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Immunology

Jnana Therapeutics Expands Leadership Team with Two Experienced Biopharmaceutical Executives – Yahoo Finance

Company appoints Nick Pullen, PhD, as Senior VP, Head of Biology and Brian Danieli as VP, Head of Finance & Operations

Jnana Therapeutics, a biotechnology company targeting the solute carrier (SLC) family of metabolite transporters to treat underserved diseases, today announced that it has expanded its leadership team with the appointment of two accomplished biopharmaceutical executives: Nick Pullen, PhD, as Senior Vice President, Head of Biology, and Brian Danieli as Vice President, Head of Finance and Operations. These new executives join Jnana at a significant time in the companys evolution as it advances its first SLC transporter-targeted therapies toward clinical development.

Nick Pullen, PhD, Senior Vice President, Head of Biology

"Nick is an experienced and passionate leader in drug discovery and development with deep knowledge in several therapeutic areas, including renal disease and inflammation, that are highly relevant to our R&D work with SLC transporters," said Joel Barrish, PhD, co-founder and Chief Scientific Officer of Jnana Therapeutics. "We are delighted to welcome Nick to our team and look forward to his contributions in building our research and development strategy and helping guide our lead programs toward the clinic."

In the role of Senior Vice President, Head of Biology, Dr. Nick Pullen will work to further leverage Jnanas RAPID platform to systematically target SLC transporters and develop novel small molecule drug candidates. Dr. Pullen is an experienced drug discovery and development leader with 20 years of experience and a proven track-record of therapeutic innovation across multiple disease areas. Before joining Jnana, he was Vice President, Integrative Sciences, Inflammation & Immunology, Cardiovascular & Fibrosis, at Bristol Myers Squibb and prior to this, he served as Executive Director, Inflammation & Immunology for Celgene. In both of these roles, Dr. Pullen was responsible for scientific and strategic leadership of externalized drug discovery programs applying novel technologies and scientific insights to the expansion of the Inflammation & Immunology portfolio as well as more broadly. Dr. Pullen brings extensive experience in Inflammation & Fibrosis, following a career at Pfizer which spanned more than 15 years and brought multiple development candidates to clinical evaluation and touched many disease areas including renal disease, IBD and NASH, a breadth of experience with significant pertinence to the emerging Jnana portfolio. Dr. Pullen received his PhD in biochemistry from the University of Southampton in the UK.

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"The Jnana team have made remarkable progress in the development of technologies that open up the therapeutic opportunity afforded by targeting the SLC gene family. I am thrilled to be joining Jnana at this exciting stage in the companys growth and to help them build a pipeline of small molecules targeting SLC transporters," said Dr. Pullen.

Brian Danieli, Vice President, Head of Finance & Operations

"Brians extensive finance background and expertise will be a critical addition to the organization," said Caroline Stark Beer, Jnanas Chief Business Officer. "Were very pleased to welcome Brian to Jnana and look forward to Brians financial and operational leadership as we enter a new stage of growth."

As the Head of Finance and Operations of Jnana Therapeutics, Brian Danieli will expand the companys finance and operations infrastructure to allow for growth to a clinical-stage drug developer. Mr. Danieli is an expert finance leader with more than 20 years of global experience with fast-growing biotechnology companies. He joins Jnana from Momenta Pharmaceuticals, where he led Financial Planning & Analysis. Previously, he served for more than 20 years in roles of increasing responsibility at Sanofi Genzyme. His most recent position at Sanofi Genzyme was Head of Finance for North America Rare Disease and Rare Blood Disorders, and he drove all aspects of strategic financial planning and operations for the North American region for two business units representing $2B in combined sales with over 500 employees and 12 products. In his roles at Sanofi Genzyme, Mr. Danieli spearheaded the integration of Bioverativ and Ablynx acquisitions, implemented financial modeling and assembled franchise performance metrics for investor audiences. Earlier in his career, he held financial positions at Blue Cross Blue Shield of Massachusetts and KPMG. He earned a BS in accounting from Boston College.

"I am eager to leverage my experience to support Jnanas evolution in the next stage of its business," said Mr. Danieli. "I see tremendous potential for Jnanas platform to bring innovation to a range of diseases, and I am excited to be part of a team that is committed to bring novel medicines to make a difference in the lives of patients."

About Jnana Therapeutics

Jnana Therapeutics is a biotechnology company focused on opening the solute carrier (SLC) family of metabolite transporters as a target class to develop transformational therapeutics. Jnana uses its RAPID platform, a proprietary, cell-based drug discovery approach, to systematically target SLC transporters and develop best-in-class therapies to treat a wide range of diseases, including immune-mediated, neurological and metabolite-dependent diseases. Headquartered in Boston, Jnana is founded by world-renowned scientists and backed by leading life science investors. For more information, please visit http://www.jnanatx.com and follow us on Twitter and on LinkedIn.

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Kathryn MorrisThe Yates Networkkathryn@theyatesnetwork.com 914-204-6412

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Jnana Therapeutics Expands Leadership Team with Two Experienced Biopharmaceutical Executives - Yahoo Finance

Immunology

[Full text] Lipid Profile and IL-17A in Allergic Rhinitis: Correlation With Diseas | JAA – Dove Medical Press

Dina Sheha,1 Lobna El-Korashi,2 Amany M AbdAllah,3 Marwa M El Begermy,4 Doaa M Elzoghby,5 Amira Elmahdi1

1Department of Internal Medicine, Allergy and Clinical Immunology, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 2Department of Medical Microbiology and Immunology, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 3Department of Family Medicine, Faculty of Medicine, Zagazig University, Zagazig, Egypt; 4Department of Otorhinolaryngology, Faculty of Medicine, Ain Shams University, Cairo, Egypt; 5Department of Clinical Pathology, Faculty of Medicine, Ain Shams University, Cairo, Egypt

Correspondence: Dina ShehaFaculty of Medicine, Ain Shams University, El-Abbassia Street, Cairo, 11566, EgyptTel +20 1001525144Email DinaSheha@med.asu.edu.eg

Background: Recent data display the possible role of cytokines such as interleukin-10 (IL-10), IL-17 and IL-23 as a link between dyslipidemia and atopy; however, the relationship between dyslipidemia, allergic rhinitis (AR), and the underlying mechanisms involved is unclear.Purpose: To measure the lipid profile and IL-17A level in AR patients in comparison to healthy controls, and correlate serum lipid level with the severity of symptoms and quality of life (QoL) of AR patients.Patients and Methods: Peripheral blood samples were collected from AR patients (n=70) and a control group (n=80). Samples were analyzed for serum total IgE by ELISA, serum lipid profile, and IL-17A level by ELISA. Severity of AR symptoms was assessed by visual analogue scale (VAS) score and the rhinoconjunctivitis QoL questionnaire.Results: Serum lipid profile and level of IL-17A in AR patients were significantly higher in comparison to controls (P < 0.001). Positive correlations were found between total cholesterol (TC) and the severity of AR and QoL. IL-17A was positively correlated with triglyceride (TG) level and low-density lipoprotein cholesterol (LDL-C) (P=0.011, r=0.303; P=0.043, r=0.242, respectively). Additionally, IL-17A was negatively correlated with high-density lipoprotein cholesterol (HDL-C) level (P=0.036, r= 0.251). IL-17A was positively correlated with both age and VAS score with statistical significance (P=0.033, r=0.225; P=0.011, r=0.302, respectively).Conclusion: Dyslipidemia might play a potential role in the severity of AR symptoms and impairment of patients QoL. Highlighting this association might alert physicians to evaluate the lipid profile in AR patients for timely diagnosis and treatment of dyslipidemia in an attempt to improve disease control and improve QoL.

