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Order Herpesvirales
Published in Paul Pumpens, Peter Pushko, Philippe Le Mercier, Virus-Like Particles, 2022
Paul Pumpens, Peter Pushko, Philippe Le Mercier
In parallel, Yuan et al. (2018) resolved to 3.1 Å the atomic structure of herpes simplex virus type 2 (HSV-2), a member of the Human alphaherpesvirus 2 species, which causes genital herpes. This structure is shown in Figure 2.3 in comparison with that of typical representatives of two other subfamilies of the Herpesviridae family, namely, Betaherpesvirinae and Gammaherpesvirinae. Again, it was found that both hexons and pentons contained the major capsid protein, VP5, while hexons also contained a small capsid protein, VP26, and triplexes comprised VP23 and VP19C. Acting as core organizers, the VP5 proteins formed extensive intermolecular networks, involving multiple disulfide bonds, about 1,500 in total, and noncovalent interactions, with VP26 proteins and triplexes (Yuan et al. 2018).
LPD Associated with Epstein–Barr Virus Infection
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Epstein–Barr virus (EBV) is a ubiquitous, oncogenic double-stranded DNA virus belonging to the Herpesviridae family, which comprises several well-known human-infecting viral pathogens including herpes simplex virus-1 (HSV-1, or human herpesvirus 1), herpes simplex virus-2 (HSV-2, or human herpesvirus 2), varicella zoster virus (VZV, or human herpesvirus 3), Epstein–Barr virus (EBV, or human herpesvirus 4), cytomegalovirus (CMV, or human herpesvirus 5), Roseolovirus (human herpesviruses 6 and 7), and Kaposi sarcoma−associated herpesvirus (KSHV, or human herpesvirus 8). Of these, EBV and KSHV are classified in the Gammaherpesvirinae subfamily, and primarily target B lymphocytes, epithelial cells, and other cells, with B cells being the site of latency.
Tea Polyphenolic Compounds against Herpes Simplex Viruses
Published in Satya Prakash Gupta, Cancer-Causing Viruses and Their Inhibitors, 2014
Tin-Chun Chu, Sandra D. Adams, Lee H. Lee
The Herpesviridae family contains more than 100 different herpesviruses that infect a multitude of host organisms, including fish, birds, horses, and humans. Herpesviruses are further classified into three subfamilies: Alphaherpesvirinae, Betaherpesvirinae, and Gammaherpesvirinae. HSV types 1 and 2 (human herpesvirus 1 and 2, or HHV-1 and -2) are members of the Alphaherpesvirinae subfamily, Simplexvirus genus. The other genus in the Alphaherpesvirinae subfamily is the Varicellovirus genus that also includes varicella zoster virus (HHV-3) that causes chicken pox and shingles. This subfamily is distinguished by its short reproductive cycle, rapid spread, destruction of host cells, and by establishing its latent cycle (Mettenleiter et al. 2009; Roizman and Baines 1991).
Prevention of viral infections in solid organ transplant recipients in the era of COVID-19: a narrative review
Published in Expert Review of Anti-infective Therapy, 2022
Paraskevas Filippidis, Julien Vionnet, Oriol Manuel, Matteo Mombelli
HHV-8 or Kaposi-Sarcoma-associated Herpes Virus belongs to the family of Gammaherpesvirinae. The seroprevalence of HHV-8 is highly variable depending on geographical location, ranging from 3% to 8% in the US [166] up to almost 90% in the sub-Saharan Africa [167,168]. In SOT recipients, the most common clinical manifestation of HHV-8 infection is cutaneous and visceral Kaposi sarcoma, multicentric Castelman disease and primary effusion lymphoma. No established preventive strategy is currently available for HHV-8 in SOT recipients. In endemic regions, determination of HHV-8 serostatus of donor and recipient followed by viral monitoring may identify patients at high risk for HHV-8-associated disease [169]. Modulation of immunosuppression (for example, switch to mTOR inhibitors) and/or administration of valganciclovir may be considered in case of reactivation or donor-related primary infection [165].
Predictive tools to determine risk of infection in kidney transplant recipients
Published in Expert Review of Anti-infective Therapy, 2020
Mario Fernández-Ruiz, Francisco López-Medrano, José María Aguado
A member of the Gammaherpesvirinae subfamily of herpesviruses, EBV is able to establish lifelong latency within the B-cell compartment following primary infection due to various mechanisms of immune-evasion [120]. The control of latent EBV infection in healthy individuals depends on the cell-mediated immunity [121]. Asymptomatic reactivation of latent infection in SOT recipients is likely underestimated, with rates of detectable circulating EBV-DNA at some point after transplantation ranging from 20% to 80% [122–125] depending on the frequency of monitoring and the sensitivity of the assay used. Uncontrolled EBV–induced B-cell proliferation underlies the pathogenesis of post-transplant lymphoproliferative disease (PTLD) [126], and the monitoring of EBV replication is routinely used to identify recipients at risk of developing this complication, particularly in the EBV-seronegative pediatric population [127–129].
Pleural effusions induced by human herpesviruses in the immunocompetent host
Published in Infectious Diseases, 2019
Erasmia Rouka, Ourania S. Kotsiou, Despoina Kyriakou, Konstantinos I. Gourgoulianis, Sotirios G. Zarogiannis
Based on their biological and genetic properties, HHVs are classified into three subfamilies termed alphaherpesvirinae [Herpes Simplex Virus type 1 (HSV-1), Herpes Simplex Virus type 2 (HSV-2), Varicella Zoster Virus (VZV)], betaherpesvirinae [Cytomegalovirus (CMV), Human Herpes Virus 6 (HHV-6), Human Herpes Virus 7 (HHV-7)] and gammaherpesvirinae [Epstein Barr Virus (EBV), Human Herpes Virus 8 (HHV-8)] [17]. The two HHV-6 variants, HHV-6A and HHV-6B have been recognized as two distinct species since 2012 [18]. Each of the aforementioned viruses replicates and establishes latency in different cell types [19]. As a result, numerous and diverse clinical entities have been associated with HHVs both in the context of primary infection and reactivation. Non-immunocompetent patients such as newborns, patients with haematological diseases, transplant recipients and acquired immunodeficiency syndrome (AIDS) patients are at high risk for HHV infection (both primary and recurrent) associated with high morbidity and mortality [19–22].