Saba Dastar, Jalal Gharesouran, Deniz Mortazavi, Hassan Hosseinzadeh, Seyed Jalal Kian, Mohammad Taheri, Soudeh Ghafouri-Fard, Elena Jamali, Maryam Rezazadeh
The outbreak of the newly emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) all over the world has caused global public health emergencies, international concern and economic crises. The systemic SARS-CoV-2 disease (COVID-19) can lead to death through causing unrestrained cytokines-storm and subsequent pulmonary shutdown among the elderly and patients with pre-existing comorbidities. Additionally, in comparison with poor nations without primary health care services, in developed countries with advanced healthcare system we can witness higher number of infections per one million people. In this review, we summarize the latest studies on genes associated with SARS-CoV-2 pathogenesis and propose possible mechanisms of the virus replication cycle and its triggered signaling pathways to encourage researchers to investigate genetic and immune profiles of the disease and try strategies for its treatment. Our review shows that immune response in people with different genetic background might vary as African and then Asian populations have lowest number of affected cases compared with European and American nations. Considering SARS-CoV-2 pathogenesis, we put forward some potentially important genetic gateways to COVID-19 infection including genes involved in the entry and replication of SARS-CoV-2 and the regulation of host immune response which might represent explanation for its spread, severity, and morality. Finally, we suggest that genetic alterations within these gateways could be critical factors in influencing geographical discrepancies of the virus, so it is essential to fully study them and design appropriated and reliable therapeutic agents against COVID-19.
{"title":"COVID-19 pandemic: Insights into genetic susceptibility to SARS-CoV-2 and host genes implications on virus spread, disease severity and outcomes.","authors":"Saba Dastar, Jalal Gharesouran, Deniz Mortazavi, Hassan Hosseinzadeh, Seyed Jalal Kian, Mohammad Taheri, Soudeh Ghafouri-Fard, Elena Jamali, Maryam Rezazadeh","doi":"10.3233/HAB-211506","DOIUrl":"https://doi.org/10.3233/HAB-211506","url":null,"abstract":"<p><p>The outbreak of the newly emerging severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) all over the world has caused global public health emergencies, international concern and economic crises. The systemic SARS-CoV-2 disease (COVID-19) can lead to death through causing unrestrained cytokines-storm and subsequent pulmonary shutdown among the elderly and patients with pre-existing comorbidities. Additionally, in comparison with poor nations without primary health care services, in developed countries with advanced healthcare system we can witness higher number of infections per one million people. In this review, we summarize the latest studies on genes associated with SARS-CoV-2 pathogenesis and propose possible mechanisms of the virus replication cycle and its triggered signaling pathways to encourage researchers to investigate genetic and immune profiles of the disease and try strategies for its treatment. Our review shows that immune response in people with different genetic background might vary as African and then Asian populations have lowest number of affected cases compared with European and American nations. Considering SARS-CoV-2 pathogenesis, we put forward some potentially important genetic gateways to COVID-19 infection including genes involved in the entry and replication of SARS-CoV-2 and the regulation of host immune response which might represent explanation for its spread, severity, and morality. Finally, we suggest that genetic alterations within these gateways could be critical factors in influencing geographical discrepancies of the virus, so it is essential to fully study them and design appropriated and reliable therapeutic agents against COVID-19.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":"30 1","pages":"1-14"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39960018","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Mohammad Taheri, Leila Gholami, Fwad Nicknafs, Bashdar Mahmud Hussen, Shahram Arsang-Jang, Arezou Sayad, Soudeh Ghafouri-Fard
