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Multiple Sclerosis
Published in Irun R. Cohen, Perspectives on Autoimmunity, 2020
It is of interest that, in a study of MS twin sets, some discordant for MS, an unusually intense peripheral blood T-cell response to measles virus was found in 7 affected twins with active MS, among 28 concordant and discordant twin pairs.211 All other individuals showed low responses to measles antigens. Patients with stable MS gave low responses as well. Responses elicited with mumps and vaccinia virus were low throughout. We shall be talking later of “original antigenic sin”. It is possible that these measles-positive cells reflect events at or about the time of the initial triggering of the MS disease process. Alternatively, there may be a deficiency of certain antigen-specific suppressor T-cells. An apparently specific finding, uncovered by Jacobson et al.,211a is the virtually total absence of “precursors” for measles-specific, class II MHC-restricted, cytotoxic T-cells in MS patients in contrast to controls. A similar deficit was not seen of precursors for mumps (class II) or influenza (class I)-restricted CTL. A parallel observation is the low level of measles-specific lymphokine-producing cells in MS patients, reported several years ago.211b
Dengue Hemorrhagic Fever
Published in James H. S. Gear, CRC Handbook of Viral and Rickettsial Hemorrhagic Fevers, 2019
These observations serve as a reminder that solid data on risk factors only have been prized from carefully planned, time consuming, and expensive prospective epidemiological studies and their spin-off research (or, hopefully, in the case of Cuba, rigorously designed retrospective studies). Even in the absence of DSS, there are important questions which can be answered through the prospective epidemiological study format in dengue endemic areas. For example, what are the long-term kinetics of neutralizing and enhancing dengue antibodies? Are heterotypic neutralizing antibodies a function of infecting strain or infected host? How accurate is the phenomenon of “original antigenic sin”? These and other studies require the addition of neutralizing and enhancing antibody assays to the standard dengue laboratory repertoire. Whether research questions concern viral virulence or immunogenetics, the most valuable resource for study remains man himself.
Neurological Dengue
Published in Sunit K. Singh, Daniel Růžek, Neuroviral Infections, 2013
Presentation of dengue antigens initiates a clonal expansion of CD8+ (cytotoxic) and CD4+ (helper) T-lymphocytes. Following resolution a significant number remain and render lifelong immunity to that serotype. However, the serotypes are sufficiently heterogenous in their antigenicity that infection with one does not confer immunity to the others. Preferential activation of memory T-lymphocytes from the primary infection at the expense of generating a new and more specific cell-mediated response (a concept dubbed “original antigenic sin”) delivers a sub-optimal response which may be at least partly responsible for the increased severity of secondary infections (Martina et al. 2009).
Toward an effective Staphylococcus vaccine: why have candidates failed and what is the next step?
Published in Expert Review of Vaccines, 2023
Chih-Ming Tsai, Jr Caldera, Irshad A. Hajam, George Y. Liu
Further investigation revealed that IsdB-specific antibodies, although abundantly generated in S. aureus pre-exposed mice, were non-neutralizing and had no effect on the opsonophagocytic killing of S. aureus by neutrophils [5]. Immunizing S. aureus-exposed mice with IsdB led to the generation of antibodies that shared these non-protective features, in sharp contrast to the protective antibodies generated by the same vaccine in naïve mice. Effectively, the preferential recall of non-protective B cell clone was the responsible mechanism and doomed the vaccine to failure. These findings largely follow the ‘original antigenic sin’ hypothesis that explains the reduced protective antibody response to influenza strains that have undergone seasonal antigenic drift [9]. Notably, we also found that the recalled non-protective anti-IsdB antibodies further suppressed the efficacy of protective IsdB-specific antibodies by competition. Together, these data provide a mechanistic basis for the significant and unexpected failures of the highly promising IsdB vaccine candidate.
Original antigen sin and COVID-19: implications for seasonal vaccination
Published in Expert Opinion on Biological Therapy, 2022
Original antigenic sin may reveal an asymmetric pattern of protective antibody cross-reactivity determined by exposure to previously existing strains of a given pathogen, and this phenomenon appears to occur more frequently in response to viruses [25–27]. Early work on immune imprinting focused primarily on the response to influenza [28–30]. This was due to the presumed influenza anamnesis of the human population born before 1956 – the year when A(H1NI) influenza viruses came out of circulation [31]. However, the phenomenon original antigenic sin has also been observed in response to dengue, a viral infection transmitted to humans through the bite of infected mosquitoes [32]. Symptoms typically occur 3 to 14 days after infection and may include fever, joint pains, rash, nausea, vomiting, and headache [33]. In some cases, the condition progresses to dengue hemorrhagic fever, which results in bleeding and severe hypotension that may be lethal [34–36].
COVID-19 during Pregnancy and Postpartum:
Published in Journal of Dietary Supplements, 2022
Sreus A. G. Naidu, Roger A. Clemens, Peter Pressman, Mehreen Zaigham, Kamran Kadkhoda, Kelvin J. A. Davies, A. Satyanarayan Naidu
The immunological imprint established by the original virus infection governs the antibody response thereafter, which is conventionally known as the doctrine of the “Original Antigenic Sin”. Some viruses (e.g. CoVs, HIV, HBV) are initially controlled by cytotoxic T-lymphocytes, but may subsequently escape through mutation of the relevant T-cell epitope. Some of these mutations preserve the normal binding to MHC class-I molecules, but present an altered surface to the T-cell antigen receptor (Klenerman and Zinkernagel 1998). Therefore, human individuals primed with a virus (i.e. SARS-CoV) may respond to a subsequent infection by related virus bearing-epitope variant (i.e. SARS-CoV-2) with a CTL response directed against the initial epitope rather than against the new variant epitope. This phenomenon of 'original antigenic sin (OAS)' was initially described with influenza and is an asymmetric pattern of protective antibody cross-reactivity determined by exposure to previously existing strains. OAS leads to impaired clearance of variant viruses infecting the same individual and may enhance the immune escape of mutant viruses evolving in an individual host.