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1.
Clin Exp Rheumatol ; 39(1): 203-213, 2021.
Article in English | MEDLINE | ID: covidwho-1068449

ABSTRACT

At the beginning of COVID-19, we underlined that this pandemic was a new challenge for rheumatologists. On the one hand, it was necessary to clarify the impact of this new viral disease on the natural history of many rheumatic diseases and, on the other hand, to define the beneficial or harmful effects of the synthetic or targeted therapies used for their treatment. In addition, we have postulated that in view of the common pathogenetic mechanisms involved, the therapeutic armamentarium currently employed in the management of viral or idiopathic systemic autoimmune rheumatic diseases could be useful to control the "cytokine storm" induced by SARS-COV-2. One year later, in the present review we have analysed the progress of the knowledge on both these aspects and updated the algorithms initially proposed for a rational use of the synthetic and targeted anti-inflammatory and immunomodulatory agents in the management of COVID-19.


Subject(s)
COVID-19 , Rheumatologists , Cytokine Release Syndrome , Humans , Pandemics , SARS-CoV-2
2.
Biol Direct ; 15(1): 30, 2020 12 29.
Article in English | MEDLINE | ID: covidwho-999756

ABSTRACT

Knowing the "point of view" of the immune system is essential to understand the characteristic of a pandemic, such as that generated by the Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV)-2, responsible for the Coronavirus Disease (COVID)-19. In this review, we will discuss the general host/pathogen interactions dictating protective immune response or immunopathology, addressing the role of immunity or immunopathology in influencing the clinical infection outcome, and debate the potential immunoprophylactic and immunotherapy strategies required to fight the virus infection.


Subject(s)
COVID-19/immunology , Immune System/physiology , Animals , Antibodies, Monoclonal/therapeutic use , Autoimmunity , COVID-19 Vaccines , Host-Pathogen Interactions , Humans , Immune Evasion , Immunity , Immunity, Innate , Immunotherapy
3.
Immunol Res ; 68(6): 325-339, 2020 12.
Article in English | MEDLINE | ID: covidwho-915244

ABSTRACT

Antibodies are considered as an excellent foundation to neutralize pathogens and as highly specific therapeutic agents. Antibodies are generated in response to a vaccine but little use as immunotherapy to combat virus infections. A new generation of broadly cross-reactive and highly potent antibodies has led to a unique chance for them to be used as a medical intervention. Neutralizing antibodies (monoclonal and polyclonal antibodies) are desirable for pharmaceutical products because of their ability to target specific epitopes with their variable domains by precise neutralization mechanisms. The isolation of neutralizing antiviral antibodies has been achieved by Phage displayed antibody libraries, transgenic mice, B cell approaches, and hybridoma technology. Antibody engineering technologies have led to efficacy improvements, to further boost antibody in vivo activities. "Although neutralizing antiviral antibodies have some limitations that hinder their full development as therapeutic agents, the potential for prevention and treatment of infections, including a range of viruses (HIV, Ebola, MERS-COV, CHIKV, SARS-CoV, and SARS-CoV2), are being actively pursued in human clinical trials."


Subject(s)
Antibodies, Monoclonal/therapeutic use , Antibodies, Neutralizing/therapeutic use , Antibodies, Viral/therapeutic use , Betacoronavirus/immunology , Coronavirus Infections/therapy , Pneumonia, Viral/therapy , Animals , Antibodies, Monoclonal/immunology , Antibodies, Neutralizing/immunology , Antibodies, Viral/immunology , COVID-19 , Coronavirus Infections/prevention & control , Epitopes/immunology , Humans , Immunotherapy/methods , Mice , Pandemics/prevention & control , Pneumonia, Viral/prevention & control , SARS-CoV-2
4.
Nat Rev Neurol ; 16(9): 493-505, 2020 09.
Article in English | MEDLINE | ID: covidwho-639750

ABSTRACT

The coronavirus disease 2019 (COVID-19) pandemic is concerning for patients with neuroimmunological diseases who are receiving immunotherapy. Uncertainty remains about whether immunotherapies increase the risk of infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) or increase the risk of severe disease and death upon infection. National and international societies have developed guidelines and statements, but consensus does not exist in several areas. In this Review, we attempt to clarify where consensus exists and where uncertainty remains to inform management approaches based on the first principles of neuroimmunology. We identified key questions that have been addressed in the literature and collated the recommendations to generate a consensus calculation in a Delphi-like approach to summarize the information. We summarize the international recommendations, discuss them in light of the first available data from patients with COVID-19 receiving immunotherapy and provide an overview of management approaches in the COVID-19 era. We stress the principles of medicine in general and neuroimmunology in particular because, although the risk of viral infection has become more relevant, most of the considerations apply to the general management of neurological immunotherapy. We also give special consideration to immunosuppressive treatment and cell-depleting therapies that might increase susceptibility to SARS-CoV-2 infection but reduce the risk of severe COVID-19.