Keywords: allergic rhinitis, cholesterol, dyslipidemia, IgE, interleukin-17, quality of life

Allergic rhinitis (AR) is a symptomatic disorder induced by exposure of the nasal mucosa to diverse aeroallergens that is mediated through immunoglobulin E (IgE) hypersensitivity reactions. AR is characterized by four cardinal symptoms of watery rhinorrhea, nasal obstruction, nasal itching and sneezing.1 AR has a wide prevalence, it is estimated to affect 2030% of adults and up to 40% of pediatrics.2 AR is associated with multiple comorbid disorders, including asthma, conjunctivitis, eczema, rhinosinusitis, adenoid hypertrophy, obstructive sleep apnea, disordered sleep with consequent educational and behavioural effects. These associated comorbidities negatively correlate with the quality of life (QoL), and work performance.3

Dyslipidemia is a major risk for atherosclerosis and cardiovascular diseases especially coronary heart disease (CHD), and may play a major role earlier than other risk factors.4 Dyslipidemia modulates the immune response through the release of pro-inflammatory mediators, activation of immune cells (eg, B-cell, T-cells and dendritic cells),5 promoting polarization of T-helper 2 (Th-2) and Th17 and downregulating interleukin-10 (IL-10) cytokine synthesis.6 Th2 and Th17 release cytokines as IL6, IL-1, IL-4, and IL-17.7 Th2 immune response with an increased production of IL-4 and tumour necrosis factor- (TNF-) has been described in AR.8

IL-17 cytokine, produced by Th17 cells, plays a pivotal role in host defense reactions, inflammatory diseases and allergic responses.IL-17 belongs to a family of cytokines that includes six members of different homology and function: IL-l7 (also IL-17A) IL-17B, IL-17C, IL-17D and IL-17 E.9 The role of TNF- and IL-17 in the pathogenesis and regulation of inflammation in autoimmune diseases such as psoriasis has been described previously.10,11 Serum IL-17A level correlated significantly with clinical and inflammatory markers in patients with persistent moderate to severe AR evaluated during the pollen season. Moreover, studies suggest that serum IL-17A level correlates with symptom scores and with the number of peripheral blood eosinophils, suggesting that Th-17 cells may be involved in the chronic allergic reaction. Authors even proposed IL-17A as a new biomarker of disease progression and allergy.12 Research suggests a link between cholesterol and the adaptive immune system, as both have the same immunological pathways involving Th1 toTh2 switch, an increase in Th2 related IgG1 and IgE release, and elevation of pro-inflammatory Th2 cytokines release such as IL-4.13

Numerous research investigated the association between dyslipidemia and allergic diseases. Fessler et al14 demonstrated the relationship between total cholesterol (TC) level and atopy in children 617 years of age. Ouyang et al15 reported increased allergic sensitisation with elevated low-density lipoprotein cholesterol (LDL-C) level. Kusunoki et al16 demonstrated a positive association between TC and LDL-C levels and the allergic sensitization in school-aged children. Similarly, a meta-analysis of ten studies investigated the lipid profile of asthmatics and found higher levels of LDL and low level of high-density lipoprotein (HDL) in asthma patients in comparison to controls.17 Vinding et al18 found higher LDL and triglycerides (TG) were associated with asthma, airway obstruction and higher incidence of aeroallergen sensitization. Elevated HDL was associated with reduction of airway obstruction and lower risk of aeroallergen sensitization. To our knowledge, only a few studies have explored the association of abnormal serum lipids in AR patients and its effect on disease severity.

Since IL-17A could represent a link between AR and dyslipidemia, we aimed to investigate the possible relationship between AR, IL-17A level and dyslipidemia, and correlate level with the severity of AR and QoL of AR patients.

Seventy adult AR patients and 80 healthy volunteers as a control group were enrolled in the current casecontrol study, conducted from March 2019 to August 2019. AR patients were selected by systematic randomization from patients attending the allergy outpatient clinic at Ain Shams University, Cairo and Zagazig University, Zagazig, Egypt. Laboratory Techniques were performed in the Medical Microbiology and Immunology Department, Zagazig University, Zagazig, Egypt. Healthy controls were apparently healthy individuals who were recruited from relatives of patients attending the internal medicine outpatient clinic. They had no chronic diseases or allergic disorders, they were not on regular medications and had no complaints concerning mental or physical health.

AR was diagnosed according to the Allergic Rhinitis and its Impact on Asthma (ARIA) guidelines.19 Inclusion criteria were atopic adult AR with a positive family history of atopy and positive skin prick test (SPT) for at least one inhalant allergen. Patients with asthma, those on statin therapy, patients with acute illness like high-grade fever, first 2 weeks following surgery, non-allergic inflammatory nasal pathology, sleep disorders, diabetics, obese patients, hypothyroid, hypertensive patients, smokers and patients with autoimmune disorders were excluded from the study. No patients received systemic steroids or immunotherapy within 1 month of enrollment. An informed verbal consent was obtained from all participants. The research ethics committee of Zagazig University approved the study (IRB number 6222-25-6-2020) and the procedure outlined for the obtainment of verbal consent. The whole process was documented and the consent was conducted with an impartial witness after which the consent was transcribed. The study procedure complies with the country regulations about subjects data protection and maintaining their integrity, and the study was conducted in accordance with the declarations of Helsinki.

Detailed medical history of allergy was collected from each participant including family history of atopy. Clinical examination (ear, nose, throat and chest examination), and SPT to common aeroallergens were performed in the clinic. Venous blood samples for serum lipid profile, serum total IgE and serum level of IL-17A weredrawn from all participants.

The severity of AR was measured using the visual analogue scale (VAS) score for global assessment of severity of nasal and non-nasal symptoms. AR patients were asked to rate the combination of the nasal and non-nasal symptoms on a scale (010 cm) as follows:

Mild: 03; Moderate: 3.17; Severe: 7.110.19

QoL was assessed in the AR group by the RQLQ total score. The instrument has 28 items in seven domains (sleep, non-rhinoconjunctivitis symptoms, practical problems, nasal symptoms, eye symptoms, activity limitations, and emotional function). The overall RQLQ score is the mean of all 28 responses.19

Skin testing was performed on AR patients according to Bernstein et al.20 A panel for the most common locally encountered inhaled allergens was used including house dust mites, cockroach, cotton, molds mix, ragweed, mugwort, Chenopodium album, hay dust, pigeon feathers, dog hair, cat hair, rabbit hair. Allergen extracts of skin testing were locally prepared at Allergy and Immunology Unit, Department of Internal Medicine, Faculty of Medicine, Ain Shams University. Aqueous allergen extracts (1:100 wt/vol) preparation was done according to allergen extract preparation guidelines developed by the AAAAI/ACAAI/JCAAI and all aqueous allergen extracts were stored at 4 C.21

The maximum or mean diameter of the wheal to various allergens was read at 15 minutes. A wheal of 3mm or more in diameter was considered positive (indicating sensitization to the allergen).

Under complete aseptic conditions, 10mL of fasting venous blood was obtained by a clean venipuncture in the early morning from all participants after 912 hours of fasting. Patients were on regular average diet 3 days before sampling. The serum was separated by centrifugation (1000 g for 15 minutes) and divided into three tubes. Serum of one tube was immediately assayed for lipid profile (TC, TG, HDL-C and LDL-C), while the serum collected in the other tube was stored at 20C for subsequent assay of the serum total IgE, IL-17A concentrations. Hemolysed samples were discarded. Repeated freezing and thawing was avoided.

Serum TC, triglycerides and HDL-C were assayed on Microlab 300 Semi Automated Clinical Chemistry Analyzer supplied by EliTech clinical system (France,www.elitechgroup.cominfo@elitechgroup.com).

TC, TG and HDL-C were assayed by (homogenous for HDL-C) enzymatic colorimetric quantitative determination at wavelength (500, 500, and 600/700 nm respectively) using kits provided by Human diagnostics kit (Human Gesellschaft fr Biomedica und Diagnostica mbH Max-Planck-Ring 21.6 5205 Wiesbaden-Germany). LDL-C was calculated according to the Friedwald equation.22

Dyslipidemia was defined according to the American College of Cardiology/American Heart Association (ACC/AHA) Blood Cholesterol 2013 Guideline, as follows: hypercholesterolemia was defined as total cholesterol (TC) level greater than 200 mg/dL and/or LDL-C level greater than 100 mg/dL, hypertriglyceridemia as TG level greater than 150 mg/dL; and low HDL-C lower than 40 mg/dL in men and 50 mg/dL in women.23

Quantitative measurement of total IgE in the serum was done using a commercially available quantitative enzyme-linked Immunosorbent assay (ELISA) Kit supplied by Calbiotech Inc. (1935 Cordell Ct., El Cajon, CA 92020, USA) according to the manufacturers instructions, and the results were expressed in IU/mL.

Human IL17-A was measured by commercially available quantitative ELISA Kit supplied by Thermo Fisher Scientific (Bender Med Systems gmbH/Campus Vienna Biocenter 2/1030 Vienna, Austria) according to the manufacturers instructions and expressed in pg/mL.

