scholarly journals Convalescent Plasma: A Potential Treatment for COVID-19

Author(s):  
Mohiuddin Ahmed Khan ◽  
Mafruha Akter

As no specific standard therapies have been approved for Coronavirus disease 2019 (COVID-19), so prevention and supportive care dominate the approach to COVID-19. Exposure to this severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) results in an adaptive immune response that commonly include antibodies with neutralization activity. Treatments directly targeting the virus and the inflammatory response to it remain investigational. Convalescent plasma (CP) is such a therapy that had been reported hundred years back in studies from the Spanish influenza era. So the idea of convalescent plasma from subjects who have recovered from viral infections has been used to both prevent or treat disease. Over the past two decades’ notable examples of the successful use of convalescent plasma (CP) include influenza, measles, Middle East respiratory syndrome (MERS), Ebola and severe acute respiratory syndrome (SARS). Two case series were recently published by China examining the therapeutic use of CP in patients with COVID-19. In the context of pandemic situation, the Food and Drug Administration (FDA) allowed to use COVID-19 convalescent plasma as Investigational New Drug (IND) since April 2020 to help patients with serious or immediately life-threatening illness associated with COVID- 19. Case series studying convalescent plasma use in the treatment of COVID-19 have been promising, but additional, high-quality studies are needed to determine the efficacy of the treatment when applied for prophylaxis, for early phases of illness and for severe illness. Bangladesh also started program to use convalescent plasma for severe and critical COVID-19 patients under limited clinical trial. J Bangladesh Coll Phys Surg 2020; 38(0): 109-115

2018 ◽  
Vol 92 (11) ◽  
Author(s):  
Steffi De Pelsmaeker ◽  
Nicolas Romero ◽  
Massimo Vitale ◽  
Herman W. Favoreel

ABSTRACTNatural killer (NK) cells play an important role in the host response against viral infections and cancer development. They are able to kill virus-infected and tumor cells, and they produce different important cytokines that stimulate the antiviral and antitumor adaptive immune response, particularly interferon gamma. NK cells are of particular importance in herpesvirus infections, which is illustrated by systemic and life-threatening herpesvirus disease symptoms in patients with deficiencies in NK cell activity and by the myriad of reports describing herpesvirus NK cell evasion strategies. The latter is particularly obvious for cytomegaloviruses, but increasing evidence indicates that most, if not all, members of the herpesvirus family suppress NK cell activity to some extent. This review discusses the different NK cell evasion strategies described for herpesviruses and how this knowledge may translate to clinical applications.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Franca Rosa Guerini ◽  
Matteo Cesari ◽  
Beatrice Arosio

AbstractThe risk of serious complications and the fatality rate due to COVID-19 pandemic have proven particularly higher in older persons, putting a further strain in healthcare system as we dramatically observed.COVID-19 is not exclusively gerophile (géro “old” and philia “love”) as young people can be infected, even if older people experience more severe symptoms and mortality due to their greater frailty. Indeed, frailty could complicate the course of COVID-19, much more than the number of years lived. As demonstration, there are centenarians showing remarkable capacity to recover after coronavirus infection.We hypothesize that centenarian’s portfolio could help in identifying protective biological mechanisms underlying the coronavirus infection.The human leukocyte antigen (HLA) is one of the major genetic regions associated with human longevity, due to its central role in the development of adaptive immune response and modulation of the individual’s response to life threatening diseases. The HLA locus seems to be crucial in influencing susceptibility and severity of COVID-19.In this hypothesis, we assume that the biological process in which HLA are involved may explain some aspects of coronavirus infection in centenarians, although we cannot rule out other biological mechanisms that these extraordinary persons are able to adopt to cope with the infection.


2007 ◽  
Vol 81 (16) ◽  
pp. 8692-8706 ◽  
Author(s):  
Mark J. Cameron ◽  
Longsi Ran ◽  
Luoling Xu ◽  
Ali Danesh ◽  
Jesus F. Bermejo-Martin ◽  
...  

