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influenza a virus h1n1 strain a pr 8 34  (ATCC)


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    ATCC influenza a virus h1n1 strain a pr 8 34
    Differentiation of nasal airway cell cultures and impact of HRV and influenza infection on mediators of airway inflammation (IL-1β and IL-6) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and <t>H1N1</t> for 24 and 48 h, as described in the methods. (A) hNEC differentiation was confirmed by qPCR using four independent differentiation genes that are not expressed in non-ciliated basal undifferentiated cells (FOX-J1, CCP-110, CDHR3) and for MUC5AC as described in Methods. (B–E) Proinflammatory cytokines interleukin 1 beta (IL-1β) (B,C) and IL-6 (D,E) were determined by multiplex Luminex immunoassay in both apical (B,D) and basal (C,E) chambers of air-liquid interface (ALI) inserts as described in methods. All panels show summary data as mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparisons between the uninfected control group and each experimental group were performed using a two-tailed Mann–Whitney test and are indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway differentiation and inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.
    Influenza A Virus H1n1 Strain A Pr 8 34, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 203 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/virus+h1n1/Influenza+A+virus/pmc13272445-48-8-19
    Average 95 stars, based on 203 article reviews
    influenza a virus h1n1 strain a pr 8 34 - by Bioz Stars, 2026-09
    95/100 stars

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    1) Product Images from "Ex vivo modeling of nasal epithelial airway inflammation in respiratory viral infections"

    Article Title: Ex vivo modeling of nasal epithelial airway inflammation in respiratory viral infections

    Journal: Frontiers in Microbiology

    doi: 10.3389/fmicb.2026.1819581

    Differentiation of nasal airway cell cultures and impact of HRV and influenza infection on mediators of airway inflammation (IL-1β and IL-6) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A) hNEC differentiation was confirmed by qPCR using four independent differentiation genes that are not expressed in non-ciliated basal undifferentiated cells (FOX-J1, CCP-110, CDHR3) and for MUC5AC as described in Methods. (B–E) Proinflammatory cytokines interleukin 1 beta (IL-1β) (B,C) and IL-6 (D,E) were determined by multiplex Luminex immunoassay in both apical (B,D) and basal (C,E) chambers of air-liquid interface (ALI) inserts as described in methods. All panels show summary data as mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparisons between the uninfected control group and each experimental group were performed using a two-tailed Mann–Whitney test and are indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway differentiation and inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.
    Figure Legend Snippet: Differentiation of nasal airway cell cultures and impact of HRV and influenza infection on mediators of airway inflammation (IL-1β and IL-6) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A) hNEC differentiation was confirmed by qPCR using four independent differentiation genes that are not expressed in non-ciliated basal undifferentiated cells (FOX-J1, CCP-110, CDHR3) and for MUC5AC as described in Methods. (B–E) Proinflammatory cytokines interleukin 1 beta (IL-1β) (B,C) and IL-6 (D,E) were determined by multiplex Luminex immunoassay in both apical (B,D) and basal (C,E) chambers of air-liquid interface (ALI) inserts as described in methods. All panels show summary data as mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparisons between the uninfected control group and each experimental group were performed using a two-tailed Mann–Whitney test and are indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway differentiation and inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Techniques Used: Infection, Ex Vivo, Multiplex Assay, Luminex, Control, Two Tailed Test, MANN-WHITNEY, Comparison, Cell Culture

    Impact of HRV and influenza infection on mediators of airway inflammation (IL-8, IL-10) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A–D) Proinflammatory cytokines interleukin 8 (IL-8 (A,B) and IL-10 (C,D) were determined by multiplex Luminex immunoassay in both the apical (A,C) and basal (B,D) chambers of air-liquid interface (ALI) inserts, as described in the methods. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test and is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.
    Figure Legend Snippet: Impact of HRV and influenza infection on mediators of airway inflammation (IL-8, IL-10) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A–D) Proinflammatory cytokines interleukin 8 (IL-8 (A,B) and IL-10 (C,D) were determined by multiplex Luminex immunoassay in both the apical (A,C) and basal (B,D) chambers of air-liquid interface (ALI) inserts, as described in the methods. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test and is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Techniques Used: Infection, Ex Vivo, Multiplex Assay, Luminex, Comparison, Control, Two Tailed Test, MANN-WHITNEY, Cell Culture

    Impact of HRV and influenza infection on mediators of airway inflammation (TNF-α, VEGF) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A–D) Proinflammatory cytokines, tumor necrosis factor alpha (TNF-α) (A,B) and Vascular endothelial growth factor (VEGF) (C,D) , were determined by multiplex Luminex immunoassay in both the apical (A,C) and basal (B,D) chambers of air-liquid interface (ALI) inserts, as described in the methods. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test and is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.
    Figure Legend Snippet: Impact of HRV and influenza infection on mediators of airway inflammation (TNF-α, VEGF) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A–D) Proinflammatory cytokines, tumor necrosis factor alpha (TNF-α) (A,B) and Vascular endothelial growth factor (VEGF) (C,D) , were determined by multiplex Luminex immunoassay in both the apical (A,C) and basal (B,D) chambers of air-liquid interface (ALI) inserts, as described in the methods. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test and is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Techniques Used: Infection, Ex Vivo, Multiplex Assay, Luminex, Comparison, Control, Two Tailed Test, MANN-WHITNEY, Cell Culture

    Impact of HRV and influenza infection on secretion of proinflammatory cytokines in apical versus basal surface in ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 (A) and 48 (B) h, as described in the methods. The mean value of each protein measurement in each apical cell culture supernatant was normalized to the mean value of protein content in the same basal cell culture supernatant of the same ALI well. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in apical versus basal surfaces of human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.
    Figure Legend Snippet: Impact of HRV and influenza infection on secretion of proinflammatory cytokines in apical versus basal surface in ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 (A) and 48 (B) h, as described in the methods. The mean value of each protein measurement in each apical cell culture supernatant was normalized to the mean value of protein content in the same basal cell culture supernatant of the same ALI well. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in apical versus basal surfaces of human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Techniques Used: Infection, Ex Vivo, Cell Culture, Comparison, Control, Two Tailed Test, MANN-WHITNEY