Periodontal diseases are common conditions in almost all age groups and a public health problem. Numerous risk factors have been demonstrated for this condition. The main mechanism of tissue destruction in the periodontitis is the functional interactions between microbial pathogens and host immune responses, thus cytokines have crucial roles in the pathogenesis periodontitis. Our previous study has demonstrated the susceptibility role of HLA-DRB1*04 allele in development of this disease. So, the individuals who were positive for HLA-DRB1*04 allele were excluded. We aimed to appraise the function of cytokines in the pathogenesis of periodontitis via assessment of tissue and blood levels of a number of cytokine coding genes, namely IL-1B, CXCL8, IL-17, IFNG, TGFB and TNFA1. Expressions of IFNG, IL-17, TGFB and TNFA1 were significantly higher in the peripheral blood of individuals with periodontitis compared with unaffected persons (Posterior beta = 1.91, P value = 0.043; Posterior beta = 1.84, P value = 0.033; Posterior beta = 0.713, P value = 0.009 and Posterior beta = 2.85, P value = 0.001, respectively). Moreover, expression of IL-17 was higher in females compared with males (Posterior beta = 1.47, P value = 0.036). As the interaction effect between gender and group was remarkable for IL-17 expression, we further conducted subgroup analysis within gender group. Expression of IL-17 was higher in male patients compared with unaffected males (Posterior beta = 1.9, P value = 0.048). We did not detect any significant difference in the expression of these cytokines in tissues obtained from affected individuals and unaffected controls. Therefore, our results imply dysregulation of cytokine coding genes in patients with periodontitis and warrant further mechanistical studies.
{"title":"Transcript levels of cytokine coding genes in peripheral blood and tissues of patients with periodontitis.","authors":"Mohammad Taheri, Leila Gholami, Fwad Nicknafs, Bashdar Mahmud Hussen, Shahram Arsang-Jang, Arezou Sayad, Soudeh Ghafouri-Fard","doi":"10.3233/HAB-211507","DOIUrl":"https://doi.org/10.3233/HAB-211507","url":null,"abstract":"<p><p>Periodontal diseases are common conditions in almost all age groups and a public health problem. Numerous risk factors have been demonstrated for this condition. The main mechanism of tissue destruction in the periodontitis is the functional interactions between microbial pathogens and host immune responses, thus cytokines have crucial roles in the pathogenesis periodontitis. Our previous study has demonstrated the susceptibility role of HLA-DRB1*04 allele in development of this disease. So, the individuals who were positive for HLA-DRB1*04 allele were excluded. We aimed to appraise the function of cytokines in the pathogenesis of periodontitis via assessment of tissue and blood levels of a number of cytokine coding genes, namely IL-1B, CXCL8, IL-17, IFNG, TGFB and TNFA1. Expressions of IFNG, IL-17, TGFB and TNFA1 were significantly higher in the peripheral blood of individuals with periodontitis compared with unaffected persons (Posterior beta = 1.91, P value = 0.043; Posterior beta = 1.84, P value = 0.033; Posterior beta = 0.713, P value = 0.009 and Posterior beta = 2.85, P value = 0.001, respectively). Moreover, expression of IL-17 was higher in females compared with males (Posterior beta = 1.47, P value = 0.036). As the interaction effect between gender and group was remarkable for IL-17 expression, we further conducted subgroup analysis within gender group. Expression of IL-17 was higher in male patients compared with unaffected males (Posterior beta = 1.9, P value = 0.048). We did not detect any significant difference in the expression of these cytokines in tissues obtained from affected individuals and unaffected controls. Therefore, our results imply dysregulation of cytokine coding genes in patients with periodontitis and warrant further mechanistical studies.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":"30 1","pages":"47-55"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39960019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Godwin Aigbedo Aikpitanyi-Iduitua, Isaiah Nnana Ibeh, Nosakhare Lawrence Idemudia, Rosemary Osamede Aikpitanyi-Iduitua, Richard Omoregie
Background: Morbidity and mortality associated with HIV infection is immune-mediated, and an understanding of HIV immunology will be beneficial in the management of HIV infectionOBJECTIVE: The objective of this research was to measure the levels of TNF-α, IL-6 and IFN-γ in asymptomatic HIV patients and non-HIV subjects, as well as their relationship with CD4 count.
