediated by membrane fusion, endocytosis or phagocytosis [13][14]. The viral capsid then enters the cell and is transported through microtubules to the nuclear pore, where the genome is injected into the nucleus and viral gene transcription initiates [15]. At this stage, productive viral infection begins with the transcription of a particular set of genes named immediate early genes (IE or alpha) [16]. A pivotal transcription factor called ICP4 (infected cell protein 4) is transcribed and translated early on (referred to as an immediate early gene; IE or alpha gene), which allows the beginning of a downstream sequential gene expression cascade that promotes the transcription and translation of early genes (E or beta genes), such as ICP8 (infected cell protein 8) or TK (thymidine kinase), and finally late genes (L or gamma genes), such as VP16 (viral protein 16) or gD (glycoprotein D) [16]. The latter are sometimes further classified as early late (gamma-1) and late (gamma-2) genes [17]. The classification of IE, E and L genes is based on the timing of their transcription during infection and dependency on different viral transcription factors [14][18].
Varicella-zoster virus (VZV), another alphaherpesvirus, causes varicella (also known as chickenpox) and zoster (also known as shingles) [19]. Current evidence suggests that primary VZV infection begins with the replication of the virus in respiratory epithelial cells [20]. Similar to other alphaherpesviruses, VZV binds to heparan sulfate receptors on the cell surface for its entry into the cell. Moreover, VZV can use the insulin-degrading enzyme (IDE) as the cellular receptor through an interaction that is mediated by the viral glycoprotein E (gE) in the MeWo cell line, which is a model of fibroblast. Once the virus is inside the cell, the expression of IE, E and L genes is initiated [21]. Infection is followed by a widely distributed vesicular rash that is a typical trait of varicella after the incubation period (approximately 10 to 21 days) [19]. This pattern likely reflects viral spread from the tonsils and other local lymphoid tissues, from where infected T cells can transport the virus via the bloodstream to the skin [22]. VZV is found in a worldwide geographic distribution, but annual epidemics are more prevalent in temperate climates, occurring most often during late winter and spring [23]. The prevalence of VZV infection in the population is elevated and, in the USA, has been reported to be over 93% in the 6- to 19-year old group and 98% in adults aged 20–49 years [24][25]. Cases of herpes zoster provide a source of VZV transmission to susceptible close contacts, causing varicella; the virus then spreads rapidly to other susceptible individuals, in part because, in contrast to other herpesviruses, VZV is transmissible by the respiratory route [19]. Varicella attack rates among susceptible household contacts exposed to VZV are approximately 90%; more limited exposures, such as those occurring in school classrooms, result in transmission rates of about 10 to 35% [26].
Two other alphaherpesviruses of interest are pseudorabies virus (PrV) and Marek’s disease virus (MDV), which can infect animals. PrV is a neurotropic virus that causes Aujeskzy’s disease in swine, although a broad spectrum of mammals can be infected with this virus, such as rodents, cats, dogs and cattle [27]. The seroprevalence of PrV in pigs in China has been reported to be approximately 35% [28]. Similar to HSV-1, neuron infection with PrV occurs through trigeminal neuron infection involving the interactions of the viral glycoprotein gD with the host nectin-1 receptor, which activates cytoskeleton remodeling, allowing viral particle entry into the cell [29]. MDV infection on other hand causes one of the most prevalent cancers described in the animal kingdom and mainly poultry [30]. The prevalence of infection can reach up to 49.5% in chicken, as reported in Iraq [31]. MDV infection is mediated by the interaction of the viral glycoprotein gC with glycosaminoglycans (GAGs) on cell surfaces and this virus mainly infects and replicates in immune cells, such as macrophages, natural killer (NK cells), as well as B cells, and establishes latency in T cells [30].
Betaherpesviruses such as CMV have a high prevalence in the infant population, with approximately 59% of children older than six years old having been exposed to the virus [32]. Strong differences in the epidemiology of CMV amongst the adult population in industrialized and emerging countries exist, where the latter have the highest frequency of infection reaching 100%, while industrialized countries display a range of infection between 60–70% [33]. CMV transmission occurs by direct contact with infected body fluids and there is evidence regarding vertical and breast-milk transmission [33]. The main cells infected by CMV are epithelial cells, fibroblasts and myeloid cells [34]. The mechanism of entry described for CMV involves molecular interactions between viral glycoprotein complexes, such as gH/gL and gH/gL/gp42, with integrins on the surface of epithelial cells and major histocompatibility complex class II (MHC-II) molecules in B cells [35]. Symptoms associated with CMV infections vary significantly, from asymptomatic to severe illness, with mononucleosis being the most common clinical presentation [36].
