ABSTRACT
The article provides information on immunopathology in sepsis and the commonality between immunopathogenetic processes of sepsis and the new coronavirus infection (COVID-19). As a result of the inability of the immune system to cope with aggression of the pathogen, inadequate immune activity occurs manifested by the systemic inflammatory response syndrome, resulting in damage to tissues of the host organism. In response, compensatory anti-inflammatory response syndrome is activated, which is manifested by inhibition of the immune response. One of its main mechanisms is signals produced by membrane receptors and their ligands. Against the background of inability of the host organism to neutralise the pathogen, numerous pathological phenomena and complications occur leading to damage to human tissues.Copyright © 2021, Krasnoyarsk State Medical University. All rights reserved.
ABSTRACT
Objective: To summarize and compare the main traditional Chinese medicineTCMsyndromes of Delta and Omicron variants of severe acute respiratory syndrome coronavirus 2SARS-CoV-2 carriers to provide references for the syndrome evolution and syndrome differentiation of SARS-CoV-2 infection. Method(s):The TCM medical records of imported and local cases of infection with Delta and Omicron variants of SARS-CoV-2 in Changsha since September 23,2021 to March 27,2022 were collected,including 18 Delta variant cases and 36 Omicron variant cases. Their TCM diagnosis information and TCM pathogenesis were analyzed and compared. Result(s): The common manifestations in Delta variant cases were cough,fever,chest distress/shortness of breath,sore muscles,nausea,dry mouth,dry or sore throat,thick and greasy tongue coating,and rapid and slippery pulse. The predominant pathogenesis was dampness-heat in the upper-energizer and heat stagnation in the lesser Yang combined with dampness. The occurrence of chest distress/shortness of breath,greasy tongue coating,slippery pulse,and the proportion of dampness-heat in the upper-energizer syndrome were higher in Delta variant cases than in Omicron variant cases P<0.05. The common manifestations in Omicron variant cases were itchy and sore throat,nasal congestion,running nose,fever,mild aversion to cold,dry mouth,dizziness,slightly reddish tongue with thin white coating,and rapid or wiry pulse. The predominant pathogenesis was wind-dryness invading defensive exterior,and heat stagnation in the lesser Yang. The occurrence of white-coated tongue and the proportion of wind-dryness invading defensive exterior syndrome were higher in Omicron variant cases than in Delta variant casesP<0.05. Conclusion(s): There are certain differences in TCM syndromes and the corresponding pathogenesis between Delta variant and Omicron variant cases in Changsha,Hunan. The Delta variant of SARS-COV-2 tends to induce dampness-heat syndrome, whereas Omicron variant infection tends to elicit wind-dampness syndrome,which is expected to provide a reference for the pathogenesis evolution of SARS-COV-2 infection.Copyright © 2022, China Academy of Chinese Medical Sciences Institute of Chinese Materia Medica. All rights reserved.
ABSTRACT
Community-acquired pneumonia is a potentially serious infection in children with high morbidity rate, risk of severe course and unfavorable outcomes. Specialists have noted the increased incidence of the destructive forms in the recent years. Aim. To present a clinical case of destructive pneumonia in a 1 year 2 month old child, hospitalized in the State Budgetary Healthcare Institution "Children's City Clinical Hospital of St. Vladimir Moscow Healthcare Department", and analyze it in terms of current understanding on the disease pathogenesis. Conclusion. During COVID-19 (COronaVIrus Disease 2019) pandemic, pulmonologists and pediatric surgeons encountered an unconventional course of destructive pneumonia. A large number of studies of pathophysiological processes in acute viral interstitial pneumonias have recently allowed to expand our understanding of the role of coagulation system. At the same time, new questions arose concerning the clinical course and development of the pathological infectious process.Copyright © Zaytseva O.V. et al., 2023.