Data analysis was performed using the software SPSS (Statistical Package for the Social Sciences) version 20 (SPSS Inc., Chicago, Illinois, USA). Quantitative variables were described using means and standard deviations. Categorical variables were described using absolute frequencies and to compare the proportion of categorical data, chi square test was used when appropriate. KolmogorovSmirnov (distribution-type) and Levene (homogeneity of variances) tests were used to verify assumptions for use in parametric tests. To compare the means of two groups, independent sample t-test was used. MannWhitney test was used to compare continuous variables between two groups when data were not normally distributed. Pearson correlation and Spearman rank correlation coefficients were used to assess the strength and direction of a linear relationship between two variables. The level of statistical significance was set at 5% (P<0.05). Highly significant difference was present if P0.001.

Descriptive data of the study groups are represented in Table 1. Patients and controls were matched regarding age and gender. The mean age of AR patients was 30.74 years ( 7.24) and controls were 32.85 years ( 7.5). Total IgE and IL17-A level were significantly higher in cases in comparison to controls (Table 1). Runny nose, sneezing, nasal obstruction, postnasal drip, itchy nose, cough and eye symptoms prevailed in 60%, 62.9%, 72.9%, 30%, 20%, 38.6% and 10% of the patients within AR group, respectively.

Table 1 Demographic and Laboratory Data Characteristics of the Study Groups

Associated allergic conjunctivitis and atopic dermatitis co-existed in 30% and 3% respectively of those patients (Table 1)

Levels of TC and LDL-C were statistically significantly higher in cases than controls. Mean SD of TC in cases and controls was 225,6562.91mg/dl and 187.9235.24mg/dl, respectively.

Regarding HDL_C, meanSD in cases was 47.255.36 mg/dl and in controls 49.834.29 mg/dl, showing statistically significantly lower levels in cases than controls. There was a non-significant difference in serum TG and very-low-density lipoprotein cholesterol (VLDL-C) between the two groups (P=0.79, P=0.175) (Table 2).

Table 2 Serum Lipid Profile of Study Subjects

AR patients had significantly increased risk of dyslipidemia by 6.27-fold (95% confidence interval (CI) of crude odds ratio (COR)=2.7114.51, P<0.001). Approximately 44% of the patients with AR had dyslipidemia versus 11.2% of the healthy controls.

Correlation studies were performed to assess the relationship between serum lipid profile and the severity of AR assessed by VAS (P=0.039, r=0.31) and RQLQ score (P=0.04, r=0.247). There was a positive correlation between IL-17A and TG and LDL-C levels (P=0.011, 0.043, respectively). IL-17A level was negatively correlated to HDL-C level (P=0.036), while no significant correlation was found for the other correlation studies listed in Table 3.

Table 3 Correlation Between Serum Lipid Profile and Different Study Parameters

There was a statistically significant correlation between IL-17A and both age and VAS score (p=0.033, r=0.225, 0=0.011, r=0.302; 95% CI; 0.078:0.486) and VAS score (95% CI; 0.078:0.486). On the other hand, there was a non-significant correlation between IL-17A and total IgE and RQLQ score (Table 4).

Table 4 Correlation Between IL-17A and All of Patients Age, VAS, RQLQ, and Total IgE

Serum lipid levels and their clinical implication in the management and monitoring of cardiovascular diseases or diabetic patients is well established.24,25 On the contrary, the role of dyslipidemia in AR is not fully elucidated.

The current casecontrol study aimed to investigate the possible relationship between AR, IL-17A level and dyslipidemia and correlate levels with the severity of AR and QoL of AR patients. We included 70 AR patients and 80 healthy controls, and found dyslipidemia in 44% of AR patients versus 11.2% of controls. Levels of TC and LDL-C were significantly higher in AR patients, while HDL-C was significantly lower. Similarly, recent studies have demonstrated a significant association between high serum lipid levels and AR.26,27 Additionally, Schfer et al investigated the effect of serum cholesterol on atopy and found that elevation of serum cholesterol is associated with an increased incidence of atopic diseases.28 Recent publications suggest the role of dyslipidemia in promoting atopic inflammation, through polarizing Th2 response.7,29 Another proposed theory is the cholesterol trafficking. Cholesterol is a critical microdomain of cell wall lipid rafts that plays an essential role in cell signaling. Changes in these cholesterol rafts trigger the toll-like receptor-signaling pathway of the innate immune reaction, which in turn aggravates the atopic inflammation.30

We report a positive correlation between TC levels and both VAS score, and RQLQ score. Ahmed et al in a recent Egyptian study reported similar results,29 which was also confirmed by regression analysis of Yon et al.31 TC and LDL-C were associated with the severity of AR high TC, which has been reported to increase allergen-specific IgE synthesis thus exacerbating allergic symptoms, which denotes a positive correlation between dyslipidemia and atopy.32 This could be attributed to the impact of dyslipidemia on the immune system where dyslipidemia induces a shift toward an immunologic Th2-oriented response and exacerbates allergic inflammation.26,33 Additionally, hypercholesterolemia is known for being pro-inflammatory, inducing the release of inflammatory cytokines30 and in turn aggravating the symptoms of AR.

We assume the poor QoL is due to the burden of increased AR severity, as well as the socioeconomic and financial burden of treatment costs, and the metabolic burden of dyslipidemia. The inflammatory nature of AR causes nasal obstruction, sleep difficulties, snoring, hypersomnolence, diminished work performance, and finally insomnia that all negatively impact the patients QoL.

Several studies have suggested that metabolic factors, such as dyslipidemia, are related to allergic diseases, but the related causal mechanisms remain elusive.3436 Hence we investigated the role of IL-17A as a link between AR and dyslipidemia, in order to explore one of the cytokines incriminated in the pathogenesis.

We found higher levels of IL-17A in AR patients compared to controls. Similarly, many studies declared this finding.3743 Moreover, other studies found higher IL-17A positive cells in peripheral blood and nasal mucosa of AR patients compared to healthy controls.44,45 It seems that Th17 cells may be involved in the process of neutrophil infiltration that occurs during the acute phase of allergic reaction.46 Besides, IL-17 induces allergen-specific Th2 cell activation, hence the production of serum IgE and eosinophil accumulation suggesting a regulatory role in Th2-allergic immune response.47

We report a positive correlation between IL-17A level and both TG and LDL-C levels, while IL-17A was negatively correlated to HDL-C level among AR patients. These findings are in line with.26 This could be explained by the fact that dyslipidemia causesTh2 and Th17 polarization and cytokines release as (IL-4, IL-17) with decreased production of IL-10. These cytokines disturbance is related to chronic inflammation that is common to both atopic predisposition and dyslipidemia6,46,48 Similarly, Vinding et al found that triglyceride levels were associated with increased risk of aeroallergen sensitization, which is one cause of AR.18

Furthermore, we found significant positive correlation between IL-17A and AR severity assessed by VAS score. IL-17 is a pro-inflammatory cytokine which in turn explains its role in increasing the severity of AR symptoms. This is consistent with many other studies.49 Also, Nieminen et al50 showed that serum IL-17A levels and allergen-induced IL-17A messenger RNA expression correlate with symptom severity, as assessed via a VAS score and symptom medication score, respectively. In addition, Lu et al51 reported significant correlations between AR symptoms and the expression of IL-17 in nasal mucosa and peripheral blood.

A study by Shahsavan et al52 found that patients with moderate to severe persistent AR demonstrated significantly greater IL-22 and IL-17A production than healthy controls, suggesting that the development of persistent AR is influenced by these cytokines. A correlation was found between IL-22 and IL-17A serum levels, along with the mean number of IL-22 and IL-17A positive cells in the nasal mucosa, and specific IgE levels, nasal eosinophil count, and total nasal symptom score.

The results of these studies are partially in conflict with Amin et al,53 who found no correlation between IL-17 and the patients symptom scores, although AR patients have significant higher serum levels of IL-17 than controls.

In our study, we did not report a correlation between IL-17 and total IgE. Huang et al,45 documented that IL-17 level was positively related to the level of total IgE, and the serum level of IL-17 and IL-23 in the AR patients were markedly higher than those in healthy subjects.

We are aware that one of the limitations of the current study is the small sample size of the study population, and large-scale multicenter studies should be performed to further elucidate the importance of measuring serum lipid profile in AR patients, and including pediatrics where AR is more prevalent. The disease duration of AR was not reported in the current study. In addition, longitudinal studies might aid in a better understanding of the causal relationship between dyslipidemia and AR, to determine whether AR is preceded by dyslipidemia or the other way round. The role of cytokines as IL-17A as a biomarker of AR severity and its role in dyslipidemia should be further elucidated. Furthermore, early detection of dyslipidemia in AR patients may help in the prevention of long-term future cardiovascular morbidity and mortality in AR patients.