Another betaherpesvirus that can infect humans is HHV-6 (also known as HHV-6A). This virus infects children at a high rate and 90% of the human population is likely to being infected before the age of three [37]. The general route of infection is by contact with contaminated saliva, after which the virus enters mainly into CD4+ T cells through the CD46 receptor [38]. Symptoms after HHV-6 infection depend on the immunological state of the host. Infection in immunosuppressed individuals is related with the development of ataxia, hypersomnia, dementia, encephalitis, and myocarditis, among others [37]. The human herpesvirus 7 (HHV-7, also known as HHV-6B), is another betaherpesvirus able to infect humans and is highly prevalent worldwide [39]. In the United States of America, the prevalence of HHV-7 is above 85% [40]. However, prevalence rates can significantly vary between ethnicities [40]. This virus enters to the target cells through the CD134 receptor which is expressed only in activated CD4+ T cells [41]. Usually, HHV-7-related symptoms after infection only occur in immunosuppressed individuals and, in these subjects, they are somewhat similar to those reported for HHV-6 [39].
Epstein Barr virus and the Kaposi’s sarcoma-associated herpesvirus (KSHV, or HHV-8) are gammaherpesviruses that can infect humans [42]. EBV infection in the population is widespread, over 90%, with asymptomatic infections mainly occurring during childhood [43]. EBV mainly infects B cells through the interaction between the viral glycoprotein-350 (gp-350) and the B cell receptor CD21 [44]. If infection occurs during adulthood, it can result in infectious mononucleosis, a self-limiting disease characterized by the inflammation of lymph nodes in the neck region [43]. Transmission of EBV is mainly through oral secretions [42], although infections after blood transfusions and organ transplants also occur [42]. EBV is known to be an oncogenic virus, as its infection is associated mainly with Hodgkin’s lymphoma [45]. Additionally, EBV reactivation in immunosuppressed individuals may cause lymphoproliferative diseases [45]. On the other hand, recent evidence links EBV with the development of multiple sclerosis [46].
As its name suggests, KSHV is responsible for the development of all Kaposi’s sarcomas [47]. Similar to other types of herpesviruses, KSHV interacts with heparan sulfates on the cell surface to enter the cell through the use of its viral glycoprotein gB [48]. In children, cases of hemophagocytic lymphohistiocytosis are described after infection with this virus [49]. The epidemiology of KSHV significantly depends on the geographical region [50]. While the prevalence of this virus in North America, Europe and Asia is lower than 5%, in Eastern Europe, the Middle East and the Caribbean the seroprevalence is above 50% [50]. Noteworthily, the highest seroprevalence of KSHV is found in Africa and regions of the Amazonas in Brazil, with values reaching 60% [50]. While the transmission route for this virus is not totally clear, its high prevalence in men that have sex with men supports the hypothesis of sexual transmission [50]. However, there is a high level of seroprevalence in children in Africa ,also suggesting salivary transmission [50]. Vertical and blood transfusion transmission are also well described [51]. Importantly, this virus is able to infect numerous cell types, such as dendritic cells (DCs), monocytes, B lymphocytes and oral epithelial cells [48][51].
Overall, herpesviruses are present in humans at a high prevalence, with the exception of HHV-8, which has a more limited penetration in the population. Importantly, these viruses elicit lifelong infections through the establishment of persistent infections and can undergo latency. Lifelong infections and frequent reactivations for some of these viruses evidences the existence of immune evasion mechanisms that allow them to persist in the host. Although there are numerous antivirals available that limit severe diseases caused by these viruses, they do not clear the virus from the host and thus, reactivations may occur during the entire life of an infected individual. Furthermore, some clinical manifestations elicited by these viruses, such as skin lesions produced by HSV-1 and HSV-2, are only mildly affected by such drugs, reducing in only a few days what are usually week-long lesions [52]. Therefore, a better understanding of the molecular determinants that favor herpesvirus infections and their persistence in the host is needed for developing better therapeutic approaches. 

This entry is adapted from the peer-reviewed paper 10.3390/microorganisms10091754

References

  1. Sharma, V.; Mobeen, F.; Prakash, T. Comparative Genomics of Herpesviridae Family to Look for Potential Signatures of Human Infecting Strains. Int. J. Genom. 2016, 2016, 9543274.
  2. Pedro Simas, J.; Cruz-Muñoz, M.E.; Fuentes-Pananá, E.M. Beta and Gamma Human Herpesviruses: Agonistic and Antagonistic Interactions with the Host Immune System. Front. Microbiol. 2018, 8, 2521.
