scholarly journals MAVS regulates the quality of the antibody response to West-Nile Virus

2020 ◽  
Vol 16 (10) ◽  
pp. e1009009
Author(s):  
Marvin O’Ketch ◽  
Spencer Williams ◽  
Cameron Larson ◽  
Jennifer L. Uhrlaub ◽  
Rachel Wong ◽  
...  
Keyword(s):  
Immune Response ◽  
West Nile Virus ◽  
Antibody Response ◽  
Adaptive Immunity ◽  
Viral Infections ◽  
Adaptive Immune Response ◽  
Neutralizing Antibody ◽  
West Nile ◽  
Humoral Immune

A key difference that distinguishes viral infections from protein immunizations is the recognition of viral nucleic acids by cytosolic pattern recognition receptors (PRRs). Insights into the functions of cytosolic PRRs such as the RNA-sensing Rig-I-like receptors (RLRs) in the instruction of adaptive immunity are therefore critical to understand protective immunity to infections. West Nile virus (WNV) infection of mice deficent of RLR-signaling adaptor MAVS results in a defective adaptive immune response. While this finding suggests a role for RLRs in the instruction of adaptive immunity to WNV, it is difficult to interpret due to the high WNV viremia, associated exessive antigen loads, and pathology in the absence of a MAVS-dependent innate immune response. To overcome these limitations, we have infected MAVS-deficient (MAVSKO) mice with a single-round-of-infection mutant of West Nile virus. We show that MAVSKO mice failed to produce an effective neutralizing antibody response to WNV despite normal antibody titers against the viral WNV-E protein. This defect occurred independently of antigen loads or overt pathology. The specificity of the antibody response in infected MAVSKO mice remained unchanged and was still dominated by antibodies that bound the neutralizing lateral ridge (LR) epitope in the DIII domain of WNV-E. Instead, MAVSKO mice produced IgM antibodies, the dominant isotype controlling primary WNV infection, with lower affinity for the DIII domain. Our findings suggest that RLR-dependent signals are important for the quality of the humoral immune response to WNV.

scholarly journals MAVS regulates the quality of the antibody response to West-Nile Virus

2019 ◽  
Author(s):  
Marvin O’Ketch ◽  
Cameron Larson ◽  
Spencer Williams ◽  
Jennifer L. Uhrlaub ◽  
Rachel Wong ◽  
...  
Keyword(s):  
Immune Response ◽  
West Nile Virus ◽  
Antibody Response ◽  
Adaptive Immunity ◽  
Viral Infections ◽  
Adaptive Immune Response ◽  
Neutralizing Antibody ◽  
West Nile ◽  
Humoral Immune

AbstractA key difference that distinguishes viral infections from protein immunizations is the recognition of viral nucleic acids by cytosolic pattern recognition receptors (PRRs) such as RNA-sensing Rig-I-like receptors (RLRs). Insights into the specific functions of cytosolic PRRs in the instruction of adaptive immunity are therefore critical for the understanding of protective immunity to infections. West Nile virus (WNV) infection of mice deficent of MAVS, the essential RLR signaling adaptor, results in a defective adaptive immune response. While this finding suggests a role for RLRs in the instruction of adaptive immunity to WNV, it is difficult to interpret due to the high WNV viremia, associated exessive antigen loads, and pathology in the absence of a MAVS-dependent innate immune response. To overcome these limitations, we have infected MAVS-deficient mice with a single-round-of-infection mutant of WNV called RepliVAX (RWN). RWN-infected MAVS-deficient (MAVSKO) mice failed to produce an effective neutralizing antibody response to WNV despite normal titers of antibodies targeting the viral WNV-E protein. This defect occurred indepedently of antigen loads or overt pathology. The specificity of the antibody response in RWN-infected MAVSKO mice remained unchanged and was still dominated by antibodies that bound the neutralizing lateral ridge (LR) epitope in the DIII domain of WNV-E. Instead, MAVSKO mice produced IgM antibodies, the dominant isotype controlling primary WNV infection, with lower affinity for the DIII domain. Our findings suggest that RLR-dependent signals are important for the quality of the humoral immune response to WNV.

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.

Live-attenuated recombinant equine herpesvirus type 1 (EHV-1) induces a neutralizing antibody response against West Nile virus (WNV)

2007 ◽  
Vol 125 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Cristina T. Rosas ◽  
B. Karsten Tischer ◽  
Gillian A. Perkins ◽  
Bettina Wagner ◽  
Laura B. Goodman ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Antibody Response ◽  
Neutralizing Antibody ◽  
Equine Herpesvirus ◽  
West Nile ◽  
Herpesvirus Type ◽  
Equine Herpesvirus Type ◽  
Equine Herpesvirus Type 1

scholarly journals Estimating biologically relevant parameters under uncertainty for experimental within-host murine West Nile virus infection

2016 ◽  
Vol 13 (117) ◽  
pp. 20160130 ◽  
Author(s):  
Soumya Banerjee ◽  
Jeremie Guedj ◽  
Ruy M. Ribeiro ◽  
Melanie Moses ◽  
Alan S. Perelson
Keyword(s):  
Immune Response ◽  
West Nile Virus ◽  
Humoral Immune Response ◽  
Basic Reproductive Number ◽  
Response Model ◽  
Wild Type ◽  
West Nile ◽  
Humoral Immune ◽  
Infectious Virion ◽  
The Mean