Measuring of serum lipid profile and IL-17A in AR patients could be a potential indicator of severe disease, and future research ought to explore the impact of timely treatment of dyslipidemia on severity of AR and QoL of patients.

The research ethics committee of Zagazig University approved the study (IRB number 6222-25-6-2020), and an informed verbal consent was obtained from all participants.

We thank all patients who participated in the study.

All authors made substantial contributions to conception and design, acquisition of data, or analysis and interpretation of data; took part in drafting the article or revising it critically for important intellectual content; agreed to submit to the current journal; gave final approval of the version to be published; and agree to be accountable for all aspects of the work.

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

The authors report no conflicts of interest in this work.

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27. Alwan A, Alobaidi A. Lipid profile in patients with asthma and allergic rhinitis. Int J Med Sci. 2018;1(2):924.

28. Schafer T, Ruhdorfer S, Weigl L, et al. Intake of unsaturated fatty acids and HDL cholesterol levels are associated with manifestations of atopy in adults. Clin Exp Allergy. 2003;33(10):13601367. doi:10.1046/j.1365-2222.2003.01780.x

29. Ahmed M, Madian Y, El-Tabbakh M, El-Serafi A, Nasr G, Hessam W. Correlation between dyslipidemia and severity of allergic rhinitis. Egypt J Otolaryngol. 2018;34(2):111. doi:10.4103/ejo.ejo_90_17

30. Ko SH, Jeong J, Baeg MK, et al. Lipid profiles in adolescents with and without asthma: Korea National Health and Nutrition Examination Survey data. Lipids Health Dis. 2018;17(1):158. doi:10.1186/s12944-018-0807-4

31. Yon DK, Lee SW, Ha EK, et al. Serum lipid levels are associated with allergic rhinitis, nasal symptoms, peripheral olfactory function, and nasal airway patency in children. Allergy. 2018;73(9):1905190828. doi:10.1111/all.13484

32. Craig T, McCann J, GurevichH F, Davies M. The correlation between allergic rhinitis and sleep disturbance. J Allergy Clin Immunol. 2004;114:S13945. doi:10.1016/j.jaci.2004.08.044

33. Robertson AKL, Zhou X, Strandvik B, Hansson GK. Severe hypercholesterolaemia leads to strong Th2 responses to an exogenous antigen. Scand J Immunol. 2004;59(3):285293. doi:10.1111/j.0300-9475.2004.01403.x

34. Huang SL, Lin KC, Pan WH. Dietary factors associated with physician-diagnosed asthma and allergic rhinitis in teenagers: analyses of the first Nutrition and Health Survey in Taiwan. Clin Exp Allergy. 2001;31:259264. doi:10.1046/j.1365-2222.2001.00938.x

35. Lumia M, Luukkainen P, Kaila M, et al. Maternal dietary fat and fatty acid intake during lactation and the risk of asthma in the offspring. Acta Paediatr. 2012;101:e33743. doi:10.1111/j.1651-2227.2012.02718.x

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38. Ciprandi G, De Amici M, Murdaca G, et al. Serum interleukin-17 levels are related to clinical severity in allergic rhinitis. Allergy. 2009;64(9):13751378. doi:10.1111/j.1398-9995.2009.02010.x

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41. Tsvetkova-Vicheva VM, Gecheva SP, Komsa-Penkova R, Velkova AS, Lukanov TH. IL-17 producing T cells correlate with polysensitization but not with bronchial hyperresponsiveness in patients with allergic rhinitis. Clin Transl Allergy. 2014;4(1):3. doi:10.1186/2045-7022-4-3

42. Xuekun H, Qintai Y, Yulian C, Zhang G. Correlation of gammadelta-T-cells, Th17 cells and IL-17 in peripheral blood of patients with allergic rhinitis. Asian Pac J Allergy Immunol. 2014;32(3).

43. Bayrak Degirmenci P, Aksun S, Altin Z, et al. Allergic rhinitis and its relationship with IL-10, IL-17, TGF-, IFN-, IL 22, and IL-35. Dis Markers. 2018;2018:9131432. doi:10.1155/2018/9131432

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Immunology

IncellDx Files Patent for COVID Long Hauler Index and Active COVID-19 Severity Score – BioSpace

Company launches http://www.covidlonghaulers.com website to facilitate immune profiling and therapy

SAN CARLOS, Calif., Feb. 3, 2021 /PRNewswire/ -- IncellDx, a leading precision medicine diagnostics company, has filed patents for algorithms identifying immunologic profiles unique to COVID long haulers and patients with severe COVID.

IncellDx has developed and patented two distinct algorithms using machine learning, built on a tailored panel of cytokines and chemokines specific for abnormalities in cytokine storm conditions and in chronic COVID patients (often referred to as COVID "long haulers"). These have been submitted for publication (pre-print available through BioRx https://www.biorxiv.org/content/10.1101/2020.12.16.423122v1).

The first algorithm generates a severity score based on analysis of hundreds of COVID-19 patients spanning the spectrum of disease severity from mild to critical. The second algorithm derived from the same cytokine/chemokine immune panel, demonstrates that the immunology of long haulers is distinct from active COVID-19. This objective algorithm offers the opportunity for precision medicine to be used by physicians as a guide in the care of COVID-19 patients.

Bruce Patterson, M.D., CEO of IncellDx, commented that "Since the beginning of the COVID-19 pandemic, IncellDx has led the way in using biomarkers to develop precision medicine approaches to therapy including the post-COVID-19 long haulers. A recent preprint of a meta-analysis suggests as many as 80% of individuals infected by COVID-19 may have at least one symptom long after infection."

IncellDx, in collaboration with Drs. Ram Yogendra and Purvi Parikh, launched the website http://www.covidlonghaulers.com on January 29, 2021. The site will serve as a resource for patients and clinicians who are dealing with the long-term complications of COVID-19. The new COVID long hauler index and severity score will likely play an important role in providing clinicians with immunological information that will aid them in caring for these patients.

Ram Yogendra, M.D. of the ECA Wellness Center, said that "through our research on chronic COVID, we recognize that there is a significant group of patients who have debilitating symptoms and complications weeks and months after the initial infection. We believe our long hauler index and treatment center are key steps in addressing this growing public health crisis."

Purvi Parikh, M.D., Immunologist, Allergist and COVID -19 researcher, stated that "as with everything in this pandemic, many of the devastating and long-term side effects of this virus are mysterious and uncertain. So much attention is paid to the death rate, but we are missing those whose quality of life has been completely changed by this terrible virus. I am happy we are at the start of a journey to help find answers for these COVID patients who continue to struggle months later. "

About IncellDx

IncellDx, Inc., located in San Carlos, California, is a single-cell, molecular diagnostics company dedicated to revolutionizing healthcare, one cell at a time. By combining molecular diagnostics with high throughput cellular analysis, the company's focus is on critical life threatening diseases in the areas of COVID-19, infectious disease and oncology/immuno-oncology, i.e., cervical, head and neck, lung, bladder, breast and prostate cancers.

CONTACT: Chris Meda, 650-777-7630

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SOURCE IncellDx, Inc.

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Immunology

The Role of the Host Immune Response in COVID-19: Friend or Foe? – Technology Networks

One of the biggest mysteries of the current pandemic is why outcomes from SARS-CoV-2 infection vary so widely between different people. Researchers are searching for clues in the host immune response to the virus.Most people who are infected with SARS-CoV-2 will clear the virus with few or no symptoms, whereas others will develop a severe illness that can lead to hospitalization and death.As with any virus, its your immune system that protects you against the deleterious consequences of an infection, says Arne Akbar, professor of immunology at University College London. But theres something about the immune system that isnt quite right in combating SARS-CoV-2 that gives these very bad outcomes in some individuals.But exactly what this immune dysfunction looks like is poorly understood and is likely to differ between patients with severe disease.It appears that if the infection isnt cleared straight away, some of the disease pathologies might be caused by the immune system rushing to try and fight it, describes Deborah Dunn-Walters, professor of immunology at the University of Surrey and chair of the British Society of Immunology COVID-19 taskforce. So its important to try and understand the balance of the immune response whats good and whats not.Unraveling the complex interactions between SARS-CoV-2 and the immune system is challenging, but hugely important in shaping our response to the virus. Our knowledge of the host immune response is already helping to identify existing drugs for treating critically ill patients. It is also underpinning work to develop novel vaccines that offer our best hope of escaping the devastating impact of the current pandemic.