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    Anti-influenza effects of stevioside, curcuminoids, and C-S/M in MDCK cells. ( A ) Cytotoxicity of stevioside (25–200 µg/mL), curcuminoids (6.25–50 µg/mL), and C–S/M (25–200 µg/mL) in MDCK cells was assessed using an MTT assay and is presented as relative cell viability compared with untreated control. ( B ) MDCK cells were <t>infected</t> <t>with</t> <t>A/PR/8/34</t> at an MOI of 0.001 and treated with the indicated concentrations of stevioside, curcuminoids, or C-S/M. At 72 hpi, IAV-induced cytopathic effects (CPE) under different treatments were evaluated using a neutral red assay. Data are presented as the mean ± SEM. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s multiple comparisons test. * p < 0.05; ** p < 0.01; and *** p < 0.001.
    Iav H1n1 Strain A Pr8 8 34, supplied by ATCC, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    influenza virus h1n1  (ATCC)
    93
    ATCC influenza virus h1n1
    Synthesis of compound <t>H1N1-17.</t> Reagents and conditions: (a) NaHCO 3 , (Boc) 2 O, acetone/H 2 O = 1:1, 0 °C to rt; (b) N , O -dimethylhydroxylamine hydrochloride, i PrMgCl, THF, 0 °C to rt; (c) allylmagnesium chloride, THF, −60 °C; (d) (i) 9-BBN, THF, 0 °C to rt; (ii) H 2 O, NaBO 3 ·4H 2 O, THF, 0 °C to rt; (e) methoxyammonium chloride, pyridine, 80 °C; (f) NaOAc, MeOH, 40 °C; (g) K 2 CO 3 , [Ru( p -cymene)Cl 2 ] 2 , 2,2,2-trifluoroethan-1-ol, 65 °C; (h) (i) TFA, DCM, rt; (ii) HATU, DIPEA, DMF, 0 °C to rt; (i) NaOH, MeOH/H 2 O = 1:1, 0–50 °C; (j) (i) 2,4,6-trichlorobenzoyl chloride, Et 3 N, THF, 0 °C to rt; (ii) DMAP, THF, 40 °C.
    Influenza Virus H1n1, supplied by ATCC, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    human h1n1 influenza virus a nws 33  (ATCC)
    99
    ATCC human h1n1 influenza virus a nws 33
    Synthesis of compound <t>H1N1-17.</t> Reagents and conditions: (a) NaHCO 3 , (Boc) 2 O, acetone/H 2 O = 1:1, 0 °C to rt; (b) N , O -dimethylhydroxylamine hydrochloride, i PrMgCl, THF, 0 °C to rt; (c) allylmagnesium chloride, THF, −60 °C; (d) (i) 9-BBN, THF, 0 °C to rt; (ii) H 2 O, NaBO 3 ·4H 2 O, THF, 0 °C to rt; (e) methoxyammonium chloride, pyridine, 80 °C; (f) NaOAc, MeOH, 40 °C; (g) K 2 CO 3 , [Ru( p -cymene)Cl 2 ] 2 , 2,2,2-trifluoroethan-1-ol, 65 °C; (h) (i) TFA, DCM, rt; (ii) HATU, DIPEA, DMF, 0 °C to rt; (i) NaOH, MeOH/H 2 O = 1:1, 0–50 °C; (j) (i) 2,4,6-trichlorobenzoyl chloride, Et 3 N, THF, 0 °C to rt; (ii) DMAP, THF, 40 °C.
    Human H1n1 Influenza Virus A Nws 33, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    h1n1 influenza virus  (ATCC)
    99
    ATCC h1n1 influenza virus
    Synthesis of compound <t>H1N1-17.</t> Reagents and conditions: (a) NaHCO 3 , (Boc) 2 O, acetone/H 2 O = 1:1, 0 °C to rt; (b) N , O -dimethylhydroxylamine hydrochloride, i PrMgCl, THF, 0 °C to rt; (c) allylmagnesium chloride, THF, −60 °C; (d) (i) 9-BBN, THF, 0 °C to rt; (ii) H 2 O, NaBO 3 ·4H 2 O, THF, 0 °C to rt; (e) methoxyammonium chloride, pyridine, 80 °C; (f) NaOAc, MeOH, 40 °C; (g) K 2 CO 3 , [Ru( p -cymene)Cl 2 ] 2 , 2,2,2-trifluoroethan-1-ol, 65 °C; (h) (i) TFA, DCM, rt; (ii) HATU, DIPEA, DMF, 0 °C to rt; (i) NaOH, MeOH/H 2 O = 1:1, 0–50 °C; (j) (i) 2,4,6-trichlorobenzoyl chloride, Et 3 N, THF, 0 °C to rt; (ii) DMAP, THF, 40 °C.
    H1n1 Influenza Virus, supplied by ATCC, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    quantitative genomic rna  (ATCC)
    94
    ATCC quantitative genomic rna
    Synthesis of compound <t>H1N1-17.</t> Reagents and conditions: (a) NaHCO 3 , (Boc) 2 O, acetone/H 2 O = 1:1, 0 °C to rt; (b) N , O -dimethylhydroxylamine hydrochloride, i PrMgCl, THF, 0 °C to rt; (c) allylmagnesium chloride, THF, −60 °C; (d) (i) 9-BBN, THF, 0 °C to rt; (ii) H 2 O, NaBO 3 ·4H 2 O, THF, 0 °C to rt; (e) methoxyammonium chloride, pyridine, 80 °C; (f) NaOAc, MeOH, 40 °C; (g) K 2 CO 3 , [Ru( p -cymene)Cl 2 ] 2 , 2,2,2-trifluoroethan-1-ol, 65 °C; (h) (i) TFA, DCM, rt; (ii) HATU, DIPEA, DMF, 0 °C to rt; (i) NaOH, MeOH/H 2 O = 1:1, 0–50 °C; (j) (i) 2,4,6-trichlorobenzoyl chloride, Et 3 N, THF, 0 °C to rt; (ii) DMAP, THF, 40 °C.
    Quantitative Genomic Rna, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    flua virus h1n1 strain a pr 8 34  (ATCC)
    94
    ATCC flua virus h1n1 strain a pr 8 34
    Synthesis of compound <t>H1N1-17.</t> Reagents and conditions: (a) NaHCO 3 , (Boc) 2 O, acetone/H 2 O = 1:1, 0 °C to rt; (b) N , O -dimethylhydroxylamine hydrochloride, i PrMgCl, THF, 0 °C to rt; (c) allylmagnesium chloride, THF, −60 °C; (d) (i) 9-BBN, THF, 0 °C to rt; (ii) H 2 O, NaBO 3 ·4H 2 O, THF, 0 °C to rt; (e) methoxyammonium chloride, pyridine, 80 °C; (f) NaOAc, MeOH, 40 °C; (g) K 2 CO 3 , [Ru( p -cymene)Cl 2 ] 2 , 2,2,2-trifluoroethan-1-ol, 65 °C; (h) (i) TFA, DCM, rt; (ii) HATU, DIPEA, DMF, 0 °C to rt; (i) NaOH, MeOH/H 2 O = 1:1, 0–50 °C; (j) (i) 2,4,6-trichlorobenzoyl chloride, Et 3 N, THF, 0 °C to rt; (ii) DMAP, THF, 40 °C.
    Flua Virus H1n1 Strain A Pr 8 34, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Differentiation of nasal airway cell cultures and impact of HRV and influenza infection on mediators of airway inflammation (IL-1β and IL-6) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A) hNEC differentiation was confirmed by qPCR using four independent differentiation genes that are not expressed in non-ciliated basal undifferentiated cells (FOX-J1, CCP-110, CDHR3) and for MUC5AC as described in Methods. (B–E) Proinflammatory cytokines interleukin 1 beta (IL-1β) (B,C) and IL-6 (D,E) were determined by multiplex Luminex immunoassay in both apical (B,D) and basal (C,E) chambers of air-liquid interface (ALI) inserts as described in methods. All panels show summary data as mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparisons between the uninfected control group and each experimental group were performed using a two-tailed Mann–Whitney test and are indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway differentiation and inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Journal: Frontiers in Microbiology

