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The Viruses
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Despite the difficulty of the problem some effective antiviral drugs have been developed against herpesviruses and retroviruses. The nucleoside analogue acycloguanosine (Acyclovir) is activated by phosphorylation via thymidine kinase, a herpesvirus encoded enzyme. The phosphorylated analogue acts then to inhibit the activity of the virus-encoded polymerase. Nucleoside and nonnucleoside inhibitors have been developed against retroviral infections as a result of the massive efforts developed in response to the AIDS epidemic (see below). Nucleoside analogues such as azidothymidine (AZT) selectively inhibit reverse transcriptase (RT) and thereby inhibit the replication of the retroviruses including HIV. A variety of nucleoside analogs have been produced to combat HIV infections (e.g., ddl, didanosine). The need for additional antiviral drugs against HIV has been driven, in part, by the ability of retroviruses like HIV to mutate and become resistant to the effects of drugs that have been developed. The introduction of protease inhibitors like nelfinavir has provided additional types of drugs active against HIV infection. These drugs in combination with RT inhibitors have provided new hope in the battle against AIDS. However, before long-term success against HIV is achieved elimination of sites of latent virus production and continued development of drugs against resistant strains will be required.
A Treatise on the Role of Herpesvirus in Neurodegeneration
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi, Kenneth Blum
Herpesviruses have been demonstrated to exert significant neurological morbidity. Herpes simplex virus type 1 (HSV-1), HSV-2, and varicella zoster viruses, three of the nine known human herpesviruses, demonstrate latency in the peripheral sensory ganglia and exist in the host for lifetime. Primary infection takes place at a mucocutaneous surface with a declining transportation of the virus to the peripheral sensory ganglia, conserving the integrity of the viral genome within the peripheral sensory ganglia, as well as regular reactivation with antegrade transmission to the nerve endings and mucocutaneous surface. HSV-1 is primarily transmitted by oral-to-oral contact and in most cases causes orolabial herpes or “cold sores” around the mouth. HSV-2 is almost entirely sexually transmitted through skin-to-skin contact, causing genital herpes.
Host Defense II: Acquired Immunity
Published in Constantin A. Bona, Francisco A. Bonilla, Textbook of Immunology, 2019
Constantin A. Bona, Francisco A. Bonilla
Another technique for avoiding immune elimination is to establish latency. This is a popular method with herpesviruses. The viral genome integrates into the host’s DNA and remains dormant (transcriptionally silent) for varying periods of time. The viral genome is present for the entire life of the individual, and may be reactivated by various stimuli such as other viral infections, hormonal changes, or depressed immunity. When reactivated, infectious virus is produced and may be transmitted.
Critical roles of adherens junctions in diseases of the oral mucosa
Published in Tissue Barriers, 2023
Christina Kingsley, Antonis Kourtidis
A family of viruses that manifest in the oral cavity are Herpes viruses, of which several types are found in humans. Herpes simplex virus type 1 (HSV-1) and Herpes simplex virus type 2 (HSV-2) cause common opportunistic viral infections. Other types of herpesviruses are Varicella zoster, Cytomegalovirus, and Epstein-Barr Virus. HSV-1 reactivates and replicates in the oral epithelium, leading to localized painful vesicles, colloquially often referred to as “cold sores”. These viruses cause lifelong infections and establish latency with periodic reactivations. HSV-1 viruses often spread by close contact and through sharing saliva and are highly infectious, while most people infected are asymptomatic. To infiltrate the cell, HSV-1 viral particles utilize nectin-1 as their cell surface receptor (Figure 2). In this case, disruption of AJs can expose nectin-1, allowing HSV to bind to it and further infiltrate the tissue.93 Therefore, the integrity of the AJs in the oral epithelium can determine the course of HSV infection, opening up an important area of future study.94
Myocarditis: causes, mechanisms, and evolving therapies
Published in Expert Opinion on Therapeutic Targets, 2023
Tin Kyaw, Grant Drummond, Alex Bobik, Karlheinz Peter
Herpesviruses: Herpesvirus is one of the most frequent causes of viral myocarditis. It is present in up to 36% of identified cases, frequently associated with acute and chronic heart failure [41]. Herpesviruses implicated in myocarditis include human herpesvirus 6 (HHV-6) [42], Epstein–Barr virus (EBV) [43], cytomegalovirus (CMV) [44], and varicella-zoster virus (VZV) [45]. Herpesviruses are enveloped double-stranded DNA viruses with an icosahedral capsid. The capsid is surrounded by an amorphous protein layer and an envelope containing viral glycoprotein spikes [46]. These viruses are complex and encode a large number of enzymes involved in nucleic acid metabolism, DNA synthesis, and processing of proteins. HHV-6 capsid maturation, DNA packaging, glycoprotein modification, and the formation of mature virus require the U53-encoded protease [47]; the protease has been sequenced and characterized and may be a possible therapeutic target [48]. HHV-6 comprises two variants HHV-6A and HHV-6B [43] but only HHV-6B seems pathogenic [49]. HVV-6B utilizes a number of strategies to reduce host immune responses, producing chemokines and chemokine receptors [50], downregulating ligands that trigger natural killer cell activation, ULBP1, MICB, and B7-H6 as well as downregulating MHC class I to attenuate anti-viral CD8+ T cell activation [49]; It also upregulates PD-L1 on the surface of infected monocytes further impairing anti-viral immunity [51].
Pediatric Scleritis: An Update
Published in Ocular Immunology and Inflammation, 2023
Maria Tarsia, Carla Gaggiano, Elisa Gessaroli, Salvatore Grosso, Gian Marco Tosi, Bruno Frediani, Luca Cantarini, Claudia Fabiani
Bacteria, fungi, parasites, and viruses have all been reported as inciting infectious agents in pediatric cases.48 In line with adult-onset scleritis, Herpesviruses seem the microbial agents most frequently implicated in the pediatric setting.42,49,50 Gungor et al. described for the first time a case of unilateral progressive necrotizing scleritis caused by primary Varicella zoster virus infection in a 6-year-old boy, with characteristic circumferential limbal involvement and scleral ischemia42; Walton et al. reported a series of seven children affected by Herpes zoster ophthalmicus with scleritis following bone marrow transplantation50; Naseri et al. presented a 9-year-old boy with unilateral diffuse anterior scleritis, marginal keratitis and moderately severe anterior uveitis due to Herpes zoster virus, 3 years after varicella vaccine administration.49 Mycobacterium tuberculosis is not uncommon as etiologic agent of scleritis in endemic regions in Asia, accounting for 15% of pediatric cases in an Indian cohort.8,51,52 The most common pattern of tubercular scleritis is the nodular one and a complete resolution with antitubercular drugs is reported.53,54 Infections by Staphylococcus aureus, Giardia lamblia, Borrelia burgdorferi and poststreptococcal etiology have been reported in children as well.25,43,55