ABSTRACT
Certolizumab is a Fab fragment of a humanized monoclonal antibody against tumor necrosis factor-alpha (TNF-alpha). Differing from the other TNF-alpha inhibitors due to the absence of Fc fragment and pegylation, it binds to both the soluble and transmembrane forms of TNF-alpha, creating a strong TNF-alpha blockage. Previously approved for psoriatic arthritis, certolizumab received another approval from FDA in 2018 for the treatment of moderate to severe chronic plaque psoriasis that does not respond to conventional systemic treatments or for which these treatments are contraindicated. Administered via subcutaneous injections, certolizumab also has a low-dose option for patients weighing less than 90 kg. Certolizumab is considered a safe biological drug that can be preferred during pregnancy and lactation.Copyright © 2022 by Turkish Society of Dermatology and Venereology.
ABSTRACT
Respiratory mucosal immune system is the body's first line of defense against infection. Since the outbreak of novel coronavirus disease 2019 (COVID-19) in 2019, nasal mucosal immune vaccine, with its ability to induce cellular, humoral and mucosal triple immune responses, has become a research hotspot. This article focuses on novel coronavirus, with an understanding of its structure and pathogenesis, a brief introduction to the immune mechanism of nasal mucosa, a summary of the different types of nasal mucosal immune vaccines and their clinical research, aiming to provide some theoretical reference for the development of new vaccines, and exploration of the best methods and strategies to combat COVID-19.
ABSTRACT
BackgroundAnti-MDA5 antibody positive dermatomyositis (MDA5-DM) is characterized by high mortality due to rapid progressive ILD. MDA5 is a cytosolic protein and a family of RIG-I like receptor, which functions as a virus RNA sensor and induces the production of such as type-1 IFN. Although little is known about the pathogenesis of MDA5-DM, it is notable that the similarities were reported between COVID-19 infection and MDA5-DM. It may suggest that there is a common underlying autoinflammatory mechanism. We reported that in MDA5-DM, (1) RIG-I-like receptor signaling is enhanced and (2) antiviral responses such as type 1 IFN signaling are also enhanced as compare with anti-ARS-antibody positive DM, and (3) the key for survival is suppression of RIG-I-like and IFN signaling (EULAR2022, POS0390). We also found that a significant role for uncontrolled macrophage in the pathogenesis of ILD by our autopsy case. Recently, it has been reported that tacrolimus (TAC) and cyclophosphamide (CY) combination therapy (TC-Tx) has improved the prognosis of cases with early onset of the disease, but there are cases that cannot be saved. Therefore, we devised BRT therapy (BRT-Tx). The Tx combines baricitinib (BAR), which inhibits GM-CSF and IFN-mediated signaling and effectively suppresses uncontrolled macrophages, with rituximab (RTX) and TAC, which rapidly inhibits B and T cell interaction and ultimately prevents anti-MDA5 antibody production.ObjectivesTo determine the differences in gene expression between BRT and TC-Tx for MDA5-DM in peripheral blood.MethodsTotal of 6 MDA5-DM (TC: 3, BRT: 3) were included and all of them had multiple poor prognostic factors. Peripheral whole blood was collected at just before and 2-3 months after the treatment. RNA was extracted, and quantified using a next-generation sequencer. Differentially Expressed Genes (DEGs) were identified by pre vs. post treatment. Gene Ontology (GO), clustering and Gene Set Variation Analysis (GSVA) were performed to DEGs. As one BRT case was added since our last year's report, we also reanalyzed the surviving vs. fatal cases. The IFN signature was scored separately for Types 1, 2, and 3, and the changes between pre- and post-treatment were investigated.ResultsTwo of three cases with TC died during treatment, while all three cases on BRT recovered. The cluster analysis of the DEGs separated deaths from survivors, not by type of treatment. Comparing surviving and dead cases, GO analysis revealed that the immune system via immunoglobulins and