    Article Title: Ex vivo modeling of nasal epithelial airway inflammation in respiratory viral infections

    doi: 10.3389/fmicb.2026.1819581

    Figure Lengend Snippet: Differentiation of nasal airway cell cultures and impact of HRV and influenza infection on mediators of airway inflammation (IL-1β and IL-6) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A) hNEC differentiation was confirmed by qPCR using four independent differentiation genes that are not expressed in non-ciliated basal undifferentiated cells (FOX-J1, CCP-110, CDHR3) and for MUC5AC as described in Methods. (B–E) Proinflammatory cytokines interleukin 1 beta (IL-1β) (B,C) and IL-6 (D,E) were determined by multiplex Luminex immunoassay in both apical (B,D) and basal (C,E) chambers of air-liquid interface (ALI) inserts as described in methods. All panels show summary data as mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparisons between the uninfected control group and each experimental group were performed using a two-tailed Mann–Whitney test and are indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway differentiation and inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Article Snippet: Human rhinovirus 16 strain 11757 (Cat# VR-283), and Influenza A virus (H1N1) strain A/PR/8/34 (Cat# VR-95) were procured from ATCC.

    Techniques: Infection, Ex Vivo, Multiplex Assay, Luminex, Control, Two Tailed Test, MANN-WHITNEY, Comparison, Cell Culture

    Impact of HRV and influenza infection on mediators of airway inflammation (IL-8, IL-10) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A–D) Proinflammatory cytokines interleukin 8 (IL-8 (A,B) and IL-10 (C,D) were determined by multiplex Luminex immunoassay in both the apical (A,C) and basal (B,D) chambers of air-liquid interface (ALI) inserts, as described in the methods. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test and is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Journal: Frontiers in Microbiology

    Article Title: Ex vivo modeling of nasal epithelial airway inflammation in respiratory viral infections

    doi: 10.3389/fmicb.2026.1819581

    Figure Lengend Snippet: Impact of HRV and influenza infection on mediators of airway inflammation (IL-8, IL-10) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A–D) Proinflammatory cytokines interleukin 8 (IL-8 (A,B) and IL-10 (C,D) were determined by multiplex Luminex immunoassay in both the apical (A,C) and basal (B,D) chambers of air-liquid interface (ALI) inserts, as described in the methods. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test and is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Article Snippet: Human rhinovirus 16 strain 11757 (Cat# VR-283), and Influenza A virus (H1N1) strain A/PR/8/34 (Cat# VR-95) were procured from ATCC.

    Techniques: Infection, Ex Vivo, Multiplex Assay, Luminex, Comparison, Control, Two Tailed Test, MANN-WHITNEY, Cell Culture

    Impact of HRV and influenza infection on mediators of airway inflammation (TNF-α, VEGF) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A–D) Proinflammatory cytokines, tumor necrosis factor alpha (TNF-α) (A,B) and Vascular endothelial growth factor (VEGF) (C,D) , were determined by multiplex Luminex immunoassay in both the apical (A,C) and basal (B,D) chambers of air-liquid interface (ALI) inserts, as described in the methods. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test and is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Journal: Frontiers in Microbiology

    Article Title: Ex vivo modeling of nasal epithelial airway inflammation in respiratory viral infections

    doi: 10.3389/fmicb.2026.1819581

    Figure Lengend Snippet: Impact of HRV and influenza infection on mediators of airway inflammation (TNF-α, VEGF) in an ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 and 48 h, as described in the methods. (A–D) Proinflammatory cytokines, tumor necrosis factor alpha (TNF-α) (A,B) and Vascular endothelial growth factor (VEGF) (C,D) , were determined by multiplex Luminex immunoassay in both the apical (A,C) and basal (B,D) chambers of air-liquid interface (ALI) inserts, as described in the methods. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test and is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Article Snippet: Human rhinovirus 16 strain 11757 (Cat# VR-283), and Influenza A virus (H1N1) strain A/PR/8/34 (Cat# VR-95) were procured from ATCC.

