scholarly journals The impact of the interferon-lambda family on the innate and adaptive immune response to viral infections

2014 ◽  
Vol 3 (1) ◽  
pp. 1-12 ◽  
Author(s):  
Adrian Egli ◽  
Deanna M Santer ◽  
Daire O’Shea ◽  
D Lorne Tyrrell ◽  
Michael Houghton
Keyword(s):  
Immune Response ◽  
Viral Infections ◽  
Adaptive Immune Response ◽  
Adaptive Immune ◽  
Interferon Lambda ◽  
The Impact

scholarly journals Rapid Weight Loss, Central Obesity Improvement and Blood Glucose Reduction Are Associated with a Stronger Adaptive Immune Response Following COVID-19 mRNA Vaccine

Vaccines ◽  
2022 ◽  
Vol 10 (1) ◽  
pp. 79
Author(s):  
Mikiko Watanabe ◽  
Angela Balena ◽  
Davide Masi ◽  
Rossella Tozzi ◽  
Renata Risi ◽  
...  
Keyword(s):  
Immune Response ◽  
Weight Loss ◽  
Blood Glucose ◽  
Adaptive Immune Response ◽  
Humoral Response ◽  
Rapid Weight Loss ◽  
Low Carbohydrate Diet ◽  
Adaptive Immune ◽  
Glucose Reduction ◽  
The Impact

Obesity is associated with a poor COVID-19 prognosis, and it seems associated with reduced humoral response to vaccination. Public health campaigns have advocated for weight loss in subjects with obesity, hoping to eliminate this risk. However, no evidence proves that weight loss leads to a better prognosis or a stronger immune response to vaccination. We aimed to investigate the impact of rapid weight loss on the adaptive immune response in subjects with morbid obesity. Twenty-one patients followed a hypocaloric, very-low-carbohydrate diet one week before to one week after the two mRNA vaccine doses. The diet’s safety and efficacy were assessed, and the adaptive humoral (anti-SARS CoV-2 S antibodies, Abs) and cell-mediated responses (IFNγ secretion on stimulation with two different SARS CoV-2 peptide mixes, IFNγ-1 and IFNγ-2) were evaluated. The patients lost ~10% of their body weight with metabolic improvement. A high baseline BMI correlated with a poor immune response (R −0.558, p = 0.013 for IFNγ-1; R −0.581, p = 0.009 for IFNγ-2; R −0.512, p = 0.018 for Abs). Furthermore, there was a correlation between weight loss and higher IFNγ-2 (R 0.471, p = 0.042), and between blood glucose reduction and higher IFNγ-1 (R 0.534, p = 0.019), maintained after weight loss and waist circumference reduction adjustment. Urate reduction correlated with higher Abs (R 0.552, p = 0.033). In conclusion, obesity is associated with a reduced adaptive response to a COVID-19 mRNA vaccine, and weight loss and metabolic improvement may reverse the effect.

scholarly journals Immune Response to COVID-19

2021 ◽  
Author(s):  
Ricardo Wesley Alberca
Keyword(s):  
Immune Response ◽  
Adaptive Immune Response ◽  
Multiple Organ ◽  
Disease Course ◽  
Angiotensin Converting Enzyme 2 ◽  
Damage And Failure ◽  
Adaptive Immune ◽  
General Aspects ◽  
Inflammatory Molecules ◽  
The Impact

The severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) invades the host’s cells via the angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2). ACE2 and TMPRSS2 molecules are highly expressed on the respiratory tract but are also expressed in other organs such as kidneys, heart, and intestine, which could partially explain the multiple organ infection, damage, and failure. During the COVID-19 disease course, patients may develop a dysregulation in the immune response, with an exacerbated production of pro-inflammatory molecules and hypercoagulation, which can collaborate to the increase in tissue damage and death. This chapter will cover general aspects of the innate and adaptive immune response during COVID-19, the impact of comorbidities on the immune response to SARS-CoV-2, and the immune response generated by COVID-19 vaccines.