The next stage is the adaptive immune response, which takes longer to get up and running but generates a highly specific response against the virus. The immune system has B cells that can produce neutralizing antibodies against the virus and T cells that can recognize and kill virus-infected cells, continues Akbar. During the lag phase, as B and T cells become activated, innate immune cells can offer some protection, but theyre not as specialized in what they do.

During the early stages of the pandemic, some people expressed concern that the host immune response to SARS-CoV-2 might deviate from the normal pattern.Its been really positive to see the data accumulate, says Lucy Walker, professor of immune regulation at University College London. Its panned out pretty much as we would expect, with most people generating antibodies and nice T-cell responses.

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But like any army, it needs to be tightly controlled, says Akbar. If its not, this can lead to autoimmune conditions, like rheumatoid arthritis or type 1 diabetes, where the immune system starts to attack a persons body tissues.

Researchers are exploring what happens when the balance starts to shift the wrong way in COVID-19, leading to the immune system turning on the host.

Its rather like autoimmunity, says Walker. Most people clear the virus with few problems and switch off the immune response but some end up with a prolonged response and immune-mediated damage.

Researchers have uncovered a variety of factors that are known to increase the risk of severe COVID-19, including age and certain pre-existing health conditions which could provide clues as to what might be going wrong.

Theres a phenomenon called inflamm-aging where people have more background inflammation as they get older, says Akbar. Interestingly, some of the pre-existing health conditions that predispose to severe COVID-19 are associated with higher levels of these inflammatory mediators.

Researchers are exploring the hypothesis that background inflammation could interfere with the bodys ability to get rid of the virus quickly without inducing tissue damage.

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This immune memory should trigger a faster and bigger response if you encounter the virus again, explains Walker. That means you should clear the infection with far fewer symptoms compared to the first time and hopefully none at all.A recent study showed that healthcare workers who have previously had COVID-19 are provided with 83% protection for at least 5 months. Another study showed that immunity may last up to eight months, indicated by the presence of neutralizing antibodies, memory B cells and T cells in the bloodstream.For the vast majority of people, once youve had it you dont tend to get it again, says Akbar. A few anecdotal cases have generated a lot of attention, but its actually only a small number of people who get reinfected.

Understanding how long protection lasts will be important for informing future vaccination strategies. Some researchers predict that immunization against SARS-CoV-2 may even generate a better immune memory compared to a natural infection.

Viruses often have ways to evade the immune response, explains Walker. Thats one of the things that SARS-CoV-2 is quite good at delaying or suppressing the initial immune response very early on in an infection, whereas vaccines dont have those characteristics.

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Weve needed to draw on pre-existing knowledge about the normal immune response and the types of immune response you want to elicit with vaccines, says Walker. And weve also relied on the availability of immunological assays to measure these effects.

Every vaccine candidate must first undergo extensive pre-clinical testing to find out whether they offer protection against the infection and the disease.

You need the immunology to assess the safety and efficacy of a candidate vaccine before taking it into clinical trials, explains Dunn-Walters. You need to monitor for the presence of neutralizing antibodies and T-cell responses that are specific to the virus.Defining whats known as the correlates of protection is key, providing scientists with the ability to assess a vaccines efficacy by measuring the immune response rather than through clinical outcomes.It gives you the tools to then look at different populations without having to challenge thousands of people with the virus, says Dunn-Walters. Once a vaccine is proven to work, it may even become unethical for people to take part in randomized placebo-controlled trials.

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Every pandemic is going to be different so you cant necessarily write a complete rule book, reflects Dunn-Walters. But we can learn lessons that will help us to be better prepared to deal with future threats.

Others emphasize the importance of investing in a breadth of basic science, which has underpinned so much of what has been achieved.

We dont know where the next problem for humanity is going to come from and what were going to need to tackle it, says Walker. But having up-to-date textbooks about the basic principles will certainly put us in the best position to succeed.

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The Role of the Host Immune Response in COVID-19: Friend or Foe? - Technology Networks

Immunology

Screening, Within and Without | In the Pipeline – Science Magazine

So Im a small-molecule drug discovery person at heart, since I started out as a synthetic organic chemist. Talking about vaccines and antibodies nonstop is a bit of a strain, then, because immunology is full of stuff thats rather far removed from good ol small-molecule ligands. Actually immunology eventually wears out everyone. Even immunologists. It just keeps on going: detail on top of detail, layer upon layer of complex, interconnected, rococo feedback loops and backup systems, repurposed evolutionary holdovers, insanely subdivided cell lineages, all the rest of it.

But in the end, even a medicinal chemist starts to feel at home in some parts of it. Because one of the key events in the adaptive immune system is exactly like one of the key events in so many small-molecule drug research programs: high-throughput screening. I know that I have a lot of people reading this who have never done any such thing, so its worth some explanation. Now, in traditional med-chem and its allied fields, HTS has been a way of life for around 30 years now (before that it was low-throughput screening!) Its had a lot of refinements and extensions, but the fundamental process has not changed one bit: round up some of your biological target (an enzyme, a receptor, an interaction between two proteins, whatever youve got), and find some setup where you can get a signal when a compound does what you want to it. Do you want to set off a signal from a receptor? Keep two proteins from coming together? Gum up the works of some enzyme? Work up some assay system where when that desired event happens, you get a signal that come up out of the noise.

It could be (and often is) a flash of fluorescence at a particular wavelength. That idea has had plenty of changes rung on it maybe youre looking at two wavelengths at the same time and checking the ratio between them. Or you can set things up where its the polarization of that fluorescent light thats telling you something. Maybe youre running things in a way where the fluorescence is already going on and your desired stuff will shut it off. You can have fluorescent probe compounds; there are whole careers involved with those things. Then there are of course fluorescent proteins (like the famous Green Fluorescent Protein), and listing the ways that those are used in assays would take us the rest of the week. Theres are physical phenomena that will allow fluorescence to be set off only when two suitable species are close enough together in space, and as you can imagine, these have been turned into workhorse assays.

Luminescence can be used in similar ways. The enzyme luciferase has been exploited six ways from Sunday, with a long list of variations. Any good screening lab has a list of their compounds that have been shown to directly interfere with the enzyme (and can thus hose up your data). We love luciferase so much that we use both the firefly kind and one from a deep-sea critter called a sea pansy because they come in both green and red versions (and sometimes you use both of those at the same time, too). That same sort of only when they come close together trick can be worked with luminescence, too. No. there are all sorts of tricks you can play with funny wavelengths of colorful light, and all sorts of interesting ways you can set up assays to emit them.

But it doesnt have to be light. A classic way to do receptor assays (and others) is to have a radioactive compound already stuck to your target. You add some of your test substance and see if it kicks any of the hot stuff off, which you read off after a filtration step: the more radioactive your filtrate, the better your compound bound to the target. You can mix radioactivity and a light-driven readout, with a scintillation proximity assay: a radioligand that gives off a beta-particle lights things up only when its next to your target, and not under other conditions.

No matter how you run any of these, the idea is to get such an assay set up so that theres a high signal-to-noise, low chances for false positives and false negatives, no need for too many picky dispensing or mixing steps to get it running, and (especially) the ability to run at the smallest scale you can handle. I well recall when doing such things in assay plates with 8 wells by 12 (96 total) was considered kind of high-tech, but for a long time now any assay that cant be shrunk down to 384 wells (1624) or 1536 (3248) has been greeted with a weary sigh and a roll of the eyes. There are legions of commercial assay kits and associated dispensers, plate-handling robots, and plate-reading machines that will assist you in getting all this going.

You want this miniaturization, of course, because you want to put the HT in the HTS. A full-deck screen at a big drug company can be a few million compounds if you pull out all the stops (which we dont so often any more, to be honest), and doing that 96 wells at a time will take you a while. Especially when you consider controls and duplicates, and youd better if you dont want to seriously waste your time. No, if youre going to screen a really impressive set of compounds, youre going to need all the help you can get. The latter 1990s and early 2000s in the drug business was a period when the high-throughput screeners and the combinatorial chemists tried to outdo each other

And heres where we get back to coronaviruses, antibodies, and vaccines. Because high-throughput screening is what goes on in your bloodstream constantly, as your adaptive immune system watches for pathogens. Everyone carries around a huge variety of different antibodies, all of which fit into some basic structural templates. No one is quite sure just how many different antibodies a person has, actually, because a real count is just an overwhelming task: the usual guesses are in the tens of billions, hundreds of billions, maybe a trillion different ones, which is a hard number to grasp. Imagine a company with a million compounds in its screening deck (OK), and then try to picture a million such companies (nope, not happening). And it might be a lot more incomprehensible than that the first link in this paragraph will take you to a paper that estimates that the available diversity for circulating antibodies is on the order of 10 to the 18th, and whats yet another factor of a million between friends? Given the combinatorial possibilities, it is beyond certain that no two humans have ever had the same repertoire of antibodies, and that no two humans ever will.