  3. Klupp, B.G. Pseudorabies Virus Infections. Pathogens 2021, 10, 719.
  4. Song, B.; Zeb, J.; Hussain, S.; Aziz, M.U.; Circella, E.; Casalino, G.; Camarda, A.; Yang, G.; Buchon, N.; Sparagano, O. A Review on the Marek’s Disease Outbreak and Its Virulence-Related meq Genovariation in Asia between 2011 and 2021. Animals 2022, 12, 540.
  5. Tognarelli, E.I.; Retamal-Díaz, A.; Farías, M.A.; Duarte, L.F.; Palomino, T.F.; Ibañez, F.J.; Riedel, C.A.; Kalergis, A.M.; Bueno, S.M.; González, P.A. Pharmacological Inhibition of IRE-1 Alpha Activity in Herpes Simplex Virus Type 1 and Type 2-Infected Dendritic Cells Enhances T Cell Activation. Front. Immunol. 2022, 12.
  6. Khadr, L.; Harfouche, M.; Omori, R.; Schwarzer, G.; Chemaitelly, H.; Abu-Raddad, L.J. The Epidemiology of Herpes Simplex Virus Type 1 in Asia: Systematic Review, Meta-analyses, and Meta-regressions. Clin. Infect. Dis. 2018, 68, 757–772.
  7. McQuillan, G.; Kruszon-Moran, D.; Flagg, E.W.; Paulose-Ram, R. Prevalence of Herpes Simplex Virus Type 1 and Type 2 in Persons Aged 14–49: United States, 2015–2016. NCHS Data Brief 2018, 304, 1–8.
  8. Zhu, S.; Viejo-Borbolla, A. Pathogenesis and virulence of herpes simplex virus. Virulence 2021, 12, 2670–2702.
  9. Xu, X.; Che, Y.; Li, Q. HSV-1 tegument protein and the development of its genome editing technology. Virol. J. 2016, 13, 1–7.
  10. Hilterbrand, A.T.; Daly, R.E.; Heldwein, E.E. Contributions of the Four Essential Entry Glycoproteins to HSV-1 Tropism and the Selection of Entry Routes. mBio 2021, 12, e00143-21.
  11. O’Donnell, C.D.; Shukla, D. The importance of heparan sulfate in herpesvirus infection. Virol. Sin. 2008, 23, 383–393.
  12. Atanasiu, D.; Cairns, T.M.; Whitbeck, J.C.; Saw, W.T.; Rao, S.; Eisenberg, R.J.; Cohen, G.H. Regulation of Herpes Simplex Virus gB-Induced Cell-Cell Fusion by Mutant Forms of gH/gL in the Absence of gD and Cellular Receptors. mBio 2013, 4, e00046-13.
  13. Farooq, A.V.; Valyi-Nagy, T.; Shukla, D. Mediators and Mechanisms of Herpes Simplex Virus Entry into Ocular Cells. Curr. Eye Res. 2010, 35, 445–450.
  14. Tognarelli, E.; Reyes, A.; Corrales, N.; Carreño, L.; Bueno, S.; Kalergis, A.; González, P. Modulation of Endosome Function, Vesicle Trafficking and Autophagy by Human Herpesviruses. Cells 2021, 10, 542.
  15. Copeland, A.M.; Newcomb, W.W.; Brown, J.C. Herpes Simplex Virus Replication: Roles of Viral Proteins and Nucleoporins in Capsid-Nucleus Attachment. J. Virol. 2009, 83, 1660–1668.
  16. Ibáñez, F.J.; Farías, M.A.; Gonzalez-Troncoso, M.P.; Corrales, N.; Duarte, L.F.; Retamal-Díaz, A.; Gonzalez, P.A. Experimental Dissection of the Lytic Replication Cycles of Herpes Simplex Viruses in vitro. Front. Microbiol. 2018, 9, 2406.
  17. Tunnicliffe, R.B.; Lockhart, M.; Levy, C.; Mould, P.; Jowitt, T.; Sito, H.; Baldock, C.; Sandri-Goldin, R.M.; Golovanov, A.P. The herpes viral transcription factor ICP4 forms a novel DNA recognition complex. Nucleic Acids Res. 2017, 45, 8064–8078.
  18. Egruffat, H.; Emarchione, R.; Manet, E. Herpesvirus Late Gene Expression: A Viral-Specific Pre-initiation Complex Is Key. Front. Microbiol. 2016, 7, 869.