ABSTRACT It is not understood how immune inflammation influences the pathogenesis of severe acute respiratory syndrome (SARS). One area of strong controversy is the role of interferon (IFN) responses in the natural history of SARS. The fact that the majority of SARS patients recover after relatively moderate illness suggests that the prevailing notion of deficient type I IFN-mediated immunity, with hypercytokinemia driving a poor clinical course, is oversimplified. We used proteomic and genomic technology to systematically analyze host innate and adaptive immune responses of 40 clinically well-described patients with SARS during discrete phases of illness from the onset of symptoms to discharge or a fatal outcome. A novel signature of high IFN-α, IFN-γ, and IFN-stimulated chemokine levels, plus robust antiviral IFN-stimulated gene (ISG) expression, accompanied early SARS sequelae. As acute illness progressed, SARS patients entered a crisis phase linked to oxygen saturation profiles. The majority of SARS patients resolved IFN responses at crisis and expressed adaptive immune genes. In contrast, patients with poor outcomes showed deviated ISG and immunoglobulin gene expression levels, persistent chemokine levels, and deficient anti-SARS spike antibody production. We contend that unregulated IFN responses during acute-phase SARS may culminate in a malfunction of the switch from innate immunity to adaptive immunity. The potential for the use of the gene signatures we describe in this study to better assess the immunopathology and clinical management of severe viral infections, such as SARS and avian influenza (H5N1), is therefore worth careful examination.


Author(s):  
Akpanda Etido ◽  
Emmanuel Ifeanyi Obeagu ◽  
Chukwuma J. Okafor ◽  
Udunma Olive Chijioke ◽  
C. C. N. Vincent ◽  
...  

This article deals with the dynamics of the innate and adaptive immune response to severe acute respiratory syndrome coronavirus 2 (SARSCoV2) infection. SARSCoV2 is the viral factor that causes the current global coronavirus pandemic disease 2019 (COVID2019). In terms of person-to-person transmission, it is contacted by inhaling the sneeze droplets of infected people. Severe acute respiratory syndrome Coronavirus 2 attacks lung cells first in its binding mechanism because there are many conservative receptor entries, such as angiotensin converting enzyme 2. The presence of this virus in host cells triggers a variety of protective immune responses, resulting in leads to pneumonia and acute respiratory distress syndrome. In the SarsCoV2 infection process, virus replication, immune response, and inflammatory response are dynamic events that can change rapidly; leading to different results, involving the dynamic expression of pro-inflammatory genes, peaking after the lowest point of respiratory function and leading to a cytokine storm, research on the interleukin 1 (IL1) pathway has shown that it is a factor related in severe respiratory diseases. The weakened expression of cytokines associated with mild infections will also delay T cell immunity to SARSCoV2, thereby prolonging the infection time; this indicates that such afebrile (afebrile) infections and undifferentiated COVID19 cases may promote the virus in the community Spread. This review aims to provide a general overview of the dynamics involved in the human immune response to this viral infection. It also includes a brief description of its structure, discovery history and pathogenesis to facilitate the understanding of this article.


2022 ◽  
Vol 23 (2) ◽  
pp. 803
Author(s):  
Alessandro Lazzaro ◽  
Gabriella De Girolamo ◽  
Valeria Filippi ◽  
Giuseppe Pietro Innocenti ◽  
Letizia Santinelli ◽  
...  

Sepsis is a life-threatening condition that arises when the body’s response to an infection injures its own tissues and organs. Despite significant morbidity and mortality throughout the world, its pathogenesis and mechanisms are not clearly understood. In this narrative review, we aimed to summarize the recent developments in our understanding of the hallmarks of sepsis pathogenesis (immune and adaptive immune response, the complement system, the endothelial disfunction, and autophagy) and highlight novel laboratory diagnostic approaches. Clinical management is also discussed with pivotal consideration for antimicrobic therapy management in particular settings, such as intensive care unit, altered renal function, obesity, and burn patients.


