Journal: Molecular therapy : the journal of the American Society of Gene Therapy

Article Title: Neuraminidase delivered as an APC-targeted DNA vaccine induces protective antibodies against influenza.

doi: 10.1016/j.ymthe.2023.03.012

Figure Lengend Snippet: Figure 1. In vitro characterization of MHC class II-targeted heterodimeric DNA vaccines containing NA and/or HA (A) MHC class II-targeted heterodimeric acid/base (A/B) vaccine proteins consist of A and B chains, each having a targeting, dimerization, and antigenic unit. The targeting unit is either an scFv that binds MHC class II on APCs (scFvaMHCII, green) or a non-targeted control that binds the hapten NIP (scFvaNIP, white). The targeting units are genetically linked to a shortened hinge from human IgG3 (exon h1), allowing covalent disulfide bond formation between the A and B chains (black lines). The hinge is followed by a duplicated A (red) or B (blue) heterodimerization unit based on a modified Jun/Fos leucine zipper motif enriched for acidic or basic amino acids, respectively. The A and B chains are linked to antigenic units composed of NA (dark blue) or HA (orange) derived from influenza H1N1 PR8 virus. The heterodimeric vaccine proteins are named as

Article Snippet: The copy number of viral RNA was determined with quantitative genomic RNA from H1N1 PR8 (VR-95DQ, ATCC) and shown per microgram total tissue RNA.

Techniques: In Vitro, Vaccines, Control, Derivative Assay, Virus

Journal: Molecular therapy : the journal of the American Society of Gene Therapy

Article Title: Neuraminidase delivered as an APC-targeted DNA vaccine induces protective antibodies against influenza.

doi: 10.1016/j.ymthe.2023.03.012

Figure Lengend Snippet: Figure 2. MHC class II-targeted NA-bivalent heterodimers efficiently induce antibody responses after a single DNA vaccination (A) BALB/c mice were vaccinated once i.m. with 5 mg of each A and B plasmids (10 mg DNA in total) encoding the indicated heterodimeric vaccine proteins (box), followed immediately by EP. Blood was sampled at the indicated time points. (B) NA-specific (top) and HA-specific (bottom) IgG (left), IgG1 (center), and IgG2a (right) titers were measured by ELISA at the indicated time points after immunization. Statistical analysis compared targeted vs. non-targeted and antigen-bivalent vs. monovalent groups. (C) BALB/c mice were immunized once i.m./EP with different amounts of the indicated DNA vaccines. Serum was analyzed for NA-specific IgG responses 4 weeks post vaccination. (D) IgG responses specific for inactivated H1N1 PR8 virus (left), rec. NA protein (center), or rec. HA protein (right) in sera harvested 6 weeks post vaccination from

Article Snippet: The copy number of viral RNA was determined with quantitative genomic RNA from H1N1 PR8 (VR-95DQ, ATCC) and shown per microgram total tissue RNA.

Techniques: Enzyme-linked Immunosorbent Assay, Vaccines, Virus

Journal: Molecular therapy : the journal of the American Society of Gene Therapy

Article Title: Neuraminidase delivered as an APC-targeted DNA vaccine induces protective antibodies against influenza.

doi: 10.1016/j.ymthe.2023.03.012

Figure Lengend Snippet: Figure 4. A single DNA immunization with MHC class II-targeted NA/NA vaccines protects against homologous influenza virus challenge (A) BALB/c mice were immunized once i.m./EP and challenged with homologous influenza A H1N1 PR8 virus at week 2 (short term) or between weeks 6 and 10 (long term) after vaccination. (B–F) 50 mg of each A and B plasmids (total 100 mg, B), 5 mg/ plasmid (10 mg total, C–E), or 1 mg/plasmid (2 mg total, F) of the indicated DNA vaccines (box) were used. Mice were challenged with a lethal dose of 5 LD50 (B–D and F) or 100 LD50 (E) at week 9 (B), week 10 (C), week 2 (D and E), or week 6 (F). Weight (left, mean ± SEM) and survival (right) were monitored up to 12 days post challenge. n = 8 mice/group (B, C, E, and F) or n = 6 mice/group (D). Dead mice were assigned a weight of 75%. *p % 0.05, ***p % 0.001; two-way ANOVA (weight curve) or Mantel-Cox test (survival). Statistical analysis compared MHC class II- targeted NA/NA versus HA/HA as well as targeted versus non-targeted and anti- gen-bivalent versus -monovalent NA.