B cells was significantly suppressed in surviving cases. GO analysis of DEGs in each therapeutic group showed that expression of B cell-related genes such as lymphocyte proliferation and B cell receptor signaling pathway were significantly suppressed in BRT-Tx. On the other hand, TC-Tx significantly suppressed such pathways as cell proliferation and cell surface receptor signaling, and was less specific for the target cells than BRT-Tx. The changes in IFN signature score after treatment showed an increase in type 2 and 3 IFN scores in all fatal cases and an increase in type 1 IFN score in one fatal case.ConclusionBRT-Tx significantly suppressed gene expression associated with B cells, while TC-Tx was characterized by low specificity of therapeutic targets and suppression of total cell proliferation. Comparison of surviving and dead cases revealed that the combination of RTX contributed to the success of treatment, as suppression of the immune system mediated by immunoglobulins and B cells is the key for survival. Analysis of the IFN signature revealed an increase in IFN score after treatment in fatal cases, indicating that the combination of BAR is beneficial. The superiority of BRT-Tx seems clear from the fact that all patients survived with BRT-Tx while only one/three patients survived with TC-Tx.REFERENCES:NIL.Acknowledgements:NIL.Disclosure of InterestsMoe Sakamoto: None declared, Yu Nakai: None declared, Yoshiharu Sato: None declared, Yoshinobu Koyama Speakers bureau: Abbvie, Asahikasei, Ayumi, BMS, Esai, Eli-Lilly, Mitsubishi Tanabe, Grant/research support from: Abbvie, GSK.
ABSTRACT
Diabetes mellitus (DM) is a metabolic disease characterised mainly by signs and symptoms derived from increased serum glucose or hyperglycemia. The coronavirus disease 2019 (COVID-19) pandemic affected the entire world with reports of severe prognosis in diabetic patients infected with the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and high hospital admissions in the intensive care unit (ICU) compared to non-diabetic patients. The objective of the bibliographic review was to evaluate and describe some of the biochemical mechanisms that lead to severe prognosis in patients with DM infected by the SARS-CoV-2 virus through a systematic search for information in different databases. The results showed that the high ICU admission with a severe prognosis of diabetic patients infected by the virus was due to excessive inflammation that causes acute respiratory distress syndrome, cytokine storm, severe pneu-monia, impaired immunity, and hyperglycemia. The virus enters the cell mainly through the endocytic and non-endosomal pathway;the central cellular receptors involved in the mechanisms are insulin receptors (IR), glucose transporter type 2 (GLUT-2), dipeptidyl peptidase-4 (DPP4), glucose transporter type 4 (GLUT-4), glucose converting enzyme angiotensin 2 (ACE2), and the serine transmembrane protease co-receptor 2 (TMPRSS2) essential for viral propagation. The increased susceptibility to devel-oping COVID-19 in diabetic patients is due to the overexpression of ACE2, and serious complications are increased at the microvascular and macrovascular levels, such as nephropathies, neuropathies, and cardiovascular diseases.
ABSTRACT
Despite the low incidence, low mortality and relatively mild symptoms of COVID-19 in children, there has been a rise in pediatric patients who develop a condition resembling Kawasaki disease after COVID-19 or contact with individuals infected with SARS-CoV-2. This condition is known as the pediatric inflammatory multisystem syndrome temporally associated with SARS-CoV-2 infection (PIMS-TS). This review introduces the reader to the hypotheses of PIMS-TS pathogenesis, provides information about its diagnosis and treatment, presents clinical and laboratory data and describes treatments strategies used in children and adolescents hospitalized to the intensive care unit of the Pediatric Research and Clinical Center for Infectious Diseases. Besides, the review outlines the main diagnostic and prognostic challenges of PIMS-TS.Copyright © Extreme Medicine.All right reserved.