These things are floating around in your blood and being displayed on the surface of your various B cells (a mere hundred thousand or so per B cell), just waiting to see if there might someday be something that they bind to. Theyre just like a compound collection in a drug company, actually, except theyre not being stored in separate vials or wells, but are rather dumped all together in your bloodstream. And the assay conditions have been long worked out by evolution, with a huge signal/noise: activation of complement or of the various types of effector cells that respond so dramatically to the presence of antibodies bound to an antigen target.

Theres actually a screening method used in drug discovery thats broadly similar to this: DNA-encoded libraries. Thats where you build up a huge set of small molecules, each of which has its own DNA bar code attached to it. You screen these all at once, too you can hold up a small plastic Eppendorf vial that has (easily) tens of millions of different compounds in it, each with its own DNA identifier. You run the assay in a way that you pan for the potent binders, washing the less potent ones out of the system. Then after you finally knock the strong binders off with stronger conditions, you amplify and sequence their DNA barcode regions and get a reading of what small-molecule structures they must have been. That makes it sound relatively straightforward, but doing this right takes a good deal of care and a lot of data analysis of the hits at the end.

But you can see how it works in a roughly similar fashion to the way native antibodies work in our own bloodstreams. You start with a large variety of compounds, all mixed together, and you try them against a given target. When one of them binds strongly, you use some sort of amplification to pick out this rare event which is present in extremely small concentration. With DNA-encoded libraries, its getting rid of all the weaker binders by washing them off, and using PCR to make far more copies of the DNA sequences you have left. In the immune system, the amplification is built into the cellular responses, which propagate strongly through the immune system and set off further responses in turn.

The immune system is a lot more impressive, of course. Its had a long time to get better, under constant whole-organism threats of illness and death and subsequent inability to reproduce. The screening collection in any single humans bloodstream is far larger than any human efforts have ever reached, so the amplification of any given binding signal has to be a lot more robust. Thats been under serious selection pressure as well, of course: if we pick the wrong compound in a screening effort we will waste time and money, but if the immune system picks the wrong antigen to go off on, it can start attacking your own bodys tissues and kill you. The amount of infrastructure thats been built up over the millennia to avoid that is pretty intimidating all by itself.

Note that we wouldnt even be able to do the DEL trick without piggybacking on all that evolutionary work, either. The ligase enzymes that allow us to build up the DNA barcodes and the PCR that lets us amplify the DNA at the end yeah, we stole all that and repurposed it, and theres no way that you could ever get things to work without them. But its just like the fluorescent proteins mentioned above molecular biology and chemical biology depend on being able to repurpose the amazing array of tools found in living cells. Weve added plenty of our own technologies as well. No living organism does anything like electrospray mass spectrometry, Frster resonance energy transfer, NMR, surface plasmon resonance or the like. But combining what weve learned of chemistry and physics with what evolution has developed, you can run some pretty fancy systems, which are getting fancier all the time.

But for sheer library size and ability to pick out hits, nothing we humans have been able to put together rivals the adaptive immune system. Perhaps thats been one minor side effect of the pandemic: people who have taken the time to learn a bit about immunology can only come away with a sense of awe when they start to see the huge panorama of whats been going on inside their bodies for every second of their lives.

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Screening, Within and Without | In the Pipeline - Science Magazine

Immunology

Efficacy of Tezepelumab in Patients with Severe, Uncontrolled Asthma w | JAA – Dove Medical Press

Claire Emson,1 Jonathan Corren,2 Kinga Saapa,3 sa Hellqvist,4 Jane R Parnes,5 Gene Colice6

1Translational Science and Experimental Medicine, Research and Early Development, Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA; 2David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA, USA; 3Biometrics, Late-Stage Development, Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Warsaw, Poland; 4Biometrics, Late-Stage Development, Respiratory and Immunology, AstraZeneca, Gothenburg, Sweden; 5Amgen, Thousand Oaks, CA, USA; 6Late-Stage Development Respiratory and Immunology, BioPharmaceuticals R&D, AstraZeneca, Gaithersburg, MD, USA

Correspondence: Claire EmsonAstraZeneca, One MedImmune Way, Gaithersburg, MD, 20878, USATel +13013980304Email Claire.emson@astrazeneca.com

Background: Tezepelumab is a human monoclonal antibody that blocks thymic stromal lymphopoietin, an epithelial cytokine implicated in asthma pathogenesis, from binding to its heterodimeric receptor. In the phase 2b PATHWAY study, tezepelumab significantly reduced annualized asthma exacerbation rates (AAERs) versus placebo, irrespective of baseline disease characteristics, and improved lung function and symptom control, in adults with severe, uncontrolled asthma. This post hoc analysis assessed the efficacy of tezepelumab in adults with severe, uncontrolled asthma with and without nasal polyposis (NP).Methods: In this post hoc analysis of the PATHWAY study (NCT02054130), participants (N=550) were randomized 1:1:1:1 to receive subcutaneous tezepelumab 70 mg every 4 weeks (Q4W), 210 mg Q4W or 280 mg every 2 weeks (Q2W), or placebo Q2W, for 52 weeks. The AAER over 52 weeks and the change from baseline to week 52 in blood eosinophil count, fractional exhaled nitric oxide (FeNO) levels and serum levels of interleukin (IL)-5 and IL-13 with tezepelumab 210 mg (the phase 3 dose) and placebo were analyzed in patients grouped by self-reported presence (NP+) or absence (NP) of NP at screening.Results: At baseline, NP+ patients had higher blood eosinophil counts, higher FeNO levels and higher serum IL-5 and IL-13 levels than NP patients. Tezepelumab 210 mg reduced the AAER versus placebo to a similar extent in both NP+ and NP patients (NP+, 75% [95% confidence interval (CI): 15, 93], n=23; NP, 73% [95% CI: 47, 86], n=112). Patients treated with tezepelumab 210 mg demonstrated greater reductions in blood eosinophil count and levels of FeNO, IL-5 and IL-13 than placebo-treated patients, irrespective of NP status.Discussion: Tezepelumab reduced exacerbations and reduced type 2 inflammatory biomarkers in patients with and those without NP, supporting its efficacy in a broad population of patients with severe asthma.

Keywords: asthma, biomarkers, nasal polyps, sinusitis, tezepelumab, thymic stromal lymphopoietin

This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution - Non Commercial (unported, v3.0) License.By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms.

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Immunology

Scientists fear COVID-19 variant is taking the edge off vaccines – Sydney Morning Herald

Based on early studies, Pfizer has said it does not expect a significant reduction in the effectiveness of its vaccine. The company says it can quickly adjust its vaccine if necessary.

However, that is based on laboratory studies, not human data. And all four vaccines use different technologies but have an identical core component a piece of the virus spike protein they try to generate an immune response to.

Nurse Novita Sirait gives a COVID-19 vaccine to a colleague at a community health centre in Medan, North Sumatra, Indonesia.Credit:AP

Pfizers vaccine was approved for use in Australia in January, and 53.8 million doses of AstraZenecas vaccine have been bought and will be distributed over coming months.

The South African variant of the virus has been picked up eight times in Australia.

It is hard to say for sure, but you would think there is the potential they would also be reduced, said Associate Professor Corey Smith, head of translational and human immunology at the QIMR Berghofer Medical Research Institute.

He said the results suggested the virus could mutate in ways that made antibodies and vaccines less effective. But I dont think thats a real surprise, he said. Viruses always mutate.

The South African variant, known as N501Y.V2, has several mutations that in lab tests appear to change the shape of the virus spike in a way that reduces the ability of some antibodies generated from infection with the original Wuhan variant of COVID-19 from binding.

That raises concerns about reinfection, and about how well COVID-19 vaccines based on the original variant will protect against the South African variant.

Professor David Tscharke, head of the department of immunology and infectious diseases at the Australian National University, said it was always likely that we will have to chase variants by changing our vaccines.