Article Snippet: The copy number of viral RNA was determined with quantitative genomic RNA from H1N1 PR8 (VR-95DQ, ATCC) and shown per microgram total tissue RNA.

Techniques: Vaccines, Virus, Plasmid Preparation

Journal: Molecular therapy : the journal of the American Society of Gene Therapy

Article Title: Neuraminidase delivered as an APC-targeted DNA vaccine induces protective antibodies against influenza.

doi: 10.1016/j.ymthe.2023.03.012

Figure Lengend Snippet: Figure 5. MHC class II-targeted NA DNA vaccine induces superior NA-specific antibody responses compared with conventional inactivated virus after one vaccination (A, B) BALB/c mice were immunized once i.m. with 0.2, 1, or 5 mg of formalin-inactivated H1N1 PR8 virus or with 5 mg/ plasmid (10 mg total) of the indicated DNA vaccines, fol- lowed by EP (box). (A) NA-specific (left) and HA-specific (right) titers were measured by ELISA at the indicated time points after immunization. Mean ± SEM is shown. (B) Mice were challenged with 5 LD50 H1N1 PR8 virus 11 week post vaccination. Weight (left, mean ± SEM) and survival (right) were monitored up to 12 days post challenge. Dead mice were assigned a weight of 75%; n = 8 mice/group. Statistical analysis compared the different doses of inactivated virus with DNA vaccination with MHC class II-targeted NA and/or HA. **p % 0.01, ***p % 0.001; two-way ANOVA (IgG titers, weight curve) or Mantel-Cox test (survival).

Article Snippet: The copy number of viral RNA was determined with quantitative genomic RNA from H1N1 PR8 (VR-95DQ, ATCC) and shown per microgram total tissue RNA.

Techniques: Virus, Plasmid Preparation, Vaccines, Enzyme-linked Immunosorbent Assay

Journal: Molecular therapy : the journal of the American Society of Gene Therapy

Article Title: Neuraminidase delivered as an APC-targeted DNA vaccine induces protective antibodies against influenza.

doi: 10.1016/j.ymthe.2023.03.012

Figure Lengend Snippet: Figure 6. Vaccine-induced NA-specific antibodies mediate protection against homologous influenza infection, inhibit NA enzymatic activity, and block viral replication (A–D) BALB/c mice were immunized once i.m./EP with 50 mg each of A and B plasmids (100 mg total) as indicated. (A) Pooled sera (350 mL) from mice 5 weeks after vaccination were transferred i.p. to naive BALB/c mice. One day after transfer, mice were challenged with 2.5 LD50 H1N1 PR8 virus. (B) 2 weeks after vaccination with the indicated DNA vaccines, mice were challenged with 5 LD50 H1N1 PR8 virus. Starting on day 12 after vaccination, mice were treated with anti-CD4 and anti- CD8 mAbs or isotype-matched control mAbs every second day. n = 8 mice/group; weight (left, mean ± SEM) and survival (right) were monitored up to 12 days post challenge, and dead mice were assigned a weight of 75% (A and B). (C) Neutrali- zation of influenza A H1N1 PR8 virus by serum from vaccinated mice (box) obtained 4 weeks after immunization was measured by microneutralization assay and is shown as IC50. (D) The same sera were tested for ability to inhibit NA enzyme activity by ELLA, using a reassorted influenza A H6N1 virus containing NA from H1N1 PR8. IC50 is indicated. (E and F) BALB/c mice were immunized once i.m./EP with 50 mg of each A and B plasmids (100 mg total, E) or 5 mg of each A and B plasmids (10 mg total, F) as indicated. Mice were challenged with homologous H1N1 PR8 virus 6 weeks after vaccination, and lungs were harvested on day 5 post challenge. Viral loads were determined by qRT-PCR (left), showing gene copy number per micro- gram total tissue RNA, and by measuring in vitro cell culture infectivity (right), pre- sented as 50% tissue culture infectious dose (TCID50) per milliliter of lung homog- enates. Individual mice and mean ± SEM are shown; n = 4–6 mice/group (C–F). *p % 0.05, **p % 0.01, ***p % 0.001; two-way ANOVA (weight curve), Mantel-Cox test (survival), Kruskal-Wallis multiple-comparisons test with Dunn’s correction (C and D, TCID50), or multiple-comparisons one-way ANOVA with Tukey’s correction (copy number).