scholarly journals Immune-Mediated Control of a Dormant Neurotropic RNA Virus Infection

2019 ◽  
Vol 93 (18) ◽  
Author(s):  
Katelyn D. Miller ◽  
Christine M. Matullo ◽  
Katelynn A. Milora ◽  
Riley M. Williams ◽  
Kevin J. O’Regan ◽  
...  
Keyword(s):  
Immune Response ◽  
Protein Synthesis ◽  
Measles Virus ◽  
Viral Infections ◽  
Acute Infection ◽  
Adaptive Immune Response ◽  
Viral Control ◽  
Cns Disease ◽  
Adaptive Immune ◽  
Immune Mediated

ABSTRACTGenomic material from many neurotropic RNA viruses (e.g., measles virus [MV], West Nile virus [WNV], Sindbis virus [SV], rabies virus [RV], and influenza A virus [IAV]) remains detectable in the mouse brain parenchyma long after resolution of the acute infection. The presence of these RNAs in the absence of overt central nervous system (CNS) disease has led to the suggestion that they are viral remnants, with little or no potential to reactivate. Here we show that MV RNA remains detectable in permissive mouse neurons long after challenge with MV and, moreover, that immunosuppression can cause RNA and protein synthesis to rebound, triggering neuropathogenesis months after acute viral control. Robust recrudescence of viral transcription and protein synthesis occurs after experimental depletion of cells of the adaptive immune response and is associated with a loss of T resident memory (Trm) lymphocytes within the brain. The disease associated with loss of immune control is distinct from that seen during the acute infection: immune cell-depleted, long-term-infected mice display severe gait and motor problems, in contrast to the wasting and lethal disease that occur during acute infection of immunodeficient hosts. These results illuminate the potential consequences of noncytolytic, immune-mediated viral control in the CNS and demonstrate that what were once considered “resolved” RNA viral infections may, in fact, induce diseases later in life that are distinct from those caused by acute infection.IMPORTANCEViral infections of neurons are often not cytopathic; thus, once-infected neurons survive, and viral RNAs can be detected long after apparent viral control. These RNAs are generally considered viral fossils, unlikely to contribute to central nervous system (CNS) disease. Using a mouse model of measles virus (MV) neuronal infection, we show that MV RNA is maintained in the CNS of infected mice long after acute control and in the absence of overt disease. Viral replication is suppressed by the adaptive immune response; when these immune cells are depleted, viral protein synthesis recurs, inducing a CNS disease that is distinct from that observed during acute infection. The studies presented here provide the basis for understanding how persistent RNA infections in the CNS are controlled by the host immune response, as well as the pathogenic consequences of noncytolytic viral control.

Respiratory and gastrointestinal epithelial modulation of the immune response during viral infection

2011 ◽  
Vol 18 (1) ◽  
pp. 179-189 ◽  
Author(s):  
Paul M Fitch ◽  
Paul Henderson ◽  
Jürgen Schwarze
Keyword(s):  
Immune Response ◽  
Human Body ◽  
World Wide ◽  
Viral Infections ◽  
Adaptive Immune Response ◽  
Significant Morbidity ◽  
Viral Pathogens ◽  
Adaptive Immune ◽  
Adaptive Interface ◽  
Portal Of Entry

Respiratory and enteric viral infections cause significant morbidity and mortality world-wide and represent a major socio-economic burden. Many of these viruses have received unprecedented public and media interest in recent years. A popular public misconception is that viruses are a threat to which the human body has only limited defences. However, the majority of primary and secondary exposures to virus are asymptomatic or induce only minor symptoms. The mucosal epithelial surfaces are the main portal of entry for viral pathogens and are centrally involved in the initiation, maintenance and polarisation of the innate and adaptive immune response to infection. This review describes the defences employed by the epithelium of the respiratory and gastrointestinal tracts during viral infections with focus on epithelial modulation of the immune response at the innate/adaptive interface.