ABSTRACT
The severe acute respiratory syndrome corona virus 2 (SARS-CoV-2) Omicron variants BA.5.2 and BF.7 have become the main epidemic strains in China since the quarantine policy was lifted in 7th December 2022. Cough is one of the main symptoms induced by SARS-CoV-2 infection. SARS-CoV-2 infection-associated cough injuries the lung and upper respiratory tract, while the infected people cough out virus and liquid which forms virus-containing aerosols, a medium for quickly spreading. Furthermore, cough is one of primary sequelae of discharged patients in corona virus disease 2019 (COVID-19). By now, there are no efficacious drugs for treatment of upper respiratory tract infection associated cough induced by omicron. Traditional Chinese medicine (TCM) has a long history on treating cough. By reviewing the mechanisms of the occurrence of cough after SARS-CoV-2 infection, potential therapeutic targets and cough suppressant herbs with significant efficacy in clinical and basic research, we provide a reference for the treatment of cough after SARS-Cov-2 infection and a basis for the majority of infected patients to select appropriate herbs for cough relief under guidance of physicians.Copyright © 2023 Editorial Office of Chinese Traditional and Herbal Drugs. All rights reserved.
ABSTRACT
The placenta is a vital yet poorly understood organ and given the increased interest in recent years in its role in human development and the birth process, histologic examinations are increasingly being performed and cause some consternation to both pathologists and histology laboratories. Different aspects of the placenta are covered including chapters on the normal histology and physiology, immunology, endocrinology, and imaging characteristics of the placenta. [Extracted from the article] Copyright of Journal of Histotechnology is the property of Taylor & Francis Ltd and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full . (Copyright applies to all s.)
ABSTRACT
The safety of COVID-19 pharmacotherapy is a relevant issue, first of all, because of the current lack of experience with using particular medicinal products and with off-label prescribing. The aim of the study was to analyse information on potential adverse drug reactions (ADRs) and their predictors in etiology- and pathogenesis-oriented COVID-19 therapy. According to literature data, the main clinically significant risk factors for COVID-19 patients to develop an ADR are the duration of their hospital stay, combined use of antivirals, polypharmacy, and their history of drug allergies. The most common adverse reactions to antivirals, to virus-neutralising antibodies, and to human anti-COVID-19 immunoglobulin and convalescent plasma are, respectively, gastrointestinal and hepatobiliary disorders;gastrointestinal disorders, neurological disorders, and allergic reactions;and transfusion reactions (fever, chills, etc.). For pathogenesis-oriented therapy with systemic glucocorticosteroids, the most characteristic ADR is hyperglycaemia. Janus kinase inhibitors and interleukin inhibitors are most often associated with gastrointestinal disorders and hypertransaminasemia;neutropenia is also characteristic of a number of interleukin inhibitors. Haemostatic adverse reactions to anticoagulants depend on the patient's dosing regimen and condition. Drug-drug interactions are a common problem in COVID-19 treatment, with the combination of nirmatrelvir and ritonavir showing the largest number of significant interactions attributed to their pharmacokinetics. Currently, there is data on the role of pharmacogenetic biomarkers in the safety and clinical outcomes of COVID-19 therapy. Thus, to improve the safety of COVID-19 therapy, an integrated approach is needed that will take into account both the clinical, demographic, and pharmacogenetic predictors of ADRs and the risk of drug-drug interactions.Copyright © 2023 Safety and Risk of Pharmacotherapy. All rights reserved.