Article Snippet: The copy number of viral RNA was determined with quantitative genomic RNA from H1N1 PR8 (VR-95DQ, ATCC) and shown per microgram total tissue RNA.

Techniques: Infection, Activity Assay, Blocking Assay, Virus, Vaccines, Control, Microneutralization Assay, Quantitative RT-PCR, In Vitro, Cell Culture

Journal: Journal of Virology

Article Title: Tetherin Sensitivity of Influenza A Viruses Is Strain Specific: Role of Hemagglutinin and Neuraminidase

doi: 10.1128/JVI.00615-15

Figure Lengend Snippet: Tetherin inhibits release of neuraminidase-based FLUAV-like particles. (A) 293T cells were transfected with expression plasmids encoding the indicated NA and HA proteins with a C-terminal V5 antigenic tag or transfected with empty plasmid (control). At 40 h posttransfection, HA and NA expression in cell lysates and supernatants was detected via Western blotting, using a V5-specific antibody. Tetherin and Vpu expression was visualized using antibodies raised against these proteins. Detection of β-actin expression in cell lysates served as loading control. Similar results were obtained in at least four independent experiments. (B) The experiment was carried out as described for panel A, but cells were additionally cotransfected with an empty plasmid (control) or tetherin-encoding plasmid. In addition, a Vpu-encoding plasmid was cotransfected as indicated. The results of a representative experiment are shown and were confirmed in six separate experiments. (C) The signal intensities measured for panel B were quantified using ImageJ software. The NA signal present in supernatants was normalized to NA in cell lysates, and normalized NA signals in supernatants measured in the absence of tetherin and Vpu were set as 100%. 1918, pandemic 1918 FLUAV; WSN, A/WSN/1933; HA, hemagglutinin; NA, neuraminidase; Sups, supernatants.

Article Snippet: A/PR/8/1934 (H1N1), A/WSN/1933 (H1N1), A/Panama/2007/1999 (H3N2), PR8 × 2009 HA/NA, and PR8 × 1968 HA/NA were propagated in the chorio-allantoic cavities of 10-day-old embryonated hen eggs (Valo BioMedia GmbH, Germany) for 48 h at 37°C.

Techniques: Transfection, Expressing, Plasmid Preparation, Western Blot, Software

Journal: Journal of Virology

Article Title: Tetherin Sensitivity of Influenza A Viruses Is Strain Specific: Role of Hemagglutinin and Neuraminidase

doi: 10.1128/JVI.00615-15

Figure Lengend Snippet: Neuraminidase and hemagglutinin of pandemic FLUAV confer resistance to tetherin in transfected cells. (A) Empty plasmid (control) or the indicated amounts of tetherin (left panel)- or angiotensin-converting enzyme 2 (ACE2) (right panel)-encoding plasmids were transfected into 293T cells, and the cells were infected with A/PR/8/1934 (H1N1) (abbreviated PR8) or A/Hamburg/4/2009 (H1N1) (abbreviated 2009) at MOIs of 0.1 and 0.3, respectively. At 1 h postinfection, the input viruses were removed by washing, and at 24 h postinfection, the supernatants were harvested and titers determined using the focus formation assay. The results of a single, representative experiment performed with triplicate samples are shown and were confirmed in three separate experiments. The statistical significance of differences between infection of control cells and tetherin- or ACE2-expressing cells was assessed employing Student's t test. (B) 293T cells transfected with a plasmid encoding tetherin or transfected with empty plasmid (control) were infected with laboratory-adapted FLUAV PR8 and A/WSN/1933 (H1N1) (abbreviated WSN), seasonal FLUAV A/Panama/2007/1999 (H3N2) (abbreviated PAN), or pandemic FLUAV 2009 at an MOI of 0.1 (PR8), 0.3 (PAN and 2009), or 0.01 (WSN) for 1 h. Subsequently, cells were processed and viral titers determined as described for panel A. The results of a single experiment performed with quintuplicate samples are shown. Error bars indicate standard deviations (SD). Similar results were obtained in two separate experiments. (C) MDCK cells transduced to express tetherin or control transduced were infected with PR8 or 2009 at an MOI of 0.01, 0.1, or 1.0 and processed as described for panel B. The results of a single experiment performed with triplicate samples are shown and were confirmed in three separate experiments. Error bars indicate SD. (D and E) Infection was carried out as described for panel B, using wt PR8 and reassortant PR8 viruses equipped with HA and NA of 2009 (PR8 × 2009 HA/NA) (D) or A/Aichi/2/1968 (H3N2) (PR8 × 1968 HA/NA) (E) at an MOI of 0.01. The results of single, representative experiments performed with sextuplicate samples are shown and were confirmed in a separate experiment. FFU, focus-forming units/ml; MOI, multiplicity of infection.