However, he said it was not clear cut that AstraZeneca and Pfizers vaccines faced the same problems as Novavax and Johnson & Johnson.

You might guess that but the extent of that is going to be varied, he said. Although they have the same antigens, they are presented in a different way.

Virus-killing T-cells also played a role in immunity, he said, and they might allow Pfizer and AstraZenecas jabs to still offer strong protection against the variant.

Early lab evidence suggested Pfizers vaccine would be less effective against the South African variant, but would still cover the virus.

But those studies were carried out using pseudoviruses viruses manipulated to look like N501Y.V2 and were done on cells in a lab. Such studies do not always translate to humans.

Science and health explained and analysed with a rigorous focus on the evidence. Examine is a weekly newsletter by science reporter Liam Mannix. Sign up to receive it every Tuesday.

Novavax and Johnson & Johnson are the first vaccine developers to report human data on the variants.

Novavaxs trial of more than 4400 patients in South Africa reported efficacy of 49.4 per cent (excluding HIV-positive patients, efficacy rose to 60 per cent). Nearly all the cases of infection among vaccinated subjects were from the South African variant.

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Johnson & Johnsons trial of 6576 people in South Africa reported efficacy of 57 per cent; 95 per cent of infections in people vaccinated were from the South African variant.

These trials were small and the results were preliminary, experts said. South Africa also presents a unique environment to test vaccines: a runaway epidemic means people may be exposed to unusually high levels of virus.

But even with all that in mind, said Associate Professor Stuart Turville, a virologist at the Kirby Institute, the data early on, looks like the edge has been taken off by the South African variant.

What were seeing in the real world is this thing has the potential to take the edge off vaccines. Which may mean we need to update the formulation.

It is anticipated that the Pfizer and AstraZeneca vaccines will have significant efficacy against the newer strains of COVID-19, a spokesman for the Therapeutic Goods Administration said.

The vaccines work by inducing what is known as a polyclonal response a collection of immunological responses to many different parts of the COVID spike protein. In the new variants, only a limited part of the spike protein is changed, and much is unchanged. So the vaccines should still work against the main, unchanged parts to the COVID-19 spike protein.

The results from the Novavax and Johnson & Johnson vaccines cannot be directly extrapolated to the other COVID-19 vaccines, such as the Pfizer BioNTech or Oxford AZ vaccine as each vaccine produces differing immune responses in vaccinated individuals.

The experts emphasised it was important to wait for real-world data from Pfizer and AstraZeneca. It may be the vaccines different designs work better against the variant.

These vaccines also stimulate T-cell immunity although it is not clear what role that plays in protection from COVID-19.

And even a vaccine with reduced effectiveness was much better than no vaccine at all.

To put this into context, were still getting significant protection, said Professor Tscharke. We could be living in a world where all these vaccines were giving numbers like that all around the world and we would still be pretty happy.

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Liam is The Age and Sydney Morning Herald's science reporter

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Scientists fear COVID-19 variant is taking the edge off vaccines - Sydney Morning Herald

Immunology

Herd immunity could be reached by end of summer: Weill Cornell Medicine-Qatar immunology expert – The Peninsula Qatar

The first COVID-19 vaccines have now been administered in Qatar and around the world, offering hope that an end to the pandemic could be in sight. Professor of Teaching in Microbiology and Immunology at Weill Cornell Medicine in Qatar (WMC-Q), DrAli Sultan, says if the ongoing vaccination campaign goes well, herd immunity could be reached by end of summer and situation closer to normal by the end of 2021.

How would you see the pre-COVID vaccine and post COVID vaccine times?Scientists, including myself, are very excited at the prospect of an effective vaccine and the prospect of returning to normality. Starting a mass vaccination program is an important first step towards ending this pandemic. And it has come relatively quickly. Producing an effective vaccine against an infectious disease is a long process that in the past has usually taken many years. The development of the COVID-19 vaccine within a span of 8-9 months, on the other hand, has been extraordinarily fast. It has shown how quickly scientific development can be achieved via collaborative hard work, and how much the will can produce the means.

In addressing the above question, I will consider the following issues:1: What next after vaccination: One has to remember that COVID-19 vaccine won't be available immediately for everybody. Early evidence suggests that the available vaccines reduce peoples risk of developing COVID-19 by around 80-95 percent. Coronavirus is likely to continue its rapid spread until a large majority of the population is vaccinated or has survived a natural infection. The bottom line is that although an effective vaccine will certainly diminish greatly the relative risk of transmission, we still should not completely abandon basic public health measures, including the wearing of masks, hand hygiene and physical distancing.

2: Another issue to consider is re-infection, though rare, may still occur. Hence, strict practice of physical distancing, wearing a mask when in public, and frequent hand washing remain key. In the winter, it is particularly important to not gather indoors in small or large groups. Also, get a flu shot.

3: Post-COVID effect on the health of those infected: We are just beginning to learn more about the after effects of the infection. Some people, now referred to as long-haulers, are also reporting that their COVID symptoms keep dragging on for weeks. These symptoms include everything from headaches and cognitive problems to mood changes, fatigue, decreased exercise tolerance, and body ache.

4: The most important lessons that that this pandemic taught us are:a) Science and data should guide our decision now and in the future.b) Practicing good hygienic measures in hospitals, schools and other public places, could drastically reduce the spread and thereby eliminate new cases of COVID-19 and help to protect us from other infectionsc) Health authorities and government bodies should have plans and preparedness programs in place in order to avoid future pandemics.d) The COVID-19 pandemic has been a test, demonstrating that multilateral cooperation is the key to overcoming global challenges.

The first COVID-19 vaccines have now been administered in Qatar and around the world, offering hope that an end to the pandemic could be in sight: How long could it take to reach this in reality?If the ongoing vaccination campaign goes well, herd immunity could be reached by end of summer and situation closer to normal by the end of 2021. This estimate is dependent on significant numbers of people in Qatar and around the world being willing to be vaccinated with one of several vaccines in various stages of development.

If 75% to 80% of people are vaccinated, then we should reach the herd immunity threshold by the end of summer and by the time we may actually have enough herd immunity protecting our society that as we get to the end of 2021. This may allow us to reach some degree of normality that is close to where we were before the pandemic. If vaccination levels are significantly lower, (for example less than 50%), it could take a very long time to reach that level of protection and herd immunity.

Confidence in the COVID-19 vaccine grows, but at same time global concerns about side effects are on the rise: How could the confidence be built in people?There are number of surveys done on vaccine confidence, which showed that strong intent to get a COVID-19 vaccine has risen in countries like USA, UK, China, Brazil, Australia and South Korea. One of the main reasons for people who dont want to get a COVID-19 vaccine is concern about side effects. Even in countries where vaccines available to wider sections of the population, one hurdle will be public resistance to vaccination, or what is known as vaccine hesitancy or anti-vaxxers. Through the following facts and information we can build the people confidence in taking the COVID-19 vaccine:1. The first fact is that the public health authority in each country and the media have important role to play by explaining that there are some temporary side effects that happen with any vaccine injection such as pain at the site of the injection, mild fever, aches and sometimes headaches. These temporary side effects are good news because it means that the vaccine is doing its job by stimulating the immune system to fight. So it is common for highly effective vaccines to give people some symptoms. This is a sign the vaccine is doing what it was meant to do: Wake up the immune system and prepare it to fight off an infection in the future.2. The second fact is that COVID-19 vaccines do not contain a live or whole coronavirus, so the vaccinated person cant get COVID-19 from the vaccine.3. COVID-19 vaccines do not contain microchips or tracer technology.

There has been a lot of debate on whether people who had COVID-19 shall/shall not take the vaccine, whats your intake on that?The current data pointing to the fact that the people who have become sick with COVID-19 have some immunity, but we don't have enough evidence about antibody persistence to confidently say recovered patients are protected. Data suggest that immunity to SARS-CoV-2 from infection lasts at least 6-8 months, but we don't know enough yet about the degree to which previous infection confers immunity.We know that cases of reinfection have been documented; they appear to be rare. Likewise, an asymptomatic reinfection may go unnoticed, yet the individual may still transmit it to others. It would not be good if that person happens to be a healthcare worker. So, there is an argument to vaccine healthcare workers, even if they got infected because vaccines provide more robust immune protection than natural infection. Those at the highest risk of spreading the virus and those who might be tipping ICU capacity over the limit, are the ones who should be first in line for immunization.