ABSTRACT
BackgroundHuman SARS-CoV-2 infection is responsible for a large variety of clinical manifestations related to Coronavirus disease-19 (COVID-19) [1]. SARS-CoV-2 can induce microvascular damage, that can be safely detected by nailfold videocapillaroscopy (NVC), as recently demonstrated [2-4]. Virus-induced endothelial dysfunction has been implicated in the pathogenesis of both active infection and long-COVID clinical manifestations (the last as persistence of disease symptoms after at least three months from onset) [5]. The study group on capillaroscopy and microcirculation in rheumatic diseases of the Italian Society of Rheumatology (CAPSIR) carried out an internal survey on the interest of the Italian Centers that perform NVC in participating in a detailed capillaroscopic and clinical data collection in long-COVID patients.ObjectivesTo carry out an Italian multicenter cognitive survey on the interest in collecting NVC and clinical data of patients affected by long-COVID with or without previous rheumatological diseases.MethodsThe steering committee of the CAPSIR study group formulated a cognitive questionnaire, entitled "Study on the role of capillaroscopy in patients with long-COVID” (CAPSIR_2 Study), consisting of 27 open or multiple-choice questions. A Google Form of the questionnaire was emailed to all the member of the study group between September and October 2022. Data are reported with a descriptive analysis.ResultsThe online questionnaire was completed by 41 CAPSIR members, belonging to 33 different Italian centers. Of note, 63% of participants had already experienced NVC in patients with long-COVID. The primary indication to perform the NVC was the onset of a new Raynaud's phenomenon (46% of cases) and the requests come mainly from General Practitioners (33% of cases). In 2/3 of the cases, patients with long-COVID and previous rheumatic diseases, who underwent NVC examination, represented less than 20% of the total. It should be noted that always in 2/3 of the cases there was no preferential channel for the study of the microcirculation in patients affected by long-COVID nor a NVC investigation prior to the SARS-CoV-2 infection. According to the previous experience of the participants in the interview, the most important NVC parameters considered to be evaluated in long-COVID patients were number of capillaries per linear millimeter (24% of cases), presence of hemorrhages (34% of cases) and giant capillaries (22% of capillaries). All participants (100%) therefore agreed to participate in a further collection of NVC and clinical data in this cohort of patients.ConclusionThis survey highlighted the interest of Italian Rheumatologists in assessing by NVC the COVID-related microvascular involvement. A consensus has emerged that future research is needed. After this pilot survey, the second part of the CAPSIR_2 Study will concern the collection/analysis before and after the SARS-CoV-2 infection of NVC and clinical data in patients with primary and secondary (to rheumatic diseases) Raynaud's phenomenon and affected by long-COVID versus adequate controls. The aim is to investigate if the presence/severity of the microvascular damage might be involved in the pathogenesis of the clinical manifestations observed in COVID-19 patients after the active infection. CAPSIR_2 Study will be open to all Italian rheumatological centers that participated in the previous national CAPSIR_1 Project [6].References[1]Fernandes Q et al. Ann Med. 2022;54:524-540.[2]Cutolo M et al. Nat Rev Rheumatol. 2021;17:665-677.[3]Sulli A et al. Microvasc Res 2022;142:104361.[4]Natalello G et al. Microvasc Res. 2021;133:104071.[5]Charfeddine S et al. Front Cardiovasc Med. 2021;8:745758.[6]Ingegnoli F et al. Reumatismo. 2022;74.AcknowledgementsAuthors wrote the on behalf of the study group on capillaroscopy and microcirculation in rheumatic diseases of the Italian Society of Rheumatology (SIR) - CAPSIR.CAPSIR Study Group thanks the EULAR Study Group of Microcirculation in Rheumatic Diseases for the continuous cultural support.Dis losure of InterestsNone Declared.
ABSTRACT
The experience of managing patients with COVID-19 around the world has shown that, although respiratory symptoms predominate during the manifestation of infection, then many patients can develop serious damage to the cardiovascular system. However, coronary artery disease (CHD) remains the leading cause of death worldwide. The purpose of the review is to clarify the possible pathogenetic links between COVID-19 and acute coronary syndrome (ACS), taking into account which will help to optimize the management of patients with comorbid pathology. Among the body's responses to SARS-CoV-2 infection, which increase the likelihood of developing ACS, the role of systemic inflammation, the quintessence of which is a "cytokine storm" that can destabilize an atherosclerotic plaque is discussed. Coagulopathy, typical for patients with Covid-19, is based on immunothrombosis, caused by a complex interaction between neutrophilic extracellular traps and von Willebrandt factor in conditions of systemic inflammation. The implementation of a modern strategy for managing patients with ACS, focused on the priority of percutaneous interventions (PCI), during a pandemic is experiencing great difficulties due to the formation of time delays before the start of invasive procedures due to the epidemiological situation. Despite this, the current European, American and Russian recommendations for the management of infected patients with ACS confirm the inviolability of the position of PCI as the first choice for treating patients with ACS and the undesirability of replacing invasive treatment with thrombolysis.Copyright © 2023 Stolichnaya Izdatelskaya Kompaniya. All rights reserved.