Article Snippet: A/PR/8/1934 (H1N1), A/WSN/1933 (H1N1), A/Panama/2007/1999 (H3N2), PR8 × 2009 HA/NA, and PR8 × 1968 HA/NA were propagated in the chorio-allantoic cavities of 10-day-old embryonated hen eggs (Valo BioMedia GmbH, Germany) for 48 h at 37°C.

Techniques: Transfection, Plasmid Preparation, Infection, Tube Formation Assay, Expressing

Journal: Journal of Virology

Article Title: Tetherin Sensitivity of Influenza A Viruses Is Strain Specific: Role of Hemagglutinin and Neuraminidase

doi: 10.1128/JVI.00615-15

Figure Lengend Snippet: Neuraminidase and hemagglutinin of pandemic FLUAV confer resistance to endogenous tetherin in NCI-H358 cells. (A) NCI-H358 cells were transfected with scrambled siRNA (control) or tetherin-specific siRNA, and tetherin expression was assessed by Western blotting. The results of a representative experiment are shown and were confirmed in three separate experiments. Bands corresponding to tetherin are highlighted by an asterisk. The tetherin signal is heterogeneous, due to heterogeneity in tetherin glycosylation. (B) NCI-H358 cells were transfected with scrambled siRNA (control) or tetherin-specific siRNA and subsequently infected with A/PR/8/1934 (H1N1) (abbreviated PR8), A/Hamburg/4/2009 (H1N1) (abbreviated 2009), and a reassortant PR8 virus equipped with HA and NA of 2009 (PR8 × 2009 HA/NA) or A/Aichi/2/1968 (H3N2) (PR8 × 1968 HA/NA) at an MOI of 0.1 (PR8, PR8 × 2009 HA/NA, and PR8 × 1968 HA/NA) or 0.3 (2009). The average from three independent experiments performed with triplicates samples is shown. Error bars indicate standard error of the mean (SEM).

Article Snippet: A/PR/8/1934 (H1N1), A/WSN/1933 (H1N1), A/Panama/2007/1999 (H3N2), PR8 × 2009 HA/NA, and PR8 × 1968 HA/NA were propagated in the chorio-allantoic cavities of 10-day-old embryonated hen eggs (Valo BioMedia GmbH, Germany) for 48 h at 37°C.

Techniques: Transfection, Expressing, Western Blot, Infection

Journal: Journal of Virology

Article Title: Tetherin Sensitivity of Influenza A Viruses Is Strain Specific: Role of Hemagglutinin and Neuraminidase

doi: 10.1128/JVI.00615-15

Figure Lengend Snippet: Tetherin antagonism by hemagglutinin and neuraminidase depends on the virion context. (A) 293T cells were cotransfected with a plasmid encoding HIV-1 Gag and an empty plasmid or tetherin-encoding plasmid. In addition, cells were transfected with plasmids encoding Vpu, 1918 HA, or 1918 NA or encoding no protein (control). At 40 h posttransfection, the presence of Gag in culture supernatants and cell lysates was determined by Western blotting. In addition, the expression of tetherin and β-actin in cell lysates was determined. Similar results were obtained in three separate experiments. (B) 293T cells were cotransfected with a plasmid encoding HIV-1 Gag and an empty plasmid or tetherin-encoding plasmid and infected with the indicated FLUAV at the indicated MOIs. As a negative control, the cells were mock infected. At 24 h postinfection, supernatants (sups) were analyzed for expression of Gag, while cell lysates were analyzed for expression of Gag, tetherin, β-actin, and FLUAV proteins (anti-FLUAV H1N1 antibody was used for detection of viral proteins in A/Hamburg/4/2009 [H1N1]-infected cells, while an HA-specific antibody was employed to probe lysates from PR8 × 1968 HA/NA-infected cells). Similar results were obtained in at least three separate experiments. Bands with the molecular masses expected for NP and M1 proteins are marked with black-filled (NP) and gray-filled (M1) triangles. MOI, multiplicity of infection; HA, hemagglutinin; NA, neuraminidase.