scholarly journals Immune Responses Induced by mRNA Vaccination in Mice, Monkeys and Humans

Vaccines ◽  
2021 ◽  
Vol 9 (1) ◽  
pp. 61
Author(s):  
Alberto Cagigi ◽  
Karin Loré
Keyword(s):  
Immune Response ◽  
Animal Models ◽  
Immune Responses ◽  
Viral Infections ◽  
Adaptive Immune Response ◽  
Adaptive Immune ◽  
Vaccine Trials ◽  
Concise Review

In this concise review, we summarize the concepts behind mRNA vaccination. We discuss the innate and adaptive immune response generated by mRNA vaccines in different animal models and in humans. We give examples of viral infections where mRNA vaccines have shown to induce potent responses and we discuss in more detail the recent SARS-CoV-2 mRNA vaccine trials in humans.

scholarly journals Long-term and short-term immunity to SARS-CoV-2: why it matters

2021 ◽  
Vol 42 (1) ◽  
pp. 34
Author(s):  
John Zaunders ◽  
Chansavath Phetsouphanh
Keyword(s):  
Immune Response ◽  
Adaptive Immunity ◽  
Viral Infections ◽  
Adaptive Immune Response ◽  
Recurrent Infection ◽  
Adaptive Immune System ◽  
Upper Respiratory Tract ◽  
Short Term ◽  
Adaptive Immune ◽  
Tract Infections

The adaptive immune system, regulated by CD4 T cells, is essential for control of many viral infections. Endemic coronavirus infections generally occur as short-term upper respiratory tract infections which in many cases appear to be cleared before adaptive immunity is fully involved, since adaptive immunity takes approximately 1.5–2 weeks to ramp up the response to a primary infection, or approximately 1 week for a recurrent infection. However, the adaptive immune response to SARS-CoV-2 infection will be critical to full recovery with minimal long-lasting effects, and to either prevention of recurrence of infection or at least reduced severity of symptoms. The detailed kinetics of this infection versus the dynamics of the immune response, including in vaccinated individuals, will largely determine these outcomes.

scholarly journals Modulation of Adaptive Immunity and Viral Infections by Ion Channels

2021 ◽  
Vol 12 ◽  
Author(s):  
Karen Bohmwald ◽  
Nicolás M. S. Gálvez ◽  
Catalina A. Andrade ◽  
Valentina P. Mora ◽  
José T. Muñoz ◽  
...  
Keyword(s):  
Immune Response ◽  
Ion Channels ◽  
Immune Cells ◽  
Viral Infections ◽  
Immune Cell ◽  
Ion Homeostasis ◽  
Adaptive Immune Response ◽  
Ionic Channels ◽  
Cellular Functions ◽  
Adaptive Immune

Most cellular functions require of ion homeostasis and ion movement. Among others, ion channels play a crucial role in controlling the homeostasis of anions and cations concentration between the extracellular and intracellular compartments. Calcium (Ca2+) is one of the most relevant ions involved in regulating critical functions of immune cells, allowing the appropriate development of immune cell responses against pathogens and tumor cells. Due to the importance of Ca2+ in inducing the immune response, some viruses have evolved mechanisms to modulate intracellular Ca2+ concentrations and the mobilization of this cation through Ca2+ channels to increase their infectivity and to evade the immune system using different mechanisms. For instance, some viral infections require the influx of Ca2+ through ionic channels as a first step to enter the cell, as well as their replication and budding. Moreover, through the expression of viral proteins on the surface of infected cells, Ca2+ channels function can be altered, enhancing the pathogen evasion of the adaptive immune response. In this article, we review those ion channels and ion transporters that are essential for the function of immune cells. Specifically, cation channels and Ca2+ channels in the context of viral infections and their contribution to the modulation of adaptive immune responses.