West Nile virus (WNV) is an emerging pathogen that has decimated bird populations and caused severe outbreaks of viral encephalitis in humans. Currently, little is known about the within-host viral kinetics of WNV during infection. We developed mathematical models to describe viral replication, spread and host immune response in wild-type and immunocompromised mice. Our approach fits a target cell-limited model to viremia data from immunocompromised knockout mice and an adaptive immune response model to data from wild-type mice. Using this approach, we first estimate parameters governing viral production and viral spread in the host using simple models without immune responses. We then use these parameters in a more complex immune response model to characterize the dynamics of the humoral immune response. Despite substantial uncertainty in input parameters, our analysis generates relatively precise estimates of important viral characteristics that are composed of nonlinear combinations of model parameters: we estimate the mean within-host basic reproductive number, R 0 , to be 2.3 (95% of values in the range 1.7–2.9); the mean infectious virion burst size to be 2.9 plaque-forming units (95% of values in the range 1.7–4.7); and the average number of cells infected per infectious virion to be between 0.3 and 0.99. Our analysis gives mechanistic insights into the dynamics of WNV infection and produces estimates of viral characteristics that are difficult to measure experimentally. These models are a first step towards a quantitative understanding of the timing and effectiveness of the humoral immune response in reducing host viremia and consequently the epidemic spread of WNV.

scholarly journals The mechanism of cross-protection afforded by dengue virus against West Nile virus in hamsters

1972 ◽  
Vol 70 (4) ◽  
pp. 611-617 ◽  
Author(s):  
Winston H. Price ◽  
Inderjit S. Thind
Keyword(s):  
West Nile Virus ◽  
Antibody Response ◽  
Dengue Virus ◽  
Neutralizing Antibody ◽  
New Guinea ◽  
Cross Protection ◽  
West Nile ◽  
Subsequent Challenge ◽  
Dengue Virus Serotypes ◽  
The Cross

SUMMARYThe protection afforded by similar concentrations of different dengue virus serotypes against a subsequent challenge of West Nile virus was studied in hamsters. The New Guinea C strain of dengue 2 virus gave the best protection. It was found that the anamnestic neutralizing antibody response induced by the challenge West Nile virus against West Nile virus in hamsters, previously immunized with dengue 2 virus, might play a major role in the cross-protection observed in this system.

scholarly journals The Interplay between Bluetongue Virus Infections and Adaptive Immunity

Viruses ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1511
Author(s):  
Daniel Rodríguez-Martín ◽  
Andrés Louloudes-Lázaro ◽  
Miguel Avia ◽  
Verónica Martín ◽  
José M. Rojas ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Adaptive Immunity ◽  
Bluetongue Virus ◽  
Viral Infections ◽  
Adaptive Immune Response ◽  
Γδ T Cells ◽  
Neutralizing Antibody ◽  
Immune Mechanisms ◽  
Adaptive Immune

Viral infections have long provided a platform to understand the workings of immunity. For instance, great strides towards defining basic immunology concepts, such as MHC restriction of antigen presentation or T-cell memory development and maintenance, have been achieved thanks to the study of lymphocytic choriomeningitis virus (LCMV) infections. These studies have also shaped our understanding of antiviral immunity, and in particular T-cell responses. In the present review, we discuss how bluetongue virus (BTV), an economically important arbovirus from the Reoviridae family that affects ruminants, affects adaptive immunity in the natural hosts. During the initial stages of infection, BTV triggers leucopenia in the hosts. The host then mounts an adaptive immune response that controls the disease. In this work, we discuss how BTV triggers CD8+ T-cell expansion and neutralizing antibody responses, yet in some individuals viremia remains detectable after these adaptive immune mechanisms are active. We present some unpublished data showing that BTV infection also affects other T cell populations such as CD4+ T-cells or γδ T-cells, as well as B-cell numbers in the periphery. This review also discusses how BTV evades these adaptive immune mechanisms so that it can be transmitted back to the arthropod host. Understanding the interaction of BTV with immunity could ultimately define the correlates of protection with immune mechanisms that would improve our knowledge of ruminant immunology.

scholarly journals The neutralizing antibody response against West Nile virus in naturally infected horses

Virology ◽  
2007 ◽  
Vol 359 (2) ◽  
pp. 336-348 ◽  
Author(s):  
Melissa D. Sánchez ◽  
Theodore C. Pierson ◽  
Marciela M. DeGrace ◽  
Lisa M. Mattei ◽  
Sheri L. Hanna ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Antibody Response ◽  
Neutralizing Antibody ◽  
West Nile

scholarly journals Immunological imprinting of the antibody response in COVID-19 patients

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Teresa Aydillo ◽  
Alexander Rombauts ◽  
Daniel Stadlbauer ◽  
Sadaf Aslam ◽  
Gabriela Abelenda-Alonso ◽  
...  
Keyword(s):  
Immune Response ◽  
Severe Acute Respiratory Syndrome ◽  
Antibody Response ◽  
Humoral Immune Response ◽  
Nucleocapsid Protein ◽  
Spike Protein ◽  
Ongoing Research ◽  
Variable Regions ◽  
Humoral Immune ◽  
Human Coronaviruses

AbstractIn addition to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), humans are also susceptible to six other coronaviruses, for which consecutive exposures to antigenically related and divergent seasonal coronaviruses are frequent. Despite the prevalence of COVID-19 pandemic and ongoing research, the nature of the antibody response against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is unclear. Here we longitudinally profile the early humoral immune response against SARS-CoV-2 in hospitalized coronavirus disease 2019 (COVID-19) patients and quantify levels of pre-existing immunity to OC43, HKU1 and 229E seasonal coronaviruses, and find a strong back-boosting effect to conserved but not variable regions of OC43 and HKU1 betacoronaviruses spike protein. However, such antibody memory boost to human coronaviruses negatively correlates with the induction of IgG and IgM against SARS-CoV-2 spike and nucleocapsid protein. Our findings thus provide evidence of immunological imprinting by previous seasonal coronavirus infections that can potentially modulate the antibody profile to SARS-CoV-2 infection.

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