    Techniques: Infection, Ex Vivo, Multiplex Assay, Luminex, Comparison, Control, Two Tailed Test, MANN-WHITNEY, Cell Culture

    Impact of HRV and influenza infection on secretion of proinflammatory cytokines in apical versus basal surface in ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 (A) and 48 (B) h, as described in the methods. The mean value of each protein measurement in each apical cell culture supernatant was normalized to the mean value of protein content in the same basal cell culture supernatant of the same ALI well. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in apical versus basal surfaces of human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Journal: Frontiers in Microbiology

    Article Title: Ex vivo modeling of nasal epithelial airway inflammation in respiratory viral infections

    doi: 10.3389/fmicb.2026.1819581

    Figure Lengend Snippet: Impact of HRV and influenza infection on secretion of proinflammatory cytokines in apical versus basal surface in ex vivo model of nasal airways. Human nasal epithelial cells (HNECs) from three human donors were prepared and infected with HRV and H1N1 for 24 (A) and 48 (B) h, as described in the methods. The mean value of each protein measurement in each apical cell culture supernatant was normalized to the mean value of protein content in the same basal cell culture supernatant of the same ALI well. All panels show summary data as the mean ± standard error of the mean (SEM) from at least 3 biological replicates per donor. Three HNEC ALI cultures were prepared per human donor, and data from 3 donors are shown. Each data point represents the average of at least two technical replicates per one biological sample. Statistical comparison between the uninfected control group and each experimental group was performed using a two-tailed Mann–Whitney test and is indicated by a blue asterisk. A statistical comparison between two non-control experimental groups was performed using a two-tailed Mann–Whitney test, and the result is indicated by a black asterisk. The p -value for each comparison is shown above each column (* p < 0.05, ** p < 0.01, *** p < 0.001). Alt Text: Graph and data showing measures of nasal airway inflammation in apical versus basal surfaces of human nasal airway cell culture models infected with influenza or human rhinovirus over 48 h compared to uninfected cell cultures.

    Article Snippet: Human rhinovirus 16 strain 11757 (Cat# VR-283), and Influenza A virus (H1N1) strain A/PR/8/34 (Cat# VR-95) were procured from ATCC.

    Techniques: Infection, Ex Vivo, Cell Culture, Comparison, Control, Two Tailed Test, MANN-WHITNEY

    Anti-influenza effects of stevioside, curcuminoids, and C-S/M in MDCK cells. ( A ) Cytotoxicity of stevioside (25–200 µg/mL), curcuminoids (6.25–50 µg/mL), and C–S/M (25–200 µg/mL) in MDCK cells was assessed using an MTT assay and is presented as relative cell viability compared with untreated control. ( B ) MDCK cells were infected with A/PR/8/34 at an MOI of 0.001 and treated with the indicated concentrations of stevioside, curcuminoids, or C-S/M. At 72 hpi, IAV-induced cytopathic effects (CPE) under different treatments were evaluated using a neutral red assay. Data are presented as the mean ± SEM. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s multiple comparisons test. * p < 0.05; ** p < 0.01; and *** p < 0.001.

    Journal: Microorganisms

    Article Title: Water-Solubilized Curcuminoids Suppress Influenza A Virus Replication and Ameliorate Virus-Induced T-Cell Immune Dysfunction and Inflammatory Responses

    doi: 10.3390/microorganisms14051152

    Figure Lengend Snippet: Anti-influenza effects of stevioside, curcuminoids, and C-S/M in MDCK cells. ( A ) Cytotoxicity of stevioside (25–200 µg/mL), curcuminoids (6.25–50 µg/mL), and C–S/M (25–200 µg/mL) in MDCK cells was assessed using an MTT assay and is presented as relative cell viability compared with untreated control. ( B ) MDCK cells were infected with A/PR/8/34 at an MOI of 0.001 and treated with the indicated concentrations of stevioside, curcuminoids, or C-S/M. At 72 hpi, IAV-induced cytopathic effects (CPE) under different treatments were evaluated using a neutral red assay. Data are presented as the mean ± SEM. Statistical significance was analyzed using one-way ANOVA followed by Tukey’s multiple comparisons test. * p < 0.05; ** p < 0.01; and *** p < 0.001.

    Article Snippet: Influenza A/PR/8/34 (H1N1) virus (ATCC VR-1469) was propagated in MDCK cells in the presence of 2 μg/mL TPCK-treated trypsin.

    Techniques: MTT Assay, Control, Infection, Neutral Red Assay

    In vivo antiviral effect of C–S/M administration in IAV-infected mice. Female C57BL/6 mice were intranasally infected with A/PR/8/34 (10 5 ELD 50 ) and treated with C–S/M (100–400 mg/kg/day) or PBS 4 h after IAV infection. ( A ) Changes in body weight of IAV-infected mice treated with different doses of C–S/M. Body weight was measured at 1, 3, 5, and 7 dpi and expressed as a percentage of the initial body weight. ( B ) Survival rates of IAV-infected mice treated with PBS or C–S/M were assessed for 7 days after viral inoculation. ( C ) mRNA expression levels of the influenza virus NS1 gene in lung tissues at 7 dpi, determined by qRT-PCR, with GAPDH serving as an internal control. Data are presented as the mean ± SEM. Data are expressed as the mean ± SEM from two independent experiments ( n = 10 mice per group). Statistical significance for panel C was analyzed using the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. ** p < 0.01 and *** p < 0.001.

    Journal: Microorganisms

    Article Title: Water-Solubilized Curcuminoids Suppress Influenza A Virus Replication and Ameliorate Virus-Induced T-Cell Immune Dysfunction and Inflammatory Responses

    doi: 10.3390/microorganisms14051152

    Figure Lengend Snippet: In vivo antiviral effect of C–S/M administration in IAV-infected mice. Female C57BL/6 mice were intranasally infected with A/PR/8/34 (10 5 ELD 50 ) and treated with C–S/M (100–400 mg/kg/day) or PBS 4 h after IAV infection. ( A ) Changes in body weight of IAV-infected mice treated with different doses of C–S/M. Body weight was measured at 1, 3, 5, and 7 dpi and expressed as a percentage of the initial body weight. ( B ) Survival rates of IAV-infected mice treated with PBS or C–S/M were assessed for 7 days after viral inoculation. ( C ) mRNA expression levels of the influenza virus NS1 gene in lung tissues at 7 dpi, determined by qRT-PCR, with GAPDH serving as an internal control. Data are presented as the mean ± SEM. Data are expressed as the mean ± SEM from two independent experiments ( n = 10 mice per group). Statistical significance for panel C was analyzed using the Kruskal–Wallis test followed by Dunn’s multiple comparisons test. ** p < 0.01 and *** p < 0.001.

    Article Snippet: Influenza A/PR/8/34 (H1N1) virus (ATCC VR-1469) was propagated in MDCK cells in the presence of 2 μg/mL TPCK-treated trypsin.

