Association of Severe Influenza Virus Infections With CD226 (DNAM-1) Variants

2019 ◽  
Vol 220 (7) ◽  
pp. 1162-1165 ◽  
Author(s):  
Monika Redlberger-Fritz ◽  
Hannes Vietzen ◽  
Elisabeth Puchhammer-Stöckl
Keyword(s):  
Influenza Virus ◽  
Intensive Care ◽  
Cell Response ◽  
Nk Cell ◽  
Virus Disease ◽  
Cell Receptor ◽  
Influenza Viruses ◽  
Virus Infections ◽  
Severe Influenza ◽  
Nk Cell Receptor

Abstract Natural killer (NK)-cell response against influenza viruses partly depends on expression of CD112, a ligand for NK-cell receptor CD226 (DNAM-1). We analyzed whether particular CD226 variants were associated with influenza disease severity. Comparison between 145 patients hospitalized with severe influenza at intensive care units (ICU) with 139 matched influenza-positive outpatients showed that presence of the rs763362 G allele (GG, AG) was associated with occurrence of severe influenza infections (P = .0076). Also, a higher frequency of rs727088 G and rs763361 T alleles was observed in the ICU group. Thus, CD226 variants may contribute to the severity of influenza virus disease.

scholarly journals Next generation methodology for updating HA vaccines against emerging human seasonal influenza A(H3N2) viruses

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
James D. Allen ◽  
Ted M. Ross
Keyword(s):  
Influenza Virus ◽  
Immune Responses ◽  
Influenza A ◽  
Seasonal Influenza ◽  
Influenza Viruses ◽  
Next Generation ◽  
Virus Infections ◽  
Wild Type ◽  
Influenza Hemagglutinin ◽  
H3n2 Influenza

AbstractWhile vaccines remain the best tool for preventing influenza virus infections, they have demonstrated low to moderate effectiveness in recent years. Seasonal influenza vaccines typically consist of wild-type influenza A and B viruses that are limited in their ability to elicit protective immune responses against co-circulating influenza virus variant strains. Improved influenza virus vaccines need to elicit protective immune responses against multiple influenza virus drift variants within each season. Broadly reactive vaccine candidates potentially provide a solution to this problem, but their efficacy may begin to wane as influenza viruses naturally mutate through processes that mediates drift. Thus, it is necessary to develop a method that commercial vaccine manufacturers can use to update broadly reactive vaccine antigens to better protect against future and currently circulating viral variants. Building upon the COBRA technology, nine next-generation H3N2 influenza hemagglutinin (HA) vaccines were designed using a next generation algorithm and design methodology. These next-generation broadly reactive COBRA H3 HA vaccines were superior to wild-type HA vaccines at eliciting antibodies with high HAI activity against a panel of historical and co-circulating H3N2 influenza viruses isolated over the last 15 years, as well as the ability to neutralize future emerging H3N2 isolates.

scholarly journals Sequential Seasonal H1N1 Influenza Virus Infections Protect Ferrets against Novel 2009 H1N1 Influenza Virus

2012 ◽  
Vol 87 (3) ◽  
pp. 1400-1410 ◽  
Author(s):  
Donald M. Carter ◽  
Chalise E. Bloom ◽  
Eduardo J. M. Nascimento ◽  
Ernesto T. A. Marques ◽  
Jodi K. Craigo ◽  
...  
Keyword(s):  
Influenza Virus ◽  
H1n1 Influenza ◽  
Cross Reactivity ◽  
Influenza Viruses ◽  
The Novel ◽  
Virus Infections ◽  
H1n1 Influenza Virus ◽  
Virus Shedding ◽  
2009 H1n1 ◽  
Novel H1n1 Influenza