Method: Blood samples were collected from 173 subjects, consisting of 125 asymptomatic HIV patients (44 HAART-naïve and 81 on HAART) and 48 non-HIV subjects. The IFN-, IL-6, and TNF- levels in the blood were determined using enzyme-linked immunosorbent assays, and the CD4 count of all participants was determined using flow cytometry.
Results: Regardless of treatment status, the IFN-γ levels of non-HIV subjects were significantly higher than those of HIV patients (p< 0.001). The opposite was true for IL-6, as the levels of IL-6 in non-HIV subjects were significantly lower than those in HAART-naïve HIV patients (p< 0.001) and those on HAART (p< 0.01). TNF-α levels did not differ between HIV patients and their non-HIV counterparts. Generally, the levels of these cytokines was not affected (p> 0.05) by immunosuppression (measured by CD4 count < 200 cells/μL) and there was no significant correlation between CD4 count and these cytokines (p> 0.05).
Conclusion: In conclusion, asymptomatic HIV infection decreased IFN-γ, increased IL-6, and had no effect on TNF-α levels, regardless of treatment status. Immunosuppression had no impact on these cytokine levels, and there was no relationship between them and CD4 counts.
{"title":"Interferon gamma, interleukin 6 and tissue necrosis factor alpha levels among asymptomatic HIV patients in Benin City, Nigeria.","authors":"Godwin Aigbedo Aikpitanyi-Iduitua, Isaiah Nnana Ibeh, Nosakhare Lawrence Idemudia, Rosemary Osamede Aikpitanyi-Iduitua, Richard Omoregie","doi":"10.3233/HAB-220014","DOIUrl":"https://doi.org/10.3233/HAB-220014","url":null,"abstract":"<p><strong>Background: </strong>Morbidity and mortality associated with HIV infection is immune-mediated, and an understanding of HIV immunology will be beneficial in the management of HIV infectionOBJECTIVE: The objective of this research was to measure the levels of TNF-α, IL-6 and IFN-γ in asymptomatic HIV patients and non-HIV subjects, as well as their relationship with CD4 count.</p><p><strong>Method: </strong>Blood samples were collected from 173 subjects, consisting of 125 asymptomatic HIV patients (44 HAART-naïve and 81 on HAART) and 48 non-HIV subjects. The IFN-, IL-6, and TNF- levels in the blood were determined using enzyme-linked immunosorbent assays, and the CD4 count of all participants was determined using flow cytometry.</p><p><strong>Results: </strong>Regardless of treatment status, the IFN-γ levels of non-HIV subjects were significantly higher than those of HIV patients (p< 0.001). The opposite was true for IL-6, as the levels of IL-6 in non-HIV subjects were significantly lower than those in HAART-naïve HIV patients (p< 0.001) and those on HAART (p< 0.01). TNF-α levels did not differ between HIV patients and their non-HIV counterparts. Generally, the levels of these cytokines was not affected (p> 0.05) by immunosuppression (measured by CD4 count < 200 cells/μL) and there was no significant correlation between CD4 count and these cytokines (p> 0.05).</p><p><strong>Conclusion: </strong>In conclusion, asymptomatic HIV infection decreased IFN-γ, increased IL-6, and had no effect on TNF-α levels, regardless of treatment status. Immunosuppression had no impact on these cytokine levels, and there was no relationship between them and CD4 counts.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":"30 4","pages":"177-182"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9464902","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background: Little is known about the association between Human Immunodeficiency Virus (HIV) infection and risk of death among hospitalized COVID-19 patients. We aimed to investigate this association using a multicenter study.
Material and methods: This multicenter study was conducted using the registry database of Coronavirus Control Operations Headquarter from March 21, 2021 to January 18, 2020 in the province of Tehran, Iran. The interest outcome was COVID-19 death among hospitalized patients living with and without HIV. The Cox regression models with robust standard error were used to estimate the association between HIV infection and risk of COVID-19 death. The subgroup and interaction analysis were also performed in this study.