    Techniques: In Vivo, Infection, Expressing, Virus, Quantitative RT-PCR, Control

    Synthesis of compound H1N1-17. Reagents and conditions: (a) NaHCO 3 , (Boc) 2 O, acetone/H 2 O = 1:1, 0 °C to rt; (b) N , O -dimethylhydroxylamine hydrochloride, i PrMgCl, THF, 0 °C to rt; (c) allylmagnesium chloride, THF, −60 °C; (d) (i) 9-BBN, THF, 0 °C to rt; (ii) H 2 O, NaBO 3 ·4H 2 O, THF, 0 °C to rt; (e) methoxyammonium chloride, pyridine, 80 °C; (f) NaOAc, MeOH, 40 °C; (g) K 2 CO 3 , [Ru( p -cymene)Cl 2 ] 2 , 2,2,2-trifluoroethan-1-ol, 65 °C; (h) (i) TFA, DCM, rt; (ii) HATU, DIPEA, DMF, 0 °C to rt; (i) NaOH, MeOH/H 2 O = 1:1, 0–50 °C; (j) (i) 2,4,6-trichlorobenzoyl chloride, Et 3 N, THF, 0 °C to rt; (ii) DMAP, THF, 40 °C.

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: Synthesis of compound H1N1-17. Reagents and conditions: (a) NaHCO 3 , (Boc) 2 O, acetone/H 2 O = 1:1, 0 °C to rt; (b) N , O -dimethylhydroxylamine hydrochloride, i PrMgCl, THF, 0 °C to rt; (c) allylmagnesium chloride, THF, −60 °C; (d) (i) 9-BBN, THF, 0 °C to rt; (ii) H 2 O, NaBO 3 ·4H 2 O, THF, 0 °C to rt; (e) methoxyammonium chloride, pyridine, 80 °C; (f) NaOAc, MeOH, 40 °C; (g) K 2 CO 3 , [Ru( p -cymene)Cl 2 ] 2 , 2,2,2-trifluoroethan-1-ol, 65 °C; (h) (i) TFA, DCM, rt; (ii) HATU, DIPEA, DMF, 0 °C to rt; (i) NaOH, MeOH/H 2 O = 1:1, 0–50 °C; (j) (i) 2,4,6-trichlorobenzoyl chloride, Et 3 N, THF, 0 °C to rt; (ii) DMAP, THF, 40 °C.

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques:

    Effects of compound H1N1-17 on cell viability and multiplication of H1N1 (A/PR/8/34) and H3N2 (A/Hong Kong/8/68). (A) Chemical structure of compound H1N1-17 and its cytotoxicity and antiviral effects in MDCK cells. CC 50 , 50% cytotoxic concentration; EC 50 , 50% maximal effective concentration; EC 90 , 90% maximal effective concentration. Values are means ± SD ( n = 3). (B) EC 50 values for compound H1N1-17 against indicated influenza virus strains in vitro . Values are means ± SD ( n = 3). (C) Viral proteins of H1N1 in MDCK cells treated with compound H1N1-17 decreased in a dose-dependent manner in a Western blot assay. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (D) Viral proteins of H3N2 in MDCK cells were invariable following treatment with compound H1N1-17 in a Western blot assay. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (E) Compound H1N1-17 alleviated the cytopathic effects of H1N1 but not H3N2 infection in MDCK cells. TCID50, 50% tissue culture infectious dose. Cell viability and morphology were examined microscopically using a 10 × objective (scale bar: 100 μm). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by two-way Anova (or mixed model) in (C) and (D).

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: Effects of compound H1N1-17 on cell viability and multiplication of H1N1 (A/PR/8/34) and H3N2 (A/Hong Kong/8/68). (A) Chemical structure of compound H1N1-17 and its cytotoxicity and antiviral effects in MDCK cells. CC 50 , 50% cytotoxic concentration; EC 50 , 50% maximal effective concentration; EC 90 , 90% maximal effective concentration. Values are means ± SD ( n = 3). (B) EC 50 values for compound H1N1-17 against indicated influenza virus strains in vitro . Values are means ± SD ( n = 3). (C) Viral proteins of H1N1 in MDCK cells treated with compound H1N1-17 decreased in a dose-dependent manner in a Western blot assay. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (D) Viral proteins of H3N2 in MDCK cells were invariable following treatment with compound H1N1-17 in a Western blot assay. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (E) Compound H1N1-17 alleviated the cytopathic effects of H1N1 but not H3N2 infection in MDCK cells. TCID50, 50% tissue culture infectious dose. Cell viability and morphology were examined microscopically using a 10 × objective (scale bar: 100 μm). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by two-way Anova (or mixed model) in (C) and (D).

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques: Concentration Assay, Virus, In Vitro, Western Blot, Quantitative Proteomics, Infection

    Compound H1N1-17 acted on the early stage of H1N1 infection. Time course of the addition of compound H1N1-17. Compound H1N1-17 was pre-incubated with Calu3 cells (−2 h, pre-infected), or added to H1N1-infected Calu3 cells at 0 (post-infected), 2, 4, 8, and 24 h. At 48 h after infection, viruses from the cell supernatant were harvested and quantified by one-step real time PCR assay. Antiviral activity of compound H1N1-17 gradually decreased with time. Values are means ± SD ( n = 3).

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: Compound H1N1-17 acted on the early stage of H1N1 infection. Time course of the addition of compound H1N1-17. Compound H1N1-17 was pre-incubated with Calu3 cells (−2 h, pre-infected), or added to H1N1-infected Calu3 cells at 0 (post-infected), 2, 4, 8, and 24 h. At 48 h after infection, viruses from the cell supernatant were harvested and quantified by one-step real time PCR assay. Antiviral activity of compound H1N1-17 gradually decreased with time. Values are means ± SD ( n = 3).