ABSTRACTIndividuals <60 years of age had the lowest incidence of infection, with ∼25% of these people having preexisting, cross-reactive antibodies to novel 2009 H1N1 influenza. Many people >60 years old also had preexisting antibodies to novel H1N1. These observations are puzzling because the seasonal H1N1 viruses circulating during the last 60 years were not antigenically similar to novel H1N1. We therefore hypothesized that a sequence of exposures to antigenically different seasonal H1N1 viruses can elicit an antibody response that protects against novel 2009 H1N1. Ferrets were preinfected with seasonal H1N1 viruses and assessed for cross-reactive antibodies to novel H1N1. Serum from infected ferrets was assayed for cross-reactivity to both seasonal and novel 2009 H1N1 strains. These results were compared to those of ferrets that were sequentially infected with H1N1 viruses isolated prior to 1957 or more-recently isolated viruses. Following seroconversion, ferrets were challenged with novel H1N1 influenza virus and assessed for viral titers in the nasal wash, morbidity, and mortality. There was no hemagglutination inhibition (HAI) cross-reactivity in ferrets infected with any single seasonal H1N1 influenza viruses, with limited protection to challenge. However, sequential H1N1 influenza infections reduced the incidence of disease and elicited cross-reactive antibodies to novel H1N1 isolates. The amount and duration of virus shedding and the frequency of transmission following novel H1N1 challenge were reduced. Exposure to multiple seasonal H1N1 influenza viruses, and not to any single H1N1 influenza virus, elicits a breadth of antibodies that neutralize novel H1N1 even though the host was never exposed to the novel H1N1 influenza viruses.

scholarly journals Activating NK cell receptor ligands are differentially expressed during progression to cervical cancer

2008 ◽  
Vol 123 (10) ◽  
pp. 2343-2353 ◽  
Author(s):  
Sonja Textor ◽  
Matthias Dürst ◽  
Lars Jansen ◽  
Rosita Accardi ◽  
Massimo Tommasino ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Nk Cell ◽  
Cell Receptor ◽  
Differentially Expressed ◽  
Receptor Ligands ◽  
Nk Cell Receptor

scholarly journals Functionally and Structurally Distinct NK Cell Receptor Repertoires in the Peripheral Blood of Two Human Donors

Immunity ◽  
1997 ◽  
Vol 7 (6) ◽  
pp. 739-751 ◽  
Author(s):  
Nicholas M Valiante ◽  
Markus Uhrberg ◽  
Heather G Shilling ◽  
Kristin Lienert-Weidenbach ◽  
Kelly L Arnett ◽  
...  
Keyword(s):  
Peripheral Blood ◽  
Nk Cell ◽  
Cell Receptor ◽  
Nk Cell Receptor

KLRL1, a novel killer cell lectinlike receptor, inhibits natural killer cell cytotoxicity

Blood ◽  
2004 ◽  
Vol 104 (9) ◽  
pp. 2858-2866 ◽  
Author(s):  
Yanmei Han ◽  
Minghui Zhang ◽  
Nan Li ◽  
Taoyong Chen ◽  
Yi Zhang ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Natural Killer ◽  
Nk Cell ◽  
Killer Cell ◽  
Cell Receptor ◽  
Sh2 Domain ◽  
Target Cells ◽  
Lymphoid Tissues ◽  
Nk Cell Receptor ◽  
Human And Mouse

Abstract Natural killer (NK) cell inhibitory receptors play important roles in the regulation of target susceptibility to natural killing. Here, we report the molecular cloning and functional characterization of a novel NK cell receptor, KLRL1, from human and mouse dendritic cells. KLRL1 is a type II transmembrane protein with an immunoreceptor tyrosine-based inhibitory motif and a C-type lectinlike domain. The KLRL1 gene is located in the central region of the NK gene complex in both humans and mice, on human chromosome 12p13 and mouse chromosome 6F3, adjacent to the other KLR genes. KLRL1 is preferentially expressed in lymphoid tissues and immune cells, including NK cells, T cells, dendritic cells, and monocytes or macrophages. Western blot and fluorescence confocal microscopy analyses indicated that KLRL1 is a membrane-associated glycoprotein, which forms a heterodimer with an as yet unidentified partner. Human and mouse KLRL1 are both predicted to contain putative immunoreceptor tyrosine-based inhibitory motifs (ITIMs), and immunoprecipitation experiments demonstrated that KLRL1 associates with the tyrosine phosphatases SHP-1 (SH2-domain-containing protein tyrosine phosphatase 1) and SHP-2. Consistent with its potential inhibitory function, pretreatment of target cells with human KLRL1-Fc fusion protein enhances NK-mediated cytotoxicity. Taken together, our results demonstrate that KLRL1 belongs to the KLR family and is a novel inhibitory NK cell receptor.

scholarly journals The Mechanism behind Influenza Virus Cytokine Storm

Viruses ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 1362
Author(s):  
Yinuo Gu ◽  
Xu Zuo ◽  
Siyu Zhang ◽  
Zhuoer Ouyang ◽  
Shengyu Jiang ◽  
...  
Keyword(s):  
Influenza Virus ◽  
Recent Literature ◽  
Cell Communication ◽  
Influenza Viruses ◽  
Viral Clearance ◽  
Cytokine Storm ◽  
Biological Factors ◽  
Severe Influenza ◽  
Immune Pathology ◽  
Biological Differences