scholarly journals The Paradox of a Phagosomal Lifestyle: How Innate Host Cell-Leishmania amazonensis Interactions Lead to a Progressive Chronic Disease

2021 ◽  
Vol 12 ◽  
Author(s):  
Matheus B. Carneiro ◽  
Nathan C. Peters
Keyword(s):  
Immune Response ◽  
Chronic Disease ◽  
Host Cell ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
Leishmania Amazonensis ◽  
Host Cells ◽  
Adaptive Immune ◽  
Th2 Immunity ◽  
The Impact

Intracellular phagosomal pathogens represent a formidable challenge for innate immune cells, as, paradoxically, these phagocytic cells can act as both host cells that support pathogen replication and, when properly activated, are the critical cells that mediate pathogen elimination. Infection by parasites of the Leishmania genus provides an excellent model organism to investigate this complex host-pathogen interaction. In this review we focus on the dynamics of Leishmania amazonensis infection and the host innate immune response, including the impact of the adaptive immune response on phagocytic host cell recruitment and activation. L. amazonensis infection represents an important public health problem in South America where, distinct from other Leishmania parasites, it has been associated with all three clinical forms of leishmaniasis in humans: cutaneous, muco-cutaneous and visceral. Experimental observations demonstrate that most experimental mouse strains are susceptible to L. amazonensis infection, including the C57BL/6 mouse, which is resistant to other species such as Leishmania major, Leishmania braziliensis and Leishmania infantum. In general, the CD4+ T helper (Th)1/Th2 paradigm does not sufficiently explain the progressive chronic disease established by L. amazonensis, as strong cell-mediated Th1 immunity, or a lack of Th2 immunity, does not provide protection as would be predicted. Recent findings in which the balance between Th1/Th2 immunity was found to influence permissive host cell availability via recruitment of inflammatory monocytes has also added to the complexity of the Th1/Th2 paradigm. In this review we discuss the roles played by innate cells starting from parasite recognition through to priming of the adaptive immune response. We highlight the relative importance of neutrophils, monocytes, dendritic cells and resident macrophages for the establishment and progressive nature of disease following L. amazonensis infection.

scholarly journals How sticky should a virus be? The impact of virus binding and release on transmission fitness using influenza as an example

2014 ◽  
Vol 11 (92) ◽  
pp. 20131083 ◽  
Author(s):  
Andreas Handel ◽  
Victoria Akin ◽  
Sergei S. Pilyugin ◽  
Veronika Zarnitsyna ◽  
Rustom Antia
Keyword(s):  
Immune Response ◽  
Adaptive Immune Response ◽  
Virus Binding ◽  
Adaptive Immune ◽  
Cell Mediated Immune Response ◽  
Infected Cells ◽  
The Right ◽  
The Impact ◽  
Virus Fitness ◽  
Better Than

Budding viruses face a trade-off: virions need to efficiently attach to and enter uninfected cells while newly generated virions need to efficiently detach from infected cells. The right balance between attachment and detachment—the right amount of stickiness—is needed for maximum fitness. Here, we design and analyse a mathematical model to study in detail the impact of attachment and detachment rates on virus fitness. We apply our model to influenza, where stickiness is determined by a balance of the haemagglutinin (HA) and neuraminidase (NA) proteins. We investigate how drugs, the adaptive immune response and vaccines impact influenza stickiness and fitness. Our model suggests that the location in the ‘stickiness landscape’ of the virus determines how well interventions such as drugs or vaccines are expected to work. We discuss why hypothetical NA enhancer drugs might occasionally perform better than the currently available NA inhibitors in reducing virus fitness. We show that an increased antibody or T-cell-mediated immune response leads to maximum fitness at higher stickiness. We further show that antibody-based vaccines targeting mainly HA or NA, which leads to a shift in stickiness, might reduce virus fitness above what can be achieved by the direct immunological action of the vaccine. Overall, our findings provide potentially useful conceptual insights for future vaccine and drug development and can be applied to other budding viruses beyond influenza.

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