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques: Infection, Incubation, Real-time Polymerase Chain Reaction, Activity Assay

    Mechanism of action of compound H1N1-17. (A) Pseudo-type H1N1, H1N2 or H5N1 models. The membrane protein (GP120/41) on the HIV-1 genome (black) was replaced with luciferase (claret), and the viral proteins Vpr (viral protein regulatory) and Nef (negative factor) were removed, and then modified with exogenous HA (H1 or H5, red) and NA (N1 or N2, lavender). Expression of luciferase on the HIV-1 genome was driven by entry of pseudo-type H1N1, H1N2 or H5N1. Compound H1N1-17 inhibited entry of pseudo-H1N1 and pseudo-H1N2 in a dose-dependent manner, but did not affect pseudo-H5N1 entry. Amounts of pseudo-type viruses entering cells are indicated by luciferase levels. Values are means ± SD ( n = 3). (B) Compound H1N1-17 did not inhibit hemagglutination of guinea pig erythrocytes caused by H1N1 in a hemagglutination inhibition (HI) assay. PBS without virus was used as a positive control: precipitated guinea pig erythrocytes (red circles); PBS with virus alone was used as a negative control: guinea pig erythrocytes did not settle and appeared uniformly red. (C) Time course of addition of compound H1N1-17. H1N1 viruses were pre-incubated with cells (−1 h) for adsorption, and compound H1N1-17 was added at 0 h (endocytosis), 2 h (fusion), and 4 h (uncoating) and 8 h (replication). At 24 h post adsorption, viruses from cellular lysate were harvested and quantified by one-step real time PCR assay. Compound H1N1-17 significantly inhibited endocytosis and fusion at 0 h post adsorption, and antiviral activity of compound H1N1-17 gradually decreased with time. Values are means ± SD ( n = 3). (D) Inhibition of compound H1N1-17 on hemolysis of guinea pig erythrocytes mediated by H1N1 HA in acidic condition. Values are means ± SD ( n = 3). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by one-way Anova (and nonparametric or mixed) in (D).

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: Mechanism of action of compound H1N1-17. (A) Pseudo-type H1N1, H1N2 or H5N1 models. The membrane protein (GP120/41) on the HIV-1 genome (black) was replaced with luciferase (claret), and the viral proteins Vpr (viral protein regulatory) and Nef (negative factor) were removed, and then modified with exogenous HA (H1 or H5, red) and NA (N1 or N2, lavender). Expression of luciferase on the HIV-1 genome was driven by entry of pseudo-type H1N1, H1N2 or H5N1. Compound H1N1-17 inhibited entry of pseudo-H1N1 and pseudo-H1N2 in a dose-dependent manner, but did not affect pseudo-H5N1 entry. Amounts of pseudo-type viruses entering cells are indicated by luciferase levels. Values are means ± SD ( n = 3). (B) Compound H1N1-17 did not inhibit hemagglutination of guinea pig erythrocytes caused by H1N1 in a hemagglutination inhibition (HI) assay. PBS without virus was used as a positive control: precipitated guinea pig erythrocytes (red circles); PBS with virus alone was used as a negative control: guinea pig erythrocytes did not settle and appeared uniformly red. (C) Time course of addition of compound H1N1-17. H1N1 viruses were pre-incubated with cells (−1 h) for adsorption, and compound H1N1-17 was added at 0 h (endocytosis), 2 h (fusion), and 4 h (uncoating) and 8 h (replication). At 24 h post adsorption, viruses from cellular lysate were harvested and quantified by one-step real time PCR assay. Compound H1N1-17 significantly inhibited endocytosis and fusion at 0 h post adsorption, and antiviral activity of compound H1N1-17 gradually decreased with time. Values are means ± SD ( n = 3). (D) Inhibition of compound H1N1-17 on hemolysis of guinea pig erythrocytes mediated by H1N1 HA in acidic condition. Values are means ± SD ( n = 3). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by one-way Anova (and nonparametric or mixed) in (D).

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques: Membrane, Luciferase, Modification, Expressing, HI Assay, Virus, Positive Control, Negative Control, Incubation, Adsorption, Real-time Polymerase Chain Reaction, Activity Assay, Inhibition

    Direct interaction of compound H1N1-17 with H1N1 HA. (A) Antiviral activity of compound H1N1-17 was specifically antagonized by H1N1 HA in the protein competition assay. Calu3 cells were pre-incubated with H1N1 at 4 °C for adsorption, and then viruses were replaced with compound H1N1-17 incubated with and without HA protein. Viral RNAs from cell culture supernatants were extracted and quantified by one-step real time PCR assay. Values are means ± SD ( n = 3). Cell viability and morphology were viewed microscopically using a 10 × objective (scale bar: 100 μm). Calu3 cell morphology: without infection (a1, b1, c1); without infection and incubated with H1 (a2), H3 (b2), and H8 (c2); without infection and treated with compound H1N1-17 that was pre-incubated with H1 (a3), H3 (b3), and H8 (c3); infected with H1N1 (a4, b4, c4); infected with H1N1 and incubated with H1 (a5), H3 (b5), and H8 (c5); infected with H1N1 and treated with compound H1N1-17 that was pre-incubated with H1 (a6), H3 (b6), and H8 (c6); and infected with H1N1 and treated with compound H1N1-17 (a7, b7, c7). (B) Strong interaction of compound H1N1-17 with H1N1 HA determined by surface plasmon resonance assay ( K D = 2.58 μmol/L). The CM5 chip was used for amino coupling fixation of H1N1 HA protein, and compound H1N1-17 was used as the analyte to detect the affinity between H1N1 HA and compound H1N1-17. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, ns indicated no statistical significance, by one-way Anova (and nonparametric or mixed) in (A).

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: Direct interaction of compound H1N1-17 with H1N1 HA. (A) Antiviral activity of compound H1N1-17 was specifically antagonized by H1N1 HA in the protein competition assay. Calu3 cells were pre-incubated with H1N1 at 4 °C for adsorption, and then viruses were replaced with compound H1N1-17 incubated with and without HA protein. Viral RNAs from cell culture supernatants were extracted and quantified by one-step real time PCR assay. Values are means ± SD ( n = 3). Cell viability and morphology were viewed microscopically using a 10 × objective (scale bar: 100 μm). Calu3 cell morphology: without infection (a1, b1, c1); without infection and incubated with H1 (a2), H3 (b2), and H8 (c2); without infection and treated with compound H1N1-17 that was pre-incubated with H1 (a3), H3 (b3), and H8 (c3); infected with H1N1 (a4, b4, c4); infected with H1N1 and incubated with H1 (a5), H3 (b5), and H8 (c5); infected with H1N1 and treated with compound H1N1-17 that was pre-incubated with H1 (a6), H3 (b6), and H8 (c6); and infected with H1N1 and treated with compound H1N1-17 (a7, b7, c7). (B) Strong interaction of compound H1N1-17 with H1N1 HA determined by surface plasmon resonance assay ( K D = 2.58 μmol/L). The CM5 chip was used for amino coupling fixation of H1N1 HA protein, and compound H1N1-17 was used as the analyte to detect the affinity between H1N1 HA and compound H1N1-17. ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, ns indicated no statistical significance, by one-way Anova (and nonparametric or mixed) in (A).