Influenza viruses are still a serious threat to human health. Cytokines are essential for cell-to-cell communication and viral clearance in the immune system, but excessive cytokines can cause serious immune pathology. Deaths caused by severe influenza are usually related to cytokine storms. The recent literature has described the mechanism behind the cytokine–storm network and how it can exacerbate host pathological damage. Biological factors such as sex, age, and obesity may cause biological differences between different individuals, which affects cytokine storms induced by the influenza virus. In this review, we summarize the mechanism behind influenza virus cytokine storms and the differences in cytokine storms of different ages and sexes, and in obesity.

scholarly journals Influenza Virus Resistance to Human Neutralizing Antibodies

mBio ◽  
2012 ◽  
Vol 3 (4) ◽  
Author(s):  
James E. Crowe
Keyword(s):  
Influenza Virus ◽  
B Cell ◽  
Neutralizing Antibodies ◽  
Cell Receptor ◽  
B Cell Receptor ◽  
Influenza Viruses ◽  
Surface Proteins ◽  
Progeny Virus ◽  
Human Antibody ◽  
Functional Surface

ABSTRACT The human antibody repertoire has an exceptionally large capacity to recognize new or changing antigens through combinatorial and junctional diversity established at the time of V(D)J recombination and through somatic hypermutation. Influenza viruses exhibit a relentless capacity to escape the human antibody response by altering the amino acids of their surface proteins in hypervariable domains that exhibit a high level of structural plasticity. Both parties in this high-stakes game of shape shifting drive structural evolution of their functional proteins (the B cell receptor/antibody on one side and the viral hemagglutinin and neuraminidase proteins on the other) using error-prone polymerase systems. It is likely that most of the genetic mutations that occur in these systems are deleterious, resulting in the failure of the B cell or virus with mutations to propagate in the immune repertoire or viral quasispecies. A subset of mutations is tolerated in functional surface proteins that enter the B cell or virus progeny pool. In both cases, selection occurs in the population of mutated and unmutated species. In cases where the functional avidity of the B cell receptor is increased significantly, that clone may be selected for preferential expansion. In contrast, an influenza virus that “escapes” the inhibitory effect of secreted antibodies may represent a high proportion of the progeny virus in that host. The recent paper by O’Donnell et al. [C. D. O’Donnell et al., mBio 3(3):e00120-12, 2012] identifies a mechanism for antibody resistance that does not require escape from binding but rather achieves a greater efficiency in replication.

scholarly journals THE INFECTION OF MICE WITH SWINE INFLUENZA VIRUS

1935 ◽  
Vol 62 (4) ◽  
pp. 561-572 ◽  
Author(s):  
Richard E. Shope
Keyword(s):  
Influenza Virus ◽  
Virus Disease ◽  
Swine Influenza Virus ◽  
Swine Influenza ◽  
Serial Passage ◽  
Virus Infections ◽  
Human Influenza ◽  
Human Influenza Virus ◽  
The Stability ◽  
At Will

The experiments confirm the earlier observation of Andrewes, Laidlaw and Smith that the swine influenza virus is pathogenic for white mice when administered intranasally. Two field strains of the swine influenza virus were found to differ in their initial pathogenicity for mice. One strain was apparently fully pathogenic even in its 1st mouse passage while the other required 2 or 3 mouse passages to acquire full virulence for this species. Both strains, however, were initially infectious for mice, without the necessity of intervening ferret passages. There is no evidence that bacteria play any significant rôle in the mouse disease though essential in that of swine, and fatal pneumonias can be produced in mice by pure virus infections. Mice surviving the virus disease are immune to reinfection for at least a month. In mice the disease is not contagious though it is notably so in swine. The virus, while regularly producing fatal pneumonias when administered intranasally to mice, appears to be completely innocuous when given subcutaneously or intraperitoneally. Prolonged serial passage of the virus in mice does not influence its infectivity or virulence for swine or ferrets. It is a stable virus so far as its infectivity is concerned, and can be transferred at will from any one of its three known susceptible hosts to any other. In discussing these facts the stability of the swine influenza virus has been contrasted with the apparent instability of freshly isolated strains of the human influenza virus. Though the mouse is an un-natural host for the virus it is, nevertheless, useful for the study of those aspects of swine influenza which have to do with the virus only.

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