Subject(s)
Betacoronavirus , Consensus , Coronavirus Infections/immunology , Coronavirus Infections/therapy , Immunotherapy/standards , Neuroimmunomodulation/immunology , Pneumonia, Viral/immunology , Pneumonia, Viral/therapy , COVID-19 , Humans , Immunologic Factors/pharmacology , Immunologic Factors/therapeutic use , Immunosuppressive Agents/pharmacology , Immunosuppressive Agents/therapeutic use , Immunotherapy/methods , Neuroimmunomodulation/drug effects , Pandemics , SARS-CoV-2
5.
Expert Opin Biol Ther ; 20(9): 959-964, 2020 09.
Article in English | MEDLINE | ID: covidwho-615438

ABSTRACT

INTRODUCTION: The COVID-19 pandemic occurred amid the cancer immunotherapy revolution. Immune checkpoint inhibitors (ICIs) have become the standard of care for several solid cancers and are associated with peculiar toxicities, including pneumonitis which has similar features to COVID-19 pneumonia. AREAS COVERED: We summarize the main hallmarks of lung injury induced by ICIs and severe acute respiratory syndrome coronavirus 2 and discuss the critical aspects for differential diagnosis and management. Symptoms and radiological findings are often similar; conversely, treatments are quite different. Furthermore, we focus on potential interactions generating hypotheses that need confirmatory studies. EXPERT OPINION: All cancer patients treated with immunotherapy should receive screening for SARS-CoV-2. This would improve the diagnosis and management of pneumonia and guide therapeutic choices. Furthermore, clinicians could estimate the risk/benefit of continuing ICI treatment in COVID-19 positive patients. Temporary withdrawal of the immunotherapy treatment pending resolution of viral infection may be a reasonable option in long-responders patients.


Subject(s)
Betacoronavirus , Coronavirus Infections/therapy , Immunotherapy , Neoplasms/therapy , Pneumonia, Viral/therapy , COVID-19 , Coronavirus Infections/epidemiology , Coronavirus Infections/immunology , Diagnosis, Differential , Disease Management , Humans , Immunotherapy/adverse effects , Immunotherapy/trends , Neoplasms/epidemiology , Neoplasms/immunology , Pandemics/prevention & control , Pneumonia, Viral/epidemiology , Pneumonia, Viral/immunology , SARS-CoV-2
6.
Chin J Traumatol ; 23(4): 190-195, 2020 Aug.
Article in English | MEDLINE | ID: covidwho-598830

ABSTRACT

COVID-19 is known for its magical infectivity, fast transmission and high death toll based on the large number of infected people. From the perspective of the clinical manifestation, autopsy examination and pathophysiology, the essence of COVID-19 should be viewed as a sepsis induced by viral infection, and has the essential characteristics as sepsis induced by other pathogens. Therefore, in addition to etiological and supportive treatment, immunomodulatory therapy is also appropriate to severe COVID-19. Although there is still a lack of consensus on immunotherapy for sepsis so far, relatively rich experiences have been accumulated in the past decades, which will help us in the treatment of severe COVID-19. This article will elaborate immunotherapy of sepsis, though it may not be consistent.


Subject(s)
Betacoronavirus , Coronavirus Infections/complications , Immunologic Factors/therapeutic use , Pneumonia, Viral/complications , Sepsis/etiology , Adrenal Cortex Hormones/therapeutic use , COVID-19 , Glycoproteins/therapeutic use , Humans , Pandemics , SARS-CoV-2 , Sepsis/drug therapy , Thymalfasin/therapeutic use
7.
Rev Med Virol ; 30(3): e2109, 2020 05.
Article in English | MEDLINE | ID: covidwho-95194

ABSTRACT

There is a growing appreciation that the regulation of the melatonergic pathways, both pineal and systemic, may be an important aspect in how viruses drive the cellular changes that underpin their control of cellular function. We review the melatonergic pathway role in viral infections, emphasizing influenza and covid-19 infections. Viral, or preexistent, suppression of pineal melatonin disinhibits neutrophil attraction, thereby contributing to an initial "cytokine storm", as well as the regulation of other immune cells. Melatonin induces the circadian gene, Bmal1, which disinhibits the pyruvate dehydrogenase complex (PDC), countering viral inhibition of Bmal1/PDC. PDC drives mitochondrial conversion of pyruvate to acetyl-coenzyme A (acetyl-CoA), thereby increasing the tricarboxylic acid cycle, oxidative phosphorylation, and ATP production. Pineal melatonin suppression attenuates this, preventing the circadian "resetting" of mitochondrial metabolism. This is especially relevant in immune cells, where shifting metabolism from glycolytic to oxidative phosphorylation, switches cells from reactive to quiescent phenotypes. Acetyl-CoA is a necessary cosubstrate for arylalkylamine N-acetyltransferase, providing an acetyl group to serotonin, and thereby initiating the melatonergic pathway. Consequently, pineal melatonin regulates mitochondrial melatonin and immune cell phenotype. Virus- and cytokine-storm-driven control of the pineal and mitochondrial melatonergic pathway therefore regulates immune responses. Virus-and cytokine storm-driven changes also increase gut permeability and dysbiosis, thereby suppressing levels of the short-chain fatty acid, butyrate, and increasing circulating lipopolysaccharide (LPS). The alterations in butyrate and LPS can promote viral replication and host symptom severity via impacts on the melatonergic pathway. Focussing on immune regulators has treatment implications for covid-19 and other viral infections.


Subject(s)
Coronavirus Infections/physiopathology , Influenza, Human/metabolism , Melatonin/metabolism , Pneumonia, Viral/physiopathology , Animals , Betacoronavirus/physiology , Biosynthetic Pathways , COVID-19 , Circadian Rhythm , Circadian Rhythm Signaling Peptides and Proteins/genetics , Coronavirus Infections/pathology , Coronavirus Infections/virology , Cytokines/immunology , Humans , Influenza, Human/immunology , Melatonin/immunology , Mitochondria/metabolism , Orthomyxoviridae/physiology , Pandemics , Pineal Gland/metabolism , Pneumonia, Viral/pathology , Pneumonia, Viral/virology , SARS-CoV-2 , Viruses/classification
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