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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
Currently, many of the neurodegenerative diseases having a herpetic etiology evade diagnostic herpetic detection, instead relying more heavily on the nosological panel of well-documented symptoms for what are perceived as nonherpetic disorders, such as joint destruction. Unless interventions for neurodegenerative diseases include tests for viral detection, identification, and an antiviral therapeutic strategy that also boosts innate immune competence, they will not completely reverse, prevent, or contain the pathological process. Halting progressive viral pathogenesis and restoring cellular functionality is a feasible strategy that offers a reasonable expectation to restore normal cellular autophagic protection against viral neurovirulence.
Companion Animals Models of Human Disease
Published in Rebecca A. Krimins, Learning from Disease in Pets, 2020
As an example, canine oral papillomavirus (COPV) causes florid warty lesions in the mucosa of the oral cavity within 4–8 weeks post exposure in experimental settings. The mucosatrophic nature of these viruses and the resulting oropharyngeal papillomas that are morphologically similar to human vaginal papillomas caused by HPV-6 and HPV-11 make this a useful model. These lesions typically spontaneously regress 4–8 weeks after appearing; this model is therefore useful in understanding the interplay between the host immune defense and viral pathogenesis. Male and female Beagles, aged 10 weeks to 2 years, with no history of COPV, are typically used for these studies. Infection is achieved by the application of a 10 ml droplet of virus extract to multiple 0.5 cm2 scarified areas within the mucosa of the upper lip of anesthetized beagles.
An approach to pathogen discovery for viral infections of the nervous system
Published in Avindra Nath, Joseph R. Berger, Clinical Neurovirology, 2020
Prashanth S. Ramachandran, Michael R. Wilson
The last three decades have seen the development of molecular technologies that have reshaped the diagnostic landscape for neurovirology and neuroinfectious diseases more generally [1–3]. This has led to a better understanding of viral pathogenesis as well as improved diagnostics, which has in turn, translated into improved patient mortality and morbidity [4,5]. Until recently, viral diagnostics have evolved in response to traditional clinical practice, in which the treating physician evaluates a patient, generates hypotheses regarding potential etiologies, and then orders a curated set of investigations.
Novel insights into the pathogenesis of virus-induced ARDS: review on the central role of the epithelial-endothelial barrier
Published in Expert Review of Clinical Immunology, 2021
Jun Feng, Lina Liu, Yang He, Min Wang, Daixing Zhou, Junshuai Wang
Because antiviral therapies for ARDS caused by viruses (for e.g. SARS-CoV-2) are rare, knowledge about relevant immunological and pathophysiological profiles may be important for understanding viral pathogenesis and identifying possible therapeutic targets. A homologue of ACE, termed ACE2, has been identified as a receptor for SARS-CoV. ACE2, a close homologue of ACE, functions as a negative regulator of the angiotensin system and exerts protective effects against influenza virus-induced ARDS. The Ang-II and ACE2 systems may also represent a new avenue of research on sepsis-associated complications. In particular, the molecular interaction of SARS-CoV-2 with the ACE2 receptor located on the endothelial cell surface, both at the pulmonary and systemic levels, can cause early dysfunction of endothelial cells, which, in turn, is involved in inflammation and thrombosis of the peripheral vascular network. This remains an important area for future studies, where it is hoped that an increased understanding of epithelial and endothelial barrier function, combined with etiologic diagnosis, will help determine the effects of specific intervention strategies to restore respiratory function.
Platelet-endothelial associations may promote cytomegalovirus replication in the salivary gland in mice
Published in Platelets, 2020
Alicia M. Braxton, Alyssa L. Chalmin, Kevin M. Najarro, Jacqueline K. Brockhurst, Karl T. Johnson, Claire E. Lyons, Brenna Daly, Catherine G. Cryer, Shefali Vijay, Griffin Cyphers, Selena M. Guerrero-Martin, S. Andrew Aston, Kirstin McGee, Yu-Pin Su, Ravit Arav-Boger, Kelly A. Metcalf Pate
Platelet decline is a common feature of acute viral infection, including human and mouse cytomegalovirus (CMV) [1–13]. Platelets have been shown to respond to viral infection through interactions with leukocytes and endothelial cells [13–15]. This has most extensively been studied in the context of HIV with sequestration of activated platelets in platelet-monocyte aggregates (PMAs) driving platelet decline during acute HIV infections [16]. These PMAs subsequently promote monocyte extravasation, potentially facilitating virus entry into tissue [17,18]. Alternatively, platelets can be sequestered in platelet-endothelial associations (PEAs), as seen in dengue virus [9,13]. These PEAs in the brain affect blood-brain barrier permeability, directly facilitating virus entry. The mechanisms through which viral infection causes these associations and through which these associations affect viral pathogenesis have yet to be fully understood, and it is unclear if these associations are a universal downstream effect of acute viral infection or a specific response to select viruses. We sought to determine if these associations occur concurrent with platelet decline in a murine cytomegalovirus (mCMV) infected mouse model of acute viral infection, and define any downstream effects on viral entry and replication into tissues.
New strategies for treatment of COVID-19 and evolution of SARS-CoV-2 according to biodiversity and evolution theory
Published in Egyptian Journal of Basic and Applied Sciences, 2020
Fortunately, mutations in the genome region of the virus’s spikes may weaken the virus’s attachment to its receptors in the host cell. This may explain the extent of the variation in the severity of the response between people each other and between different countries of this disease (COVID-19). Interactions between the SARS-CoV spike protein receptor-binding domain (RBD) and its host receptor angiotensin-converting enzyme 2 (ACE2) regulate both the cross-species and human-to-human transmissions of SARS-CoV. The sequence of 2019-nCoV RBD, including its receptor-binding motif (RBM) that directly contacts ACE2, is similar to that of SARS-CoV, strongly suggesting that 2019-nCoV uses ACE2 as its receptor [37]. The crystal structure of the C-terminal domain of SARS-CoV-2 (SARS-CoV-2-CTD) spike (S) protein was demonstrated, in complex with human ACE2 (hACE2), which reveals a hACE2-binding mode similar overall to that observed for SARS-CoV. These findings shed light on the viral pathogenesis and provide important structural information regarding development of therapeutic countermeasures against the emerging virus [38].