Author(s):  
Jose Irazuzta ◽  
Nicolas Chiriboga Salazar

A misguided auto-reactive injury is responsible for diverse types of central nervous system (CNS) conditions. We suspect that, in some of these conditions, the adaptive immune system have a common cellular immune pathogenesis, driven predominantly by T cells, despite variability on the phenotypical clinical presentation. Aim: the main goal of this study is to characterize a portion of the adaptive immune response (AIR) on patients presenting with clinical symptoms compatible with monophasic acute neuroimmune disorders (NID) including Psychotic Disorders (PD). Methodology: flow cytometry with deep immunophenotyping of T effector (Teff) and T regulatory (Treg) cells was performed on peripheral blood obtained during the acute clinical phase and compared it to the one from an age-matched cohort group [Co). Results: our preliminary findings point toward the presence of common “immunosignature” in individuals affected by NID or PD.  We also found a shared dysregulation of immune related neurogenes in NID and PD that were not present in normal cohorts. Conclusions: this preliminary report gives some insights into the underlying shared pathobiology. If we can improve our capacity for early accurate diagnosis and meaningful disease monitoring of pathogenic T cell subsets, we will both expedite disease detection and may serve as a guide the administration of effective immunotherapeutic agents.


2020 ◽  
Author(s):  
Ademola Samuel Ojo ◽  
Paul Toluwatope Okediji ◽  
Ayotemide P. Akin-Onitolo ◽  
Olusegun S. Ojo ◽  
Oluyinka Oladele Opaleye

This paper attempts to answer the question: are recovered COVID-19 patients protected from re-infection? This review draws evidence from comparisons between immune responses to Severe Acute Respiratory Syndrome coronavirus (SARS-CoV) and Middle East Respiratory Syndrome coronavirus (MERS-CoV), which are phylogenetically closely related to Severe Acute Respiratory Syndrome coronavirus type 2 (SARS-CoV-2). Relevant studies were identified and reviewed based on searches conducted using PubMed. Full-text original studies on short- and long-term immune responses to human coronaviruses were included. The immune dysfunction and clinical manifestations in SARS-CoV-2, SARS-CoV, and MERS-CoV were found to be similar. Infections with SARS-CoV and MERS-CoV trigger the production of antibodies and memory B- and T-cells. Serum IgM is detectable within 7 days, peak at 21-30 days and become undetectable by 180 days. IgG is detectable at 7 days, peak at 90 days, and decline to undetected levels by 2 years post-infection. Memory B- and T-cells persist in the body for up to 2 and 6 years respectively after initial infection. The short-term risk of SARS-CoV-2 re-infection is predictably low based on similarities in the short term adaptive immune response to kindred coronaviruses. However, more research will be required to determine the long-term adaptive immunity to SARS-CoV-2 and factors that may influence the existence of short- and long-term immunity against the virus.


Science ◽  
2020 ◽  
Vol 370 (6518) ◽  
pp. 811-818 ◽  
Author(s):  
Chadi M. Saad-Roy ◽  
Caroline E. Wagner ◽  
Rachel E. Baker ◽  
Sinead E. Morris ◽  
Jeremy Farrar ◽  
...  

The future trajectory of the coronavirus disease 2019 (COVID-19) pandemic hinges on the dynamics of adaptive immunity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2); however, salient features of the immune response elicited by natural infection or vaccination are still uncertain. We use simple epidemiological models to explore estimates for the magnitude and timing of future COVID-19 cases, given different assumptions regarding the protective efficacy and duration of the adaptive immune response to SARS-CoV-2, as well as its interaction with vaccines and nonpharmaceutical interventions. We find that variations in the immune response to primary SARS-CoV-2 infections and a potential vaccine can lead to markedly different immune landscapes and burdens of critically severe cases, ranging from sustained epidemics to near elimination. Our findings illustrate likely complexities in future COVID-19 dynamics and highlight the importance of immunological characterization beyond the measurement of active infections for adequately projecting the immune landscape generated by SARS-CoV-2 infections.


RMD Open ◽  
2020 ◽  
Vol 6 (2) ◽  
pp. e001333 ◽  
Author(s):  
Isabelle Koné-Paut ◽  
Rolando Cimaz

A few weeks after the peak of the global 2019 novel coronavirus disease pandemic, cases of shock, multisystem inflammation and severe myocarditis have occurred in children and adolescents, generating some concerns and above all many questions. An almost immediate association raised with shock syndrome related to Kawasaki disease (KD). However, in light of bo/th experience and literature have taught us about severe acute respiratory syndrome coronavirus 2 (SARS-COV-2) infection, and what already known on the epidemiology of KD, we suggest here the hypothesis of a new ‘post-viral’ systemic inflammatory disease related to excessive adaptive immune response rather than a form of KD caused by SARS-COV-2. We discuss analogies and differences between the two forms.


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