Infection with influenza A/Victoria virus in Houston families, 1976

SUMMARYIn 1976, an epidemic caused by infections with an influenza virus antigenically similar to A/Victoria/75 (H3N2) occurred in Houston, Texas. During this outbreak, 37 families (155 members) enrolled in the Houston Family Study were under observation. The families lived throughout the metropolitan area (Houston, Texas), and were representative of low income groups. The overall frequency of infection in family members was 27·7%. The frequency of infection was the highest for infants under one year of age and for their older siblings, 14 (37·8%) of 37 and 17 (33·3%) of 51, respectively. Eighteen (48·6%) of the 37 families had at least one infected member. Twelve of the 18 ‘infected’ families had school aged children, whereas only three of the 19 ‘non-infected’ families had school aged children (P < 0·01). These infected families were also larger and had increased household density (persons/rooms). The levels of pre-existing HI antibodies to A/Victoria/75 and A/Port Chalmers/73 were inversely related to frequencies of infection and illness associated with A/Victoria/75 virus. Three children required hospitalization as direct consequence of their infection with this H3N2 influenza virus. Antibody response to infection was related to previous experience with antigenically-related influenza A (H3N2) viruses according to Francis', ‘doctrine of original antigenic sin.’

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Evaluation of cytokine production by J774.G8 macrophages after treatment with biotherapics

International Journal of High Dilution Research - ISSN 1982-6206 ◽

10.51910/ijhdr.v10i36.496 ◽

2021 ◽

Vol 10 (36) ◽

pp. 167-169

Author(s):

Camila Siqueira ◽

Diogo Kuczera ◽

Eneida Da Lozzo ◽

Dorly Buchi ◽

JosÃƒÆ’Ã‚Â© Nelson Couceiro ◽

...

Keyword(s):

Influenza Virus ◽

Viral Infection ◽

Influenza A ◽

Control Groups ◽

Viral Particles ◽

Significant Difference ◽

Infected Cells ◽

H3n2 Influenza ◽

Aseptic Conditions ◽

H3n2 Influenza Virus

Introduction: Strains of macrophages, such as murine J774.G8 macrophages, are susceptible to influenza A infection [1]. One of the responses to viral infection involves the production of various types of immunostimulatory cytokines by infected cells [2]. Methods: In the present study, the macrophage strain J774.G8, maintained in RPMI medium, was submitted to treatment with 10% V/V of two different biotherapics prepared from influenza H3N2, both at 30x. Additionally, two control groups were analyzed: macrophages stimulated with water 30x and macrophages without any treatment. Biotherapics were prepared from intact H3N2 influenza virus and H3N2 inactivated by alcohol 70%. The compounding of both biotherapics followed this procedure: one part of viral particles was diluted in 9 parts of sterile distilled water. The 1:10 sample was submitted to 100 mechanical succussions using AuticÃƒâ€šÃ‚Â® Brazilian machine, originating the first dilution, named decimal (1x). 1 ml of this solution was diluted in 9 ml of solvent and was submitted to 100 succussions, generating biotherapic 2x. This procedure was successively repeated, according to Brazilian Homeopathic Pharmacopoeia, to obtain the biotherapic 30x. By the same technique, water vehicle was prepared in the potency of 30x to be used as control. All samples were prepared under sterile and aseptic conditions, using laminar flow cabinet, class II, and were stored in the refrigerator (8Ãƒâ€šÃ‚ÂºC), to avoid microbiological contamination. J774.G8 macrophages were stimulated for 2 days, in a total of six stimuli. Immediately before infection with 25 Ãƒâ€šÃ‚Âµl of H3N2 influenza virus, the supernatants were collected and frozen at -20 Ãƒâ€šÃ‚ÂºC for later analysis. Next, 24 hours after the virus infection, the supernatants were aliquoted and frozen under the same conditions. Three independent experiments were done in triplicate. Analysis of supernatants was performed by flow cytometry using the Mouse Inflammation Kit. The cytokines detected in this experiment were IL-10, IL 12, TNF-ÃƒÅ½Ã‚Â± and MCP1. Results: In all cases, there were no significant differences compared to control groups. However, the production of TNF-ÃƒÅ½Ã‚Â± detected in macrophages treated by intact and inactivated biotherapics presented a tendency to increase after infection. In fact, similar results were previously detected in other experiments conducted only with the intact biotherapic [3]. The release of the cytokine MCP1 in all experimental situations presented a tendency to decrease after the viral infection when compared to untreated macrophages. No statistically significant difference was detected in the production of IL 12 and IL 10. These experiments will be repeated to confirm the data obtained.

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In Vitro Characterization of A-315675, a Highly Potent Inhibitor of A and B Strain Influenza Virus Neuraminidases and Influenza Virus Replication

Antimicrobial Agents and Chemotherapy ◽

10.1128/aac.46.4.1014-1021.2002 ◽

2002 ◽

Vol 46 (4) ◽

pp. 1014-1021 ◽

Cited By ~ 78

Author(s):

Warren M. Kati ◽

Debra Montgomery ◽

Robert Carrick ◽

Larisa Gubareva ◽

Clarence Maring ◽

...