ABSTRACT
Lung cancer is the most common cancer in males and the second most common among females both in Europe and worldwide. Moreover, lung cancer is the leading cause of death due to cancer in males. The European region accounts for 23% of total cancer cases and 20% of cancer-related deaths. Relationships have been described between a number of infectious agents and cancers, but our knowledge of the role of viruses, both respiratory and systemic, in the pathogenesis of lung cancer is still rudimentary and has been poorly disseminated. In this chapter, we review the available evidence on the involvement of HPV, Epstein-Barr virus, HIV, cytomegalovirus and measles virus in the epidemiology and pathogenesis of lung cancer.Copyright © ERS 2021.
ABSTRACT
The new coronavirus infection COVID-19 (Coronavirus Disease 2019) caused by SARS-CoV-2, has posed scientific and public health challenges. The problem of treating COVID-19 still remains, and the pathogenesis of COVID-19 needs to be studied in detail, including the involvement of mast cells (MCs) and their specific proteases. The aim of this study was to characterize the role of mast cell proteases chymase, tryptase, and carboxypeptidase A3 (CPA3) in the lung damage associated with COVID-19. Methods. The study included postmortem lung biopsies from 30 patients who died of severe COVID-19, and biopsies from 9 control group patients. Histological preparations were made and protease profile and degranulation activity of MCs were analyzed. In addition, some demographic, clinical, and laboratory parameters were analyzed. Results. The average number of tryptase-positive MCs without evidence of degranulation and the total number of CPA3-positive MCs were statistically significantly higher in patients with COVID-19, and the number of tryptase-positive and CPA3-positive MCs fragments was lower compared with controls. Negative correlations were established between the numbers of tryptase-positive MCs and red blood cell count. Negative correlations were found between non-granulating tryptase-positive MCs and hemoglobin levels. Positive correlations were noted between tryptase-positive MCs and the leukocytes and eosinophils counts, and negative correlations were noted between the number of CPA3-positive cells and the platelet count. A positive correlation was found between the number of adjoining MCs, as well as fragments of tryptase-positive MCs, and the erythrocyte sedimentation rate (ESR). A negative correlation was also observed between the number of non-degranulated CPA3-positive MCs and the blood level of C-reactive protein. In patients with COVID-19, reduced degranulation activity of tryptase-positive MCs was found along with increased representation of CPA3-positive MCs. Several trends and associations with laboratory test results were noted. The potential involvement of MCs in the development of anemia and thrombocytopenia is considered. Associations were established between tryptase-positive MCs and the peripheral blood counts of leukocytes and eosinophils, as well as ESR. Conclusion. The results obtained are highly contradictory. Since many aspects of the involvement of MCs and their proteases in COVID-19 pathogenesis are still unknown, studies with larger cohorts of patients are needed.Copyright © Budnevsky A.V. et al., 2023.
ABSTRACT
Lymphangitis carcinomatosa refers to pulmonary interstitial involvement by cancer and is a dreaded clinical finding in oncology because it is a late manifestation indicative of metastatic malignancy, from either a lung or a nonlung primary cancer, and is associated with poor prognosis. Its presentation is nonspecific, often with subacute dyspnoea and a nonproductive cough in a person with a known history of malignancy, but in some cases is the first manifestation of cancer. CT imaging can be suggestive, typically demonstrating thickening of the peribronchovascular interstitium, interlobular septa and fissures. However, a biopsy may be required to confirm the pathological diagnosis as these changes can also be due to concurrent disease such as heart failure, ILD, infection, radiation pneumonitis and drug reactions. Diagnosis allows symptomatic treatment, with personalised treatment directed towards the primary cancer most likely to provide a meaningful benefit. Future research should focus on prospective clinical trials to identify new interventions to improve both diagnosis and treatment of lymphangitis carcinomatosa.Copyright © ERS 2021.