Results: 326052 patients with COVID-19 were included in the study, of whom 127 (0.04%) were living with HIV. COVID-19 patients with HIV were more likely to be female, older, and to have symptoms such as fever, muscular pain, dyspnea and cough. The death proportion due to COVID-19 was 18 (14.17%) and 21595 (6.63%) among HIV and non-HIV patients, respectively. Patients living with HIV had lower mean survival time compared to those without HIV (26.49 vs. 15.31 days, P-value = 0.047). Crude risk of COVID-19 death was higher among HIV patients than in non-HIV group (hazard ratio[HR]: 1.60, 1.08-2.37). Compared to those without HIV, higher risk of COVID-19 death was observed among patients with HIV after adjusting for sex (1.60, 1.08-2.36), comorbidities (1.49, 1.01-2.19), cancer (1.59, 1.08-2.33), and PO2 (1.68, 1.12-2.50). However, the risk of COVID-19 death was similar in patients with and without HIV after adjusting for age (1.46, 0.98-2.16) and ward (1.30, 0.89-1.89).
Conclusion: We found no strong evidence of association between HIV infection and higher risk of COVID-19 death among hospitalized patients. To determine the true impact of HIV on the risk of COVID-19 death, factors such as age, comorbidities, hospital ward, viral load, CD4 count, and antiretroviral treatment should be considered.
{"title":"The impact of HIV on the risk of COVID-19 death among hospitalized patients.","authors":"Mehdi Azizmohammad Looha, Nazanin Taraghikhah, Maedeh Amini, Pegah Salimi Pormehr, Negin Talaei, Mahmood Khodadoost, Saeid Gholamzadeh, Reza Vafaee, Gohar Mohammadi","doi":"10.3233/HAB-220011","DOIUrl":"https://doi.org/10.3233/HAB-220011","url":null,"abstract":"<p><strong>Background: </strong>Little is known about the association between Human Immunodeficiency Virus (HIV) infection and risk of death among hospitalized COVID-19 patients. We aimed to investigate this association using a multicenter study.</p><p><strong>Material and methods: </strong>This multicenter study was conducted using the registry database of Coronavirus Control Operations Headquarter from March 21, 2021 to January 18, 2020 in the province of Tehran, Iran. The interest outcome was COVID-19 death among hospitalized patients living with and without HIV. The Cox regression models with robust standard error were used to estimate the association between HIV infection and risk of COVID-19 death. The subgroup and interaction analysis were also performed in this study.</p><p><strong>Results: </strong>326052 patients with COVID-19 were included in the study, of whom 127 (0.04%) were living with HIV. COVID-19 patients with HIV were more likely to be female, older, and to have symptoms such as fever, muscular pain, dyspnea and cough. The death proportion due to COVID-19 was 18 (14.17%) and 21595 (6.63%) among HIV and non-HIV patients, respectively. Patients living with HIV had lower mean survival time compared to those without HIV (26.49 vs. 15.31 days, P-value = 0.047). Crude risk of COVID-19 death was higher among HIV patients than in non-HIV group (hazard ratio[HR]: 1.60, 1.08-2.37). Compared to those without HIV, higher risk of COVID-19 death was observed among patients with HIV after adjusting for sex (1.60, 1.08-2.36), comorbidities (1.49, 1.01-2.19), cancer (1.59, 1.08-2.33), and PO2 (1.68, 1.12-2.50). However, the risk of COVID-19 death was similar in patients with and without HIV after adjusting for age (1.46, 0.98-2.16) and ward (1.30, 0.89-1.89).</p><p><strong>Conclusion: </strong>We found no strong evidence of association between HIV infection and higher risk of COVID-19 death among hospitalized patients. To determine the true impact of HIV on the risk of COVID-19 death, factors such as age, comorbidities, hospital ward, viral load, CD4 count, and antiretroviral treatment should be considered.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":"30 4","pages":"165-175"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9457546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kemal Beksac, Hanife Guler Donmez, Murat Cagan, Mehmet Sinan Beksac
Background: Thyroglobulin (anti-TG) and/or thyroid peroxidase (anti-TPO) autoantibodies are associated with higher rates of poor gestational outcomes.