Regarding the new COVID-19 variants that appeared in some countries, will the vaccine be effective in stopping them?New mutations of the coronavirus have been reported, which may change the nature of the proteins on its surface. This has led to fears that the vaccines developed so far may or may not work against these new variants because vaccines are based on teaching the body to recognize those proteins and attack them in future.The new mutations in the SARS-CoV-2 virus detected in UK created a new variant that is more transmissible than the earlier variants. However, there is no evidence that the new mutations seen in the SARS-CoV-2 will affect the vaccine efficacy or increase the severity of COVID-19.The vaccines teach the body about multiple spike proteins on the virus surface, and those spikes are also what the virus uses to get inside our cells. So a change in one protein because of a mutation doesnt automatically make the whole vaccine useless. But its important to keep looking for mutations in the coronavirus thats infecting people now. This will help researchers working on the vaccine field to know if we need to change the current vaccines or make new vaccines against COVID-19.Meanwhile, scientists are still studying whether changes in the coronavirus are making it more likely to infect children and teenagers. It will take time to find all these things out. Thats why its important to continue to wear masks in public, and stay away from large gatherings and unmasked interactions with people who dont live with you.

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Herd immunity could be reached by end of summer: Weill Cornell Medicine-Qatar immunology expert - The Peninsula Qatar

Immunology

Delaying the second Covid dose in the UK is controversial, but it’s the right decision – The Guardian

A recent YouGov poll shows that the British are among the most willing in the world to take the Covid-19 vaccine. This is good news. But there are still questions about the vaccines and the way theyre being deployed, especially after the government decided to spread out the time between the two doses from three weeks to 12 weeks. The confusion is understandable, as we are in a developing situation. Clear messages about why tough decisions are made can get lost in the noise.

First, it is absolutely clear that the two Covid-19 vaccines that are being deployed in the UK will save lives. Moreover, they will reduce the burden on hospitals. The Pfizer data, measured from day 14 post-vaccination, showed only one severe case of Covid-19 in 21,000 vaccinated people. The AstraZeneca data showed no hospitalisations or severe disease in 6,000 vaccinated trial participants. The caveat to this was that there were a small number of cases in the first two weeks after the first vaccine dose. This brings me to an important point.

The vaccines need time to work. Vaccines prepare our immune system to defend against infection by showing it a small part of the virus, in this instance a spike protein that appears on the outside of the Sars-CoV-2 virus. Our immune system produces a bespoke response to this protein, making antibodies and memory cells which it stores away against future need. Creating these initial antibodies and memory cells can take a couple of weeks, so there is a lag time before you start to be protected. If our immune system later sees the spike protein again, it can bring out all its pre-made resources to act immediately.

So why do we need two jabs? Immunity elicited by the vaccine can be boosted. When the spike protein appears a second time and the immune system brings its armoury out, the immune memory cells will rapidly increase in number and more antibody will be produced to neutralise the virus. This will happen whether the spike protein is in the vaccine or on a live virus. To get the best response possible, the current vaccines were designed to have a second boosting dose after the first priming dose.

The UK governments decision to change the timing of the second vaccine dose has been controversial. After all, if you have evidence that scheme A works, why would you use an untested scheme B? But the decision will not have been taken lightly and there is some basis in the current data available. AstraZeneca trials reported early indications that a longer interval between doses is beneficial. Pfizer trials did not have such data, but the similar Moderna vaccine elicited immunity lasting just under two months after one dose. It boiled down to simple sums based on real-world scarcity: if a vaccine protects people from disease by 89% after one dose and 95% after two doses, and someone gives you just 200 doses this month, you can choose to protect 95 people after three weeks or 178 people for 12 weeks.

One worry is that the change in timing could encourage virus escape, resulting in worrisome new variants. The rationale is that if you dont kill off a virus immediately, mutations will enable the virus to survive better. But it has equally been argued that allowing natural infection would also be a reason to cause mutations. After all, the new variants that concern us now from England, Brazil and South Africa appeared before vaccines were rolled out. Also, simply by fighting the virus with these vaccines we are putting it under pressure to evolve. An optimistic view is that our immune memory is diverse and dynamic enough to adapt and counter any viral escape. It is encouraging that early data from the mRNA vaccines show they work against some of these variants. Close monitoring of the situation is necessary, but in the face of the current emergency we should try to save as many lives as we can as soon as possible.

This is why its crucial that we do not change our good social behaviour just because of vaccination. Even with 95% vaccine efficacy, one in 20 people could get Covid-19. We also need to consider virus carriage and transmission. When we catch the virus, our immune systems immediately roll out to fight it. The response may be so effective that we dont have any symptoms or even realise that the virus has briefly inhabited our bodies, yet we could still have passed it on to others.

We do not yet know to what extent the vaccines block this type of virus transmission. The recent reports from Israel of up to 60% protection after just one dose do not really contradict the Pfizer study data (which show 89%), because the former measured the presence of the virus and the latter measured disease symptoms they may simply illustrate the point that protection from disease is not the same as protection from having the virus, and 60% protection from carrying the virus is encouraging.

Immunity is not all or nothing. There are degrees of protection depending how good the vaccine is and how good your immune system is in responding to it. Some factors, such as age, health status, and type of virus variant, may mean that immunity is reduced. What we urgently need now is robust monitoring of the vaccine rollout to help us understand how different individuals immune systems respond to the vaccine, how the vaccines work against the different variants, and how the changes in dosing schedule affect the efficacy of responses. This will help us be more certain of our answers in the future.

Deborah Dunn-Walters is professor of immunology at University of Surrey and chair of the British Society for Immunologys Covid-19 and Immunology taskforce

This article was amended on 27 January 2021. There were a small number of cases in the first two weeks after the first vaccine dose, not two months as an earlier version stated due to an editing error.

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Delaying the second Covid dose in the UK is controversial, but it's the right decision - The Guardian

Immunology

Samsung Bioepis Opens the New State-of-the-Art Headquarters to Accommodate Next Stage of Growth and Innovation – BioSpace

A photo accompanying this announcement is available at https://www.globenewswire.com/NewsRoom/AttachmentNg/370961b4-344f-49bf-86e4-e882f7265b1c

INCHEON, Korea, Jan. 25, 2021 (GLOBE NEWSWIRE) -- Samsung Bioepis Co., Ltd. today announced the opening of its new headquarters in Koreas Bio Cluster of Songdo, located in the Incheon Free Economic Zone (IFEZ), a specially-designated economic zone in the city of Incheon. The new site is approximately 52,000 square feet, and will be the hub of Samsung Bioepis drive for development of next-generation biologic medicines. Construction of the new building was completed in December 2020.

We are very excited to be opening our new headquarters which will serve as the foundation for the companys next stage of growth. Our colleagues who were previously stationed in two campuses in Korea will be working together at the new headquarters to accelerate our passion for health, said Christopher Hansung Ko, President and Chief Executive Officer, Samsung Bioepis. With the new office equipped with the state-of-the-art laboratories, we look forward to providing our high-quality biologic medicines with more agility and with stringent quality control so that patients around the world can have access to our proven medicines more quickly and more widely available.

The newly established 12-story building will house approximately 1,000 employees, who will be working at the 17,300-square-foot laboratory space and 15,200-square-foot office space. Attached to the main building is a three-story Welfare Center which includes 4,750-square-foot cafeteria, a gymnasium and a fitness center for employees to enjoy. Furthermore, the company has an onsite childcare center to support employees with young children.

Established in 2012, Samsung Bioepis has rapidly grown to have five biologic products in immunology and oncology with more than 215,000 patients treated with the companys immunology products in Europe alone. The company is continuing its work to improve access to medicines through its unique process innovation development platform and currently has five biologic candidates in its pipeline ranging from hematology and ophthalmology.

About Samsung Bioepis Co., Ltd.

Established in 2012, Samsung Bioepis is a biopharmaceutical company committed to realizing healthcare that is accessible to everyone. Through innovations in product development and a firm commitment to quality, Samsung Bioepis aims to become the world's leading biopharmaceutical company. Samsung Bioepis continues to advance a broad pipeline of biosimilar candidates that cover a spectrum of therapeutic areas, including immunology, oncology, ophthalmology and hematology. Samsung Bioepis is a joint venture between Samsung Biologics and Biogen. For more information, please visit: http://www.samsungbioepis.com and follow us on social media Twitter, LinkedIn.

MEDIA CONTACTYoon Kim: yoon1.kim@samsung.com

Samsung Bioepis New Headquarters

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Samsung Bioepis Opens the New State-of-the-Art Headquarters to Accommodate Next Stage of Growth and Innovation - BioSpace