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques: Activity Assay, Competitive Binding Assay, Incubation, Adsorption, Cell Culture, Real-time Polymerase Chain Reaction, Infection, SPR Assay

    Potential sites of interaction between compound H1N1-17 and H1N1 HA. (A) Structure of the H1N1 (A/PR/8/34) HA trimer (PDB ID: 1RU7) and functional subdomains. Subdomain: blue (R), yellow (E), purple (F, sequence HA1), and red (F, sequence HA2). (B) Resistant mutations (L43I of HA1 and D109G of HA2, red spheres) identified in the H1N1 HA to compound H1N1-17 located in F subdomain. L43I mutation of HA1 located near the interaction sites between CR6261 and H1N1 HA (L42, V40, and L292 of HA1, yellow spheres). The D109G mutation of HA2 was one of the mutation sites that mediated membrane fusion at high pH (D109G, D112, and K116 of HA2, orange spheres). HA1 and HA2 in the structure of H1N1 (A/PR/8/34) HA monomer (PDB ID: 6WCR), light pink and pale cyan, respectively. (C) Compound H1N1-17 inhibited the multiplication of H1N1 WT while H1N1 resis was insensitive to compound H1N1-17. H1N1 WT , the sixth passage of H1N1 in Calu3 cells in the absence of compound H1N1-17; H1N1 resis , the sixth passage of H1N1 in Calu3 cells in the presence of compound H1N1-17. Values are means ± SD ( n = 3). (D) Viral proteins of H1N1 WT in Calu3 cells significantly decreased with treatment of compound H1N1-17 in Western blot assay. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (E) Viral proteins of H1N1 resis in Calu3 cells were invariable following treatment with compound H1N1-17 in Western blot assay. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (F) Compound H1N1-17 alleviated the cytopathic effects of H1N1 WT but not H1N1 resis infection in Calu3 cells. Cell viability and morphology were viewed microscopically using a 10 × objective (scale bar: 100 μm). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by two-way Anova (or mixed model) in (D) and (E).

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: Potential sites of interaction between compound H1N1-17 and H1N1 HA. (A) Structure of the H1N1 (A/PR/8/34) HA trimer (PDB ID: 1RU7) and functional subdomains. Subdomain: blue (R), yellow (E), purple (F, sequence HA1), and red (F, sequence HA2). (B) Resistant mutations (L43I of HA1 and D109G of HA2, red spheres) identified in the H1N1 HA to compound H1N1-17 located in F subdomain. L43I mutation of HA1 located near the interaction sites between CR6261 and H1N1 HA (L42, V40, and L292 of HA1, yellow spheres). The D109G mutation of HA2 was one of the mutation sites that mediated membrane fusion at high pH (D109G, D112, and K116 of HA2, orange spheres). HA1 and HA2 in the structure of H1N1 (A/PR/8/34) HA monomer (PDB ID: 6WCR), light pink and pale cyan, respectively. (C) Compound H1N1-17 inhibited the multiplication of H1N1 WT while H1N1 resis was insensitive to compound H1N1-17. H1N1 WT , the sixth passage of H1N1 in Calu3 cells in the absence of compound H1N1-17; H1N1 resis , the sixth passage of H1N1 in Calu3 cells in the presence of compound H1N1-17. Values are means ± SD ( n = 3). (D) Viral proteins of H1N1 WT in Calu3 cells significantly decreased with treatment of compound H1N1-17 in Western blot assay. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (E) Viral proteins of H1N1 resis in Calu3 cells were invariable following treatment with compound H1N1-17 in Western blot assay. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (F) Compound H1N1-17 alleviated the cytopathic effects of H1N1 WT but not H1N1 resis infection in Calu3 cells. Cell viability and morphology were viewed microscopically using a 10 × objective (scale bar: 100 μm). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by two-way Anova (or mixed model) in (D) and (E).

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques: Functional Assay, Sequencing, Mutagenesis, Membrane, Western Blot, Quantitative Proteomics, Infection

    Inhibitory activity of compound H1N1-17 of HA-mediated membrane fusion of Vero cells expressing GFP and HA. Vero cells were co-transfected with plasmid carrying the encoding sequence of wild-type HA (HA-WT) or HA mutants (HA-Mut: L43I, D109G or L43I/D109G) and plasmid carrying the encoding sequence of GFP. The mutual fusion between Vero cells was triggered by conformational changes of HA at pH 4.8 and characterized by the diffusion of GFP in cells (green). Inhibition of H1N1-17 on membrane fusion mediated by HA-WT was observed, while this phenomenon did not occur in membrane fusion mediated by HA mutants that contained one or two drug-resistant mutations (L43I, D109G, or L43I/D109G). (A) Fluorescence images were visualized and photographed using a fluorescence inverted microscope with a 20 × objective (scale bar: 50 μm). (B) Relative fluorescence intensity of fluorescence images in (A). Values are means ± SD ( n = 3). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by two-way Anova (or mixed model) in (B).

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: Inhibitory activity of compound H1N1-17 of HA-mediated membrane fusion of Vero cells expressing GFP and HA. Vero cells were co-transfected with plasmid carrying the encoding sequence of wild-type HA (HA-WT) or HA mutants (HA-Mut: L43I, D109G or L43I/D109G) and plasmid carrying the encoding sequence of GFP. The mutual fusion between Vero cells was triggered by conformational changes of HA at pH 4.8 and characterized by the diffusion of GFP in cells (green). Inhibition of H1N1-17 on membrane fusion mediated by HA-WT was observed, while this phenomenon did not occur in membrane fusion mediated by HA mutants that contained one or two drug-resistant mutations (L43I, D109G, or L43I/D109G). (A) Fluorescence images were visualized and photographed using a fluorescence inverted microscope with a 20 × objective (scale bar: 50 μm). (B) Relative fluorescence intensity of fluorescence images in (A). Values are means ± SD ( n = 3). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by two-way Anova (or mixed model) in (B).

