China
Africa
Explore chapters and articles related to this topic
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).
Evolution of Herpes Simplex Viruses
Published in Marie Studahl, Paola Cinque, Tomas Bergström, Herpes Simplex Viruses, 2017
Rory J. Bowden, Duncan J. McGeoch
All alphaherpesvirus genomes contain long and short unique regions (UL and Us) and a pair of large repeat elements that flank the Us sequence in opposing orientations (Rs). Some, including HSV-1 and HSV-2, also possess a distinct pair of large repeat elements that flank UL (RL). These large-scale features are illustrated for HSV in Figure 3, with conventions of genome segment naming. All of the ancestral genes, common to the three subfamilies, lie in the UL component. An equivalent arrangement of long and short unique sequences with flanking repeats is also found in the Cytomegalovirus genus of the Betaherpesvirinae, but the Us, Rs, and RL components of these betaherpesvirus genomes are considered to be unrelated to the alphaherpesvirus sequences. It thus appears that the alphaherpesvirus S region (Us plus its flanking Rs copies) emerged after divergence from the Beta- and Gammaherpesvirinae and before the appearance of the α1 to α4 lineages.
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-6 (including HHV-6A and HHV-6B) and HHV-7 belong to the Betaherpesvirinae subfamily, and are acquired during early childhood with a seroprevalence of 90% by adulthood [161,162]. HHV-6 may reactivate in up to 40% of SOT recipients, although infection is usually asymptomatic, with only few cases of invasive disease reported. Inherited chromosomally integrated HHV-6 (ciHHV-6) refers to the persistence of HHV-6 DNA by integration in the human genome, which can be vertically transmitted through germ cell lines. ciHHV-6 needs to be differentiated from HHV-6 reactivation and disease. No preventive strategy is currently recommended in SOT recipients [163]. A strategy consisting in HHV-6 DNAemia monitoring and preemptive modulation of immunosuppression showed no clear benefit in a randomized controlled trial [164,165].
Reactivation of human herpesviruses 6 and 7 in Kawasaki disease
Published in Modern Rheumatology, 2019
Yoshihiko Kawano, Jun-ichi Kawada, Noriko Nagai, Yoshinori Ito
Kawasaki disease (KD) is an acute, self-limited systemic vasculitis for which the etiology remains unknown. The clinical and epidemiological features of KD suggest that infectious agents might be triggers of the disease, but specific pathogens have not been identified [1]. Human herpesviruses (HHV)-6 and HHV-7, causative pathogens of exanthema subitum, belong to the subfamily Betaherpesvirinae. Both KD and exanthem subitum occur in young children, and some case reports and serological studies have suggested an etiological relationship between KD and HHV-6 or -7 [2–5]. However, primary infection with or reactivation of HHV-6 and -7 has not been fully investigated in patients with KD. We encountered a case of severe KD with prolonged detection of HHV-7 DNA from the blood [6]. Based on this case, we hypothesized that primary infection with or reactivation of HHV-6 or -7 might be associated with the pathophysiology and/or severity of KD. The present study prospectively enrolled KD patients and evaluated HHV-6 and -7 viral loads in blood by quantitative real-time PCR.
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].