Article Snippet: A/PR/8/1934 (H1N1), A/WSN/1933 (H1N1), A/Panama/2007/1999 (H3N2), PR8 × 2009 HA/NA, and PR8 × 1968 HA/NA were propagated in the chorio-allantoic cavities of 10-day-old embryonated hen eggs (Valo BioMedia GmbH, Germany) for 48 h at 37°C.

Techniques: Plasmid Preparation, Transfection, Western Blot, Expressing, Infection, Negative Control

Journal: Journal of Virology

Article Title: Tetherin Sensitivity of Influenza A Viruses Is Strain Specific: Role of Hemagglutinin and Neuraminidase

doi: 10.1128/JVI.00615-15

Figure Lengend Snippet: Neuraminidase and hemagglutinin of pandemic FLUAV reduce tetherin expression. (A) 293T cells were transfected with a tetherin-encoding plasmid or empty plasmid and infected with A/PR/8/1934 (H1N1) (abbreviated PR8), A/Hamburg/4/2009 (H1N1) (abbreviated 2009), and a reassortant PR8 virus equipped with HA and NA of 2009 (PR8 × 2009 HA/NA) or A/Aichi/2/1968 (H3N2) (PR8 × 1968 HA/NA) at an MOI of 0.1 (PR8, PR8 × 2009 HA/NA, and PR8 × 1968 HA/NA) or 0.3 (2009). At 1 h postinfection, the virus-containing medium was replaced by fresh culture medium, and cells were cultured for 24 h. Thereafter, cells were lysed and expression of tetherin and β-actin in cell lysates determined by Western blotting. Similar results were obtained in three separate experiments. (B) The tetherin and β-actin signals measured for panel A were quantified using ImageJ software and relative tetherin expression determined. Results represent the average from three independent experiments. Tetherin levels in mock-infected cells were set as 100%. The statistical significance of differences between tetherin expression in mock-infected and FLUAV-infected cells was assessed by Student's t test.

Article Snippet: A/PR/8/1934 (H1N1), A/WSN/1933 (H1N1), A/Panama/2007/1999 (H3N2), PR8 × 2009 HA/NA, and PR8 × 1968 HA/NA were propagated in the chorio-allantoic cavities of 10-day-old embryonated hen eggs (Valo BioMedia GmbH, Germany) for 48 h at 37°C.

Techniques: Expressing, Transfection, Plasmid Preparation, Infection, Cell Culture, Western Blot, Software

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Pan-antiviral effects of a PIKfyve inhibitor on respiratory virus infection in human nasal epithelium and mice

doi: 10.1128/aac.01050-23

Figure Lengend Snippet: Antiviral effects of PIKfyve inhibitors against influenza isolates in MDCK cells, evaluated by CPE a

Article Snippet: In vivo H1N1 infection BALB/c mice (male, 20–30 g) were inoculated intranasally on Day 0 with H1N1 PR8 (0.65 × 10 5 PFU/mouse) in Pharmidex UK.

Techniques:

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Pan-antiviral effects of a PIKfyve inhibitor on respiratory virus infection in human nasal epithelium and mice

doi: 10.1128/aac.01050-23

Figure Lengend Snippet: Antiviral effects of PIKfyve inhibitors against influenza isolates. (A) Concentration-dependent cell toxicity and antiviral effects of apilimod mesylate (AM) in MDCK cells infected with H1N1 A/California/07/2009. (B) Concentration-dependent cell toxicity and antiviral effects of YM201636 (YM) in MDCK cells infected with H1N1 A/California/07/2009. (C) Antiviral effects of AM and YM in MDCK cells infected with H3N2, A/Ohio/88/2012 v. (D) Antiviral effects of AM and YM in MDCK cells infected with H5N1, Duck/MN/1525/81. Compounds were treated at the same time when the virus was inoculated, and CPE was determined on Day 3 post-inoculation by neutral red staining.

Article Snippet: In vivo H1N1 infection BALB/c mice (male, 20–30 g) were inoculated intranasally on Day 0 with H1N1 PR8 (0.65 × 10 5 PFU/mouse) in Pharmidex UK.