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques: Activity Assay, Membrane, Expressing, Transfection, Plasmid Preparation, Sequencing, Diffusion-based Assay, Inhibition, Fluorescence, Inverted Microscopy

    The effect of compound H1N1-17 on mice challenged with lethal H1N1 (A/PR/8/34). Six mice in each group were intranasally inoculated with MLD 100 of H1N1 (A/PR/8/34) and treated with compound H1N1-17 at 25 mg/kg/day intraperitoneally or oseltamivir phosphate at 25 mg/kg/day intragastrically from −1 to 10 days post infection (dpi). Survival and body weight were monitored daily from −1 to 21 dpi. For pathological analysis, another parallel experiment was performed. Three mice in each group were euthanized on 10 dpi, and lung tissues were isolated. (A) Survival and body weight of H1N1-infected and drug-treated mice. Compound H1N1-17 effectively protected H1N1-infected mice from death and weight loss. Values are means ± SD ( n = 6). (B) Compound H1N1-17 significantly reduced H1N1 in mice lung tissues. Virus titers in lung tissues were detected by one-step real time PCR assay at 10 dpi. LLOQ, lower limit of quantification: 10 3 copies/mL. Values are means ± SD ( n = 3). (C) Viral proteins in lung tissues were detected by Western blot assay at 10 dpi. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (D) Compound H1N1-17 effectively alleviated lung injury caused by viral infection. H1N1-induced pathogenesis was determined by H&E staining at 10 dpi. Smith lung injury score was shown on the right. Values are means ± SD ( n = 3). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by two-way Anova (or mixed model) in (C) and one-way Anova (and nonparametric or mixed) in (B) and (D).

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: The effect of compound H1N1-17 on mice challenged with lethal H1N1 (A/PR/8/34). Six mice in each group were intranasally inoculated with MLD 100 of H1N1 (A/PR/8/34) and treated with compound H1N1-17 at 25 mg/kg/day intraperitoneally or oseltamivir phosphate at 25 mg/kg/day intragastrically from −1 to 10 days post infection (dpi). Survival and body weight were monitored daily from −1 to 21 dpi. For pathological analysis, another parallel experiment was performed. Three mice in each group were euthanized on 10 dpi, and lung tissues were isolated. (A) Survival and body weight of H1N1-infected and drug-treated mice. Compound H1N1-17 effectively protected H1N1-infected mice from death and weight loss. Values are means ± SD ( n = 6). (B) Compound H1N1-17 significantly reduced H1N1 in mice lung tissues. Virus titers in lung tissues were detected by one-step real time PCR assay at 10 dpi. LLOQ, lower limit of quantification: 10 3 copies/mL. Values are means ± SD ( n = 3). (C) Viral proteins in lung tissues were detected by Western blot assay at 10 dpi. Relative quantification was shown on the right ( n = 3). Values are means ± SD. (D) Compound H1N1-17 effectively alleviated lung injury caused by viral infection. H1N1-induced pathogenesis was determined by H&E staining at 10 dpi. Smith lung injury score was shown on the right. Values are means ± SD ( n = 3). ∗ P < 0.05, ∗∗ P < 0.01, and ∗∗∗ P < 0.001, by two-way Anova (or mixed model) in (C) and one-way Anova (and nonparametric or mixed) in (B) and (D).

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques: Infection, Isolation, Virus, Real-time Polymerase Chain Reaction, Western Blot, Quantitative Proteomics, Staining

    Compound H1N1-17 showed synergistic effect with oseltamivir acid against H1N1. (A) The three-dimensional (3-D) dose-response surface of the combination therapy against H1N1 of compound H1N1-17 and oseltamivir acid. The dose-response surface exhibited a convex shape resembling a flipping sail, especially at an inhibition level of 40%–60% (green). According to the principle of Loewe additivity, the combination therapy against H1N1 of compound H1N1-17 and oseltamivir acid was synergistic. (B) The two-dimensional isobologram of the combination therapy against H1N1 of compound H1N1-17 and oseltamivir acid at the inhibition effect of 50%. By controlling the concentrations of compound H1N1-17 and oseltamivir acid as a constant separately, the EC 50 against H1N1 of another compound could be calculated to obtain a series of data points, and then the cross-sectional curve in the 3-D dose-response surface at the inhibition level of 50% was obtained, which presented a concave upward curve. According to the principle of Loewe additivity, compound H1N1-17 showed a synergistic effect with oseltamivir acid against H1N1.

    Journal: Acta Pharmaceutica Sinica. B

    Article Title: A novel entry inhibitor targeting the stalk domain of the hemagglutinin of H1N1

    doi: 10.1016/j.apsb.2026.02.003

    Figure Lengend Snippet: Compound H1N1-17 showed synergistic effect with oseltamivir acid against H1N1. (A) The three-dimensional (3-D) dose-response surface of the combination therapy against H1N1 of compound H1N1-17 and oseltamivir acid. The dose-response surface exhibited a convex shape resembling a flipping sail, especially at an inhibition level of 40%–60% (green). According to the principle of Loewe additivity, the combination therapy against H1N1 of compound H1N1-17 and oseltamivir acid was synergistic. (B) The two-dimensional isobologram of the combination therapy against H1N1 of compound H1N1-17 and oseltamivir acid at the inhibition effect of 50%. By controlling the concentrations of compound H1N1-17 and oseltamivir acid as a constant separately, the EC 50 against H1N1 of another compound could be calculated to obtain a series of data points, and then the cross-sectional curve in the 3-D dose-response surface at the inhibition level of 50% was obtained, which presented a concave upward curve. According to the principle of Loewe additivity, compound H1N1-17 showed a synergistic effect with oseltamivir acid against H1N1.

    Article Snippet: Influenza virus H1N1 (A/Puerto Rico/8/34, A/California/07/2009 pdm09, A/WS/33, A/FM/1/47), H3N2 (A/Hong Kong/8/68, A/California/2/2014) and influenza B virus (B/Taiwan/2/62) were obtained from ATCC (VR-1469, VR-1894, VR-1520, VR-97, VR-1679 and VR-1938 and VR-1735).

    Techniques: Inhibition