Objective: To demonstrate the impact of anti-TPO and anti-TG autoantibodies on the gestational outcomes of euthyroid pregnant women with a history of poor gestational outcome and thyroid gland disorders.
Methods: This retrospective study included totally 75 euthyroid pregnant, 30 of women with high thyroid autoantibodies (Anti-TPO/Thyroglobulin-positive group) and 45 of them without autoantibodies (control group).
Results: We could not demonstrate significant differences between two groups in terms of risk factors/co-morbidities, obstetric complications, gestational outcomes, and birth data (p> 0.05). However, enhanced miscarriage rates were observed among the Anti-TPO/Thyroglobulin-positive and control groups without significance (36.7% and 17.8% respectively, p= 0.116). High neonatal intensive care unit (NICU) admission rates were found for control and Anti-TPO/Thyroglobulin-positive groups (16.2% and 21.1%, respectively) (p= 0.720). Clinically, we compared the two groups in terms of the existence and the types of goiter (diffuse and nodular), and demonstrated that nodular goiter was statistically more frequent in the control group (40.0% vs. 8.7%, p= 0.015). Alongside, relatively high hereditary thrombophilia and type-2 diabetes mellitus rates were found in the Anti-TPO/Thyroglobulin-positive group (20.0% and 20.0%).
Conclusion: Thyroid autoantibody positivity is likely a risk factor for early pregnancy loss and NICU admission.
{"title":"Impact of anti-thyroid peroxidase and anti-thyroglobulin antibodies on the gestational outcome of euthyroid pregnancies: A retrospective study.","authors":"Kemal Beksac, Hanife Guler Donmez, Murat Cagan, Mehmet Sinan Beksac","doi":"10.3233/HAB-220010","DOIUrl":"https://doi.org/10.3233/HAB-220010","url":null,"abstract":"<p><strong>Background: </strong>Thyroglobulin (anti-TG) and/or thyroid peroxidase (anti-TPO) autoantibodies are associated with higher rates of poor gestational outcomes.</p><p><strong>Objective: </strong>To demonstrate the impact of anti-TPO and anti-TG autoantibodies on the gestational outcomes of euthyroid pregnant women with a history of poor gestational outcome and thyroid gland disorders.</p><p><strong>Methods: </strong>This retrospective study included totally 75 euthyroid pregnant, 30 of women with high thyroid autoantibodies (Anti-TPO/Thyroglobulin-positive group) and 45 of them without autoantibodies (control group).</p><p><strong>Results: </strong>We could not demonstrate significant differences between two groups in terms of risk factors/co-morbidities, obstetric complications, gestational outcomes, and birth data (p> 0.05). However, enhanced miscarriage rates were observed among the Anti-TPO/Thyroglobulin-positive and control groups without significance (36.7% and 17.8% respectively, p= 0.116). High neonatal intensive care unit (NICU) admission rates were found for control and Anti-TPO/Thyroglobulin-positive groups (16.2% and 21.1%, respectively) (p= 0.720). Clinically, we compared the two groups in terms of the existence and the types of goiter (diffuse and nodular), and demonstrated that nodular goiter was statistically more frequent in the control group (40.0% vs. 8.7%, p= 0.015). Alongside, relatively high hereditary thrombophilia and type-2 diabetes mellitus rates were found in the Anti-TPO/Thyroglobulin-positive group (20.0% and 20.0%).</p><p><strong>Conclusion: </strong>Thyroid autoantibody positivity is likely a risk factor for early pregnancy loss and NICU admission.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":" ","pages":"157-163"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40591442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yasmine El Abd, Ashraf Tabll, Robert Smolic, Martina Smolic
Background: The emergence of novel viruses poses severe challenges to global public health highlighting the crucial necessity for new antivirals.