Techniques: Concentration Assay, Infection, Virus, Staining

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Pan-antiviral effects of a PIKfyve inhibitor on respiratory virus infection in human nasal epithelium and mice

doi: 10.1128/aac.01050-23

Figure Lengend Snippet: Effects of Apilimod mesylate on H1N1(PR8) infected ALI-cultured nasal epithelium. (A) Kinetics of H1N1 viral load in apical washes post-virus inoculation. On Day 0, the virus was inoculated and removed after 60 min of absorption. Apical washes were collected after 1-hour incubation (and wash) on Day 0, and once daily from Day 1 to Day 3. (B) Viral load determined by TCID50 assay in apical washes from the inserts treated vehicle and AM, which were collected on Day 2 post-inoculation. (C) Kinetics of cell integrity determined as TEER post-virus inoculation. (D) TEER determined in epithelium inserts treated with vehicle and AM on Day 2 post-inoculation. (E) The kinetics of Rantes and CXCL8 release in apical washed from the epithelium inserts infected with H1N1, and the effects of AM on Rantes (F) and CXCL8 (G) in apical washes collected on Day 2 post-inoculation.

Article Snippet: In vivo H1N1 infection BALB/c mice (male, 20–30 g) were inoculated intranasally on Day 0 with H1N1 PR8 (0.65 × 10 5 PFU/mouse) in Pharmidex UK.

Techniques: Infection, Cell Culture, Virus, Incubation, TCID50 Assay

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Pan-antiviral effects of a PIKfyve inhibitor on respiratory virus infection in human nasal epithelium and mice

doi: 10.1128/aac.01050-23

Figure Lengend Snippet: H1N1 viral load in apical wash from ALI nasal epithelium treated with Apilimod or oseltamivir

Article Snippet: In vivo H1N1 infection BALB/c mice (male, 20–30 g) were inoculated intranasally on Day 0 with H1N1 PR8 (0.65 × 10 5 PFU/mouse) in Pharmidex UK.

Techniques:

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Pan-antiviral effects of a PIKfyve inhibitor on respiratory virus infection in human nasal epithelium and mice

doi: 10.1128/aac.01050-23

Figure Lengend Snippet: Effects of intranasal apilimod (Apilimod base: AB, and Apilimod mesylate: AM) treatment on H1N1-infected BALB/c mice. Mice were inoculated intranasally with H1N1 PR8 (1.0 × 105 PFU/mouse), and the animals were sacrificed 5 days post-virus inoculation. Apilimod was treated once daily on day 0 (4 hours before infection), and then on Days 1, 2, and 3. Body weight loss triggered by virus infection (A, B), viral load in lung tissue (C) and nasal tissue (D), and neutrophil accumulation in BALF (E) were evaluated. For viral load, individual data have been plotted as geometric mean. For body weight. mean ± SEM was shown. *P < 0.05, ***P < 0.001 vs H1N1-infected control.

Article Snippet: In vivo H1N1 infection BALB/c mice (male, 20–30 g) were inoculated intranasally on Day 0 with H1N1 PR8 (0.65 × 10 5 PFU/mouse) in Pharmidex UK.

Techniques: Infection, Virus, Control

Journal: Antimicrobial Agents and Chemotherapy

Article Title: Pan-antiviral effects of a PIKfyve inhibitor on respiratory virus infection in human nasal epithelium and mice

doi: 10.1128/aac.01050-23

Figure Lengend Snippet: Effects of Apilimod mesylate administered intranasally on H1N1-induced inflammation detected in bronchoalveolar lavage and nasal lavage of H1N1-infected mice a

Article Snippet: In vivo H1N1 infection BALB/c mice (male, 20–30 g) were inoculated intranasally on Day 0 with H1N1 PR8 (0.65 × 10 5 PFU/mouse) in Pharmidex UK.

Techniques: Inhibition, Saline, Virus

Journal: Frontiers in Microbiology

Article Title: Cell Receptors for Influenza a Viruses and the Innate Immune Response

doi: 10.3389/fmicb.2012.00117

Figure Lengend Snippet: Summary of cell surface or soluble host molecules reported to interact with IAV .

Article Snippet: MBL (opsonization) , Mouse model- in vivo /macrophages , PR8 (H1N1) , Dispensable for humoral immunity , Gonzalez et al. ( ) .

Techniques: Virus, In Vivo