  19. Mueller, N.H.; Gilden, D.H.; Cohrs, R.J.; Mahalingam, R.; Nagel, M.A. Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis of Disease, and Latency. Neurol. Clin. 2008, 26, 675–697.
  20. Laing, K.; Ouwendijk, W.J.D.; Koelle, D.M.; Verjans, G.M.G.M. Immunobiology of Varicella-Zoster Virus Infection. J. Infect. Dis. 2018, 218, S68–S74.
  21. Li, Q.; Krogmann, T.; Ali, M.A.; Tang, W.-J.; Cohen, J.I. The Amino Terminus of Varicella-Zoster Virus (VZV) Glycoprotein E Is Required for Binding to Insulin-Degrading Enzyme, a VZV Receptor. J. Virol. 2007, 81, 8525–8532.
  22. Campbell, T.M.; McSharry, B.P.; Steain, M.; Ashhurst, T.; Slobedman, B.; Abendroth, A. Varicella zoster virus productively infects human natural killer cells and manipulates phenotype. PLoS Pathog. 2018, 14, e1006999.
  23. Daulagala, S.W.P.L.; Noordeen, F. Epidemiology and factors influencing varicella infections in tropical countries including Sri Lanka. VirusDisease 2018, 29, 277–284.
  24. Kourieh, A.; Gheit, T.; Tommasino, M.; Dalstein, V.; Clifford, G.M.; Guily, J.L.S.; Clavel, C.; Franceschi, S.; Combes, J.-D.; for the SPLIT study group. Prevalence of human herpesviruses infections in nonmalignant tonsils: The SPLIT study. J. Med. Virol. 2018, 91, 687–697.
  25. Reynolds, M.A.; Kruszon-Moran, D.; Jumaan, A.; Schmid, D.S.; McQuillan, G.M. Varicella Seroprevalence in the U.S.: Data from the National Health and Nutrition Examination Survey, 1999–2004. Public Heal. Rep. 2010, 125, 860–869.
  26. Jackson, C.; Mangtani, P.; Fine, P.; Vynnycky, E. The Effects of School Holidays on Transmission of Varicella Zoster Virus, England and Wales, 1967–2008. PLoS ONE 2014, 9, e99762.
  27. Laval, K.; Enquist, L.W. The Neuropathic Itch Caused by Pseudorabies Virus. Pathogens 2020, 9, 254.
  28. Tan, L.; Yao, J.; Yang, Y.; Luo, W.; Yuan, X.; Yang, L.; Wang, A. Current Status and Challenge of Pseudorabies Virus Infection in China. Virol. Sin. 2021, 36, 588–607.
  29. Lyman, M.G.; Enquist, L.W. Herpesvirus Interactions with the Host Cytoskeleton. J. Virol. 2009, 83, 2058–2066.
  30. Bertzbach, L.D.; Conradie, A.M.; You, Y.; Kaufer, B.B. Latest Insights into Marek’s Disease Virus Pathogenesis and Tumorigenesis. Cancers 2020, 12, 647.
  31. Wajid, S.J.; Katz, M.E.; Renz, K.G.; Walkden-Brown, S.W. Prevalence of Marek's Disease Virus in Different Chicken Populations in Iraq and Indicative Virulence Based on Sequence Variation in the EcoRI-Q (meq) Gene. Avian Dis. 2013, 57, 562–568.
  32. Rico, A.; Dollard, S.C.; Valencia, D.; Corchuelo, S.; Tong, V.T.; Laiton-Donato, K.; Amin, M.M.; Benavides, M.; Wong, P.; Newton, S.; et al. Epidemiology of cytomegalovirus Infection among mothers and infants in Colombia. J. Med. Virol. 2021, 93, 6393–6397.
  33. Manicklal, S.; Emery, V.C.; Lazzarotto, T.; Boppana, S.B.; Gupta, R.K. The “Silent” Global Burden of Congenital Cytomegalovirus. Clin. Microbiol. Rev. 2013, 26, 86–102.
  34. Sun, L.; Chen, J.-M.; Yang, K.; Zhang, L.; Ma, Z.-Y.; Chen, X.-M.; Li, M.; Zhou, X.; Li, P.; Zhao, H.-X.; et al. Cytomegalovirus cell tropism and clinicopathological characteristics in gastrointestinal tract of patients with HIV/AIDS. Diagn. Pathol. 2022, 17, 1–8.