Keyword(s):

Cell Culture ◽

Influenza Virus ◽

Virus Replication ◽

Influenza A ◽

Strong Support ◽

Oseltamivir Carboxylate ◽

Influenza Virus Replication ◽

H3n2 Influenza ◽

H3n2 Influenza Virus

ABSTRACT A-315675 is a novel, pyrrolidine-based compound that was evaluated in this study for its ability to inhibit A and B strain influenza virus neuraminidases in enzyme assays and influenza virus replication in cell culture. A-315675 effectively inhibited influenza A N1, N2, and N9 and B strain neuraminidases with inhibitor constant (Ki ) values between 0.024 and 0.31 nM. These values were comparable to or lower than the Ki values measured for oseltamivir carboxylate (GS4071), zanamivir, and BCX-1812, except for the N1 enzymes that were found to be the most sensitive to BCX-1812. The time-dependent inhibition of neuraminidase catalytic activity observed with A-315675 is likely due to its very low rate of dissociation from the active site of neuraminidase. The half times for dissociation of A-315675 from B/Memphis/3/89 and A/Tokyo/3/67 (H3N2) influenza virus neuraminidases of 10 to 12 h are significantly slower than the half times measured for oseltamivir carboxylate (33 to 60 min). A-315675 inhibited the replication of several laboratory strains of influenza virus in cell culture with potencies that were comparable or superior to those for oseltamivir carboxylate and BCX-1812, except for the A/H1N1 viruses that were found to be two- to fourfold more susceptible to BCX-1812. A-315675 and oseltamivir carboxylate exhibited comparable potencies against a panel of A/H1N1 and A/H3N2 influenza virus clinical isolates, but A-315675 was found to be significantly more potent than oseltamivir carboxylate against the B strain isolates. The favorable in vitro results relative to other clinically effective agents provide strong support for the further investigation of A-315675 as a potential therapy for influenza virus infections.

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Structure of an H3N2 influenza virus nucleoprotein

Acta Crystallographica Section F Structural Biology Communications ◽

10.1107/s2053230x2100635x ◽

2021 ◽

Vol 77 (7) ◽

Author(s):

Michael L. Knight ◽

Haitian Fan ◽

David L. V. Bauer ◽

Jonathan M. Grimes ◽

Ervin Fodor ◽

...

Keyword(s):

Influenza Virus ◽

Influenza A ◽

Rna Binding ◽

H3n2 Virus ◽

Influenza A Viruses ◽

Seasonal Epidemic ◽

H3n2 Influenza ◽

Structural Levels ◽

Viral Genomic Rna ◽

H3n2 Influenza Virus

Influenza A viruses of the H1N1 and H3N2 subtypes are responsible for seasonal epidemic events. The influenza nucleoprotein (NP) binds to the viral genomic RNA and is essential for its replication. Efforts are under way to produce therapeutics and vaccines targeting the NP. Despite this, no structure of an NP from an H3N2 virus has previously been determined. Here, the structure of the A/Northern Territory/60/1968 (H3N2) influenza virus NP is presented at 2.2 Å resolution. The structure is highly similar to those of the A/WSN/1933 (H1N1) and A/Hong Kong/483/97 (H5N1) NPs. Nonconserved amino acids are widely dispersed both at the sequence and structural levels. A movement of the 73–90 RNA-binding loop is observed to be the key difference between the structure determined here and previous structures. The data presented here increase the understanding of structural conservation amongst influenza NPs and may aid in the design of universal interventions against influenza.

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H3N2 influenza virus infection enhances Oncostatin M expression in human nasal epithelium

10.26226/morressier.5afd6e2ed64f25002cfc3664 ◽

2018 ◽

Author(s):

TENGFEI TIAN

Keyword(s):

Influenza Virus ◽

Virus Infection ◽

Influenza Virus Infection ◽

Oncostatin M ◽

Nasal Epithelium ◽

Human Nasal Epithelium ◽

H3n2 Influenza ◽

H3n2 Influenza Virus

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

Scientific Reports ◽

10.1038/s41598-020-79590-7 ◽

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.

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Chimeric Hemagglutinin-Based Live-Attenuated Vaccines Confer Durable Protective Immunity against Influenza A Viruses in a Preclinical Ferret Model

Vaccines ◽

10.3390/vaccines9010040 ◽

2021 ◽

Vol 9 (1) ◽

pp. 40

Author(s):

Wen-Chun Liu ◽

Raffael Nachbagauer ◽

Daniel Stadlbauer ◽

Shirin Strohmeier ◽

Alicia Solórzano ◽

...

Keyword(s):

Influenza Virus ◽

Influenza A ◽

Influenza Virus Infection ◽

Influenza Virus Vaccine ◽

Antibody Responses ◽

Upper Respiratory Tract ◽

Influenza A Viruses ◽

Humoral And Cellular Immunity ◽

Stalk Domain ◽

One Year

Epidemic or pandemic influenza can annually cause significant morbidity and mortality in humans. We developed novel chimeric hemagglutinin (cHA)-based universal influenza virus vaccines, which contain a conserved HA stalk domain from a 2009 pandemic H1N1 (pH1N1) strain combined with globular head domains from avian influenza A viruses. Our previous reports demonstrated that prime-boost sequential immunizations induced robust antibody responses directed toward the conserved HA stalk domain in ferrets. Herein, we further followed vaccinated animals for one year to compare the efficacy and durability of these vaccines in the preclinical ferret model of influenza. Although all cHA-based immunization regimens induced durable HA stalk-specific and heterosubtypic antibody responses in ferrets, sequential immunization with live-attenuated influenza virus vaccines (LAIV-LAIV) conferred the best protection against upper respiratory tract infection by a pH1N1 influenza A virus. The findings from this study suggest that our sequential immunization strategy for a cHA-based universal influenza virus vaccine provides durable protective humoral and cellular immunity against influenza virus infection.

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