ABSTRACT
Hepatitis E is a zoonosis caused by hepatitis E virus (HEV), which was first discovered 40 years ago. Twenty million HEV infections worldwide are estimated each year. Most hepatitis E cases are self-limiting acute hepatitis, but the virus has been recognized to cause chronic hepatitis. Following the first case report of chronic hepatitis E (CHE) in a transplant recipient, CHE has recently been identified as associated with chronic liver damage induced by HEV genotypes 3, 4, and 7-usually in immunocompromised patients such as transplant recipients. In addition, patients infected with HIV and those receiving chemotherapy for malignancy, along with patients with rheumatic disease and COVID-19, have recently been reported as having CHE. CHE can be easily misdiagnosed by usual diagnostic methods of antibody response, such as anti-HEV IgM or IgA, because of the low antibody response in the immunosuppressive condition. HEV RNA should be evaluated in these patients, and appropriate treatments-such as ribavirin-should be given to prevent progression to liver cirrhosis or liver failure. While still rare, cases of CHE in immunocompetent patients have been reported, and care must be taken not to overlook these instances. Herein, we conduct an overview of hepatitis E, including recent research developments and management of CHE, in order to improve our understanding of such cases. The early diagnosis and treatment of CHE should be performed to decrease instances of hepatitis-virus-related deaths around the world.
ABSTRACT
Nipah virus (NiV) and Hendra virus (HeV) are highly pathogenic zoonotic viruses of the genus Henipavirus, family Paramyxoviridae that cause severe disease outbreaks in humans and also can infect and cause lethal disease across a broad range of mammalian species. Another related Henipavirus has been very recently identified in China in febrile patients with pneumonia, the Langya virus (LayV) of probable animal origin in shrews. NiV and HeV were first identified as the causative agents of severe respiratory and encephalitic disease in the 1990s across Australia and Southern Asia with mortality rates reaching up to 90%. They are responsible for rare and sporadic outbreaks with no approved treatment modalities. NiV and HeV have wide cellular tropism that contributes to their high pathogenicity. From their natural hosts bats, different scenarios propitiate their spillover to pigs, horses, and humans. Henipavirus-associated respiratory disease arises from vasculitis and respiratory epithelial cell infection while the neuropathogenesis of Henipavirus infection is still not completely understood but appears to arise from dual mechanisms of vascular disease and direct parenchymal brain infection. This brief review offers an overview of direct and indirect mechanisms of HeV and NiV pathogenicity and their interaction with the human immune system, as well as the main viral strategies to subvert such responses.
ABSTRACT
A period of about a decade has been estimated to pass for the emergence of a new infectious strain of a virus that may lead to the occurrence of a pandemic one. It is now suggested that the variants of the 1918 H1N1 and coronavirus disease-19 pandemics could have existed in humans after the initial cross-species introduction to humans and underwent multiple low-level seasonal epidemics before the occurrence of their outbreaks. They share similarities in the continuation, widespreadness due to high transmissibility, high fatality rate and clinical symptoms. They are assumed to share a similar principle of a zoonotic source and a cross-species pathway for transmission. They show some similarities in their pathogenesis with other enveloped viruses: Severe Acute Respiratory Syndrome Coronavirus-1 (SARS-CoV-1), Middle East respiratory syndrome coronavirus (MERS-CoV), human immunodeficiency virus, Ebola, Lassa and measles viruses. The highly pathogenic nature of these viruses and their genetic variants may depend on their binding affinity for host cell receptors, whereby they efficiently circumvent or block host cell immune responses triggered by cytokines (interferon). High transmission rates and viral pathogenicity are attributed to glycan moieties that facilitate virus binding to host multiple receptors and cell entry, thereby helping viruses to evade immune recognition and response. Also, mucosa glycotopes are a matter of concern that play as primary sites for virus attachment and body entry. Finding general lectins or ligands that block the viral-host receptors interaction or identifying individual glycotopes is the therapeutic and prognosis topic that demands the main focus.