  35. Vanarsdall, A.L.; Johnson, D.C. Human cytomegalovirus entry into cells. Curr. Opin. Virol. 2012, 2, 37–42.
  36. Ishii, T.; Sasaki, Y.; Maeda, T.; Komatsu, F.; Suzuki, T.; Urita, Y. Clinical differentiation of infectious mononucleosis that is caused by Epstein-Barr virus or cytomegalovirus: A single-center case-control study in Japan. J. Infect. Chemother. 2019, 25, 431–436.
  37. Eliassen, E.; Lum, E.; Pritchett, J.; Ongradi, J.; Krueger, G.; Crawford, J.R.; Phan, T.L.; Ablashi, D.; Hudnall, S.D. Human Herpesvirus 6 and Malignancy: A Review. Front. Oncol. 2018, 8, 512.
  38. Santoro, F.; E Kennedy, P.; Locatelli, G.; Malnati, M.S.; A Berger, E.; Lusso, P. CD46 Is a Cellular Receptor for Human Herpesvirus 6. Cell 1999, 99, 817–827.
  39. Parra, M.; Alcala, A.; Amoros, C.; Baeza, A.; Galiana, A.; Tarragó, D.; García-Quesada, M..; Sánchez-Hellín, V. Encephalitis associated with human herpesvirus-7 infection in an immunocompetent adult. Virol. J. 2017, 14, 97.
  40. Ablashi, D.; Berneman, Z.; Kramarsky, B.; Whitman, J.; Asano, Y.; Pearson, G. Human herpesvirus-7 (HHV-7): Current status. Clin. Diagn. Virol. 1995, 4, 1–13.
  41. Tang, H.; Serada, S.; Kawabata, A.; Ota, M.; Hayashi, E.; Naka, T.; Yamanishi, K.; Mori, Y. CD134 is a cellular receptor specific for human herpesvirus-6B entry. Proc. Natl. Acad. Sci. USA 2013, 110, 9096–9099.
  42. Smatti, M.K.; Al-Sadeq, D.W.; Ali, N.H.; Pintus, G.; Abou-Saleh, H.; Nasrallah, G.K. Epstein–Barr Virus Epidemiology, Serology, and Genetic Variability of LMP-1 Oncogene Among Healthy Population: An Update. Front. Oncol. 2018, 8, 211.
  43. Kuri, A.; Jacobs, B.M.; Vickaryous, N.; Pakpoor, J.; Middeldorp, J.; Giovannoni, G.; Dobson, R. Epidemiology of Epstein-Barr virus infection and infectious mononucleosis in the United Kingdom. BMC Public Heal. 2020, 20, 912.
  44. D’Addario, M.; Libermann, T.; Xu, J.; Ahmad, A.; Menezes, J. Epstein-Barr virus and its glycoprotein-350 upregulate IL-6 in human B-lymphocytes via CD21, involving activation of NF-κB and different signaling pathways. J. Mol. Biol. 2001, 308, 501–514.
  45. Carbone, A.; Gloghini, A. Epstein Barr Virus-Associated Hodgkin Lymphoma. Cancers 2018, 10, 163.
  46. Levin, L.I.; Munger, K.L.; O’Reilly, E.J.; Falk, K.I.; Ascherio, A. Primary infection with the epstein-barr virus and risk of multiple sclerosis. Ann. Neurol. 2010, 67, 824–830.
  47. Mesri, E.A.; Cesarman, E.; Boshoff, C. Kaposi’s sarcoma and its associated herpesvirus. Nat. Cancer 2010, 10, 707–719.
  48. Veettil, M.V.; Bandyopadhyay, C.; Dutta, D.; Chandran, B. Interaction of KSHV with Host Cell Surface Receptors and Cell Entry. Viruses 2014, 6, 4024–4046.
  49. Dow, D.E.; Cunningham, C.K.; Buchanan, A.M. A Review of Human Herpesvirus 8, the Kaposi’s Sarcoma-Associated Herpesvirus, in the Pediatric Population. J. Pediatr. Infect. Dis. Soc. 2013, 3, 66–76.
  50. Rohner, E.; Wyss, N.; Trelle, S.; Mbulaiteye, S.M.; Egger, M.; Novak, U.; Zwahlen, M.; Bohlius, J. HHV-8 seroprevalence: A global view. Syst. Rev. 2014, 3, 11.
  51. Chakraborty, S.; Veettil, M.V.; Chandran, B. Kaposi’s Sarcoma Associated Herpesvirus Entry into Target Cells. Front. Microbiol. 2012, 3, 6.
  52. Whitley, R.; Baines, J. Clinical management of herpes simplex virus infections: Past, present, and future. F1000Research 2018, 7, 1726.
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