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Herpesvirus microRNAs for Use in Gene Therapy Immune-Evasion Strategies
Published in Yashwant Pathak, Gene Delivery, 2022
Vineet Mahajan, Shruti Saptarshi, Yashwant Pathak
Herpesviridae is a large family of encapsulated DNA viruses. A typical herpes virion structure is made up of an inner core of double stranded DNA 124-235 kilobase (kbp) pair in size, a protein capsid, tegument, and an envelope derived from the nuclear membrane of the infected cell and long glycoprotein spikes. A large number of clinical manifestations, including malignancies, have been recorded for herpes virus related infections in humans. Interestingly, herpes viruses not only cause acute infections that may even be transmitted via organ transplantation, but also latent infections. The tendency to persist in the host following an initial infection, without producing overt disease is latency. Thus, herpesviruses are able to establish lifelong infections in the host and transition between the lytic (productive) and latent (non-productive) replication cycles. The microenvironment, host immunity, cell autonomous factors, as well as viral elements, may all contribute to this latency establishment, maintenance, and reactivation of herpes virus infection.1
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
The etiology and symptomatologies of an increasingly expansive array of neurodegenerative diseases associated with the herpes family of viruses are alarming. We have provided a comprehensive introductory overview on disease etiology, progression, and consequences to avail an understanding of the diversity of nosological manifestations. No therapeutic breakthrough of disease eradication has been achieved so far. Thorough mechanistic insight has been provided in this chapter detailing the propensity of viral activation, viral infection, and viral propagation. The proposed mechanistic insight to halt, reduce, and/or reverse, and/or contain neurodegenerative diseases and disorders has been elaborated. Numerous studies have demonstrated the efficacy of phytopharmaceuticals and nutraceuticals in the prevention and amelioration of Herpesviridae. We have provided an extensive discussion on the botany, pharmacology, and the therapeutic benefits of structurally diverse phytopharmaceuticals in the treatment of HSV. This chapter reveals the efficacy of a significant array of botanicals individually that have been shown to inactivate, regress, and contain Herpesviridae. These botanical phytopharmaceuticals merit further research on extensive combinations in formulas to explore potential therapeutic synergies.
Determination of Antiviral Activity
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
The known animal models for the viruses in the Herpesviridae family that cause significant clinical disease are summarized in Table 5. The references indicated may be either the initial report describing the animal model or, if more appropriate, a report of a typical chemotherapy experiment using the animal model.
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
Herpesviridae are large, enveloped, DNA-containing viruses, including CMV, EBV, HSV-1, and −2, VZV, and human herpes virus 6, 7, and 8 (HHV-6, HHV-7, and HHV-8). In particular, CMV, HSV, and VZV are responsible for the majority of post-transplant viral infections [2]. Upon primary infection, herpesviridae produce lifelong latency, and might reactivate in the presence of impaired cellular immunity [92]. Thus, in SOT recipients, infection can result from reactivation of a latent infection in the presence of preexisting immunity in seropositive recipients (recipient positive [R+] serostatus) or from primary infection from a latently infected organ in recipients without preexisting immunity (donor positive [D+]/recipient negative [R-] serostatus). Much less frequently, infection is acquired in the community in the absence of preexisting immunity in both the donor and the recipient (donor positive [D-]/recipient negative [R-] serostatus). A summary of available prophylactic strategies against Herpesviridae is provided in Table 1.
The First Iranian Cohort of Pediatric Patients with Activated Phosphoinositide 3-Kinase-δ (PI3Kδ) Syndrome (APDS)
Published in Immunological Investigations, 2022
Saba Fekrvand, Samaneh Delavari, Zahra Chavoshzadeh, Roya Sherkat, Seyed Alireza Mahdaviani, Mahnaz Sadeghi Shabestari, Gholamreza Azizi, Mohammad Taghi Arzanian, Bibi Shahin Shamsian, Shabnam Eskandarzadeh, Narges Eslami, William Rae, Antonio Condino-Neto, Javad Mohammadi, Hassan Abolhassani, Reza Yazdani, Asghar Aghamohammadi
APDS patients present a wide spectrum of clinical phenotypes ranging from mild to fatal. Symptoms and signs include recurrent respiratory tract infections, bronchiectasis, chronic non-resolving infections with Herpesviridae family viruses, non-neoplastic lymphoproliferation, autoimmunity, increased risk of lymphoma, and neurodevelopmental abnormalities (Elkaim et al. 2016, Lucas, 2014a; Singh et al. 2020). Immunological phenotypes of these patients is variable, but typically consist of low/normal serum level of immunoglobulin A (IgA) and IgG, normal or increased IgM (Fekrvand et al. 2020), decreased total and naïve CD19+ B cells with increased transitional B cells, reduced CD4+ helper T cells, normal to increased CD8+ cytotoxic T cells with an increased senescent proportion, and normal to decreased natural killer cells (Lucas, 2014a, Singh et al. 2020). Management of the affected patients varies based on the severity and extent of clinical features. Therapeutic options include antibiotic prophylaxis, immunoglobulin replacement therapy, immunomodulators, PI3Kδ inhibitors and hematopoietic stem cell transplantation (HSCT) (Azizi et al. 2016; Coulter et al. 2017; Elkaim et al. 2016).
Steroid alternatives for managing eosinophilic lung diseases
Published in Expert Opinion on Orphan Drugs, 2021
Quentin Delcros, Matthieu Groh, Mouhamad Nasser, Jean-Emmanuel Kahn, Vincent Cottin
Over and above 200 drugs have been reported to cause eosinophilic lung infiltrates with anti-epileptics, allopurinol, antibiotics, and non-steroidal anti-inflammatory drugs being the main causes [24] [. Overall, drug-induced eosinophil toxicity can be isolated or embedded within the picture of a systemic drug reaction with eosinophilia and systemic symptoms. Testing for herpesviridae (e.g. HHV-7, EBV, CMV, and more specifically HHV-6) reactivation can be helpful, especially when the diagnosis is not straightforward [25]. Of note, skin manifestations are not mandatory for the diagnosis of drug-induced eosinophilia especially in drug-induced chronic pulmonary eosinophilia. Hence, all drugs taken within the weeks or months preceding the clinical symptoms must be recorded, and online-web drug-induced ‘respiratory diseases’ database resources (e.g. www.pneumotox.com) are worth consulting.