Main body: Monoclonal antibodies (mAbs) are immunoglobulins that bind to a single epitope. Mouse mAbs are generated by classic hybridoma technology and are mainly used for immunodiagnostics. For immunotherapy, it is critical to use monoclonal antibodies in their human form to minimize adverse reactions. They have been successfully used to treat numerous illnesses, accordingly, an increasing number of mAbs, with high potency against emerging viruses is the target of every biopharmaceutical company. The diagnostic and therapeutic mAbs market grows rapidly into a multi-billion-dollar business. Biopharmaceuticals are innovative resolutions which revolutionized the treatment of significant chronic diseases and malignancies. Currently, a variety of therapeutic options that include antiviral medications, monoclonal antibodies, and immunomodulatory agents are available for the management of COVID-19.
Short conclusion: The invasion of mAbs in new medical sectors will increase the market magnitude as it is expected to generate revenue of about 300 billion $ by 2025. In the current mini-review, the applications of monoclonal antibodies in immune-diagnosis and immunotherapy will be demonstrated, particularly for COVID-19 infection and will focus mainly on monoclonal antibodies in the market.
{"title":"Mini-review: The market growth of diagnostic and therapeutic monoclonal antibodies - SARS CoV-2 as an example.","authors":"Yasmine El Abd, Ashraf Tabll, Robert Smolic, Martina Smolic","doi":"10.3233/HAB-211513","DOIUrl":"https://doi.org/10.3233/HAB-211513","url":null,"abstract":"<p><strong>Background: </strong>The emergence of novel viruses poses severe challenges to global public health highlighting the crucial necessity for new antivirals.</p><p><strong>Main body: </strong>Monoclonal antibodies (mAbs) are immunoglobulins that bind to a single epitope. Mouse mAbs are generated by classic hybridoma technology and are mainly used for immunodiagnostics. For immunotherapy, it is critical to use monoclonal antibodies in their human form to minimize adverse reactions. They have been successfully used to treat numerous illnesses, accordingly, an increasing number of mAbs, with high potency against emerging viruses is the target of every biopharmaceutical company. The diagnostic and therapeutic mAbs market grows rapidly into a multi-billion-dollar business. Biopharmaceuticals are innovative resolutions which revolutionized the treatment of significant chronic diseases and malignancies. Currently, a variety of therapeutic options that include antiviral medications, monoclonal antibodies, and immunomodulatory agents are available for the management of COVID-19.</p><p><strong>Short conclusion: </strong>The invasion of mAbs in new medical sectors will increase the market magnitude as it is expected to generate revenue of about 300 billion $ by 2025. In the current mini-review, the applications of monoclonal antibodies in immune-diagnosis and immunotherapy will be demonstrated, particularly for COVID-19 infection and will focus mainly on monoclonal antibodies in the market.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":"30 1","pages":"15-24"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39878194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hayder H Abed, Ahmed Ghdhban Al-Ziaydi, Ihab Abbas Taher, Ahmed K Al Dulaimi
Background: COVID-19 is a highly contagious virus that is rapidly spreading across the world. As the number of COVID-19 patients is quickly rising, and certain nations and areas, such as the third world countries, lack the medical resources, it is critical to track and monitor a patient's status using blood parameters on regular testing. The aim of this study is to compare the serum D-dimer levels, Ferritin, CRP, WBCs, Lymphocytes, and Neutrophils in male and female patients infected with COVID-19.
Objective and methods: The study procedure includes evaluating the D-dimer level, Ferritin, CRP, WBCs, lymphocytes, and neutrophils in 116 patients infected with COVID-19 (48 Females and 68 Males).
Result: The result of this study shows a significant increase in the D-dimer level in males 1618 ± 247.7 ng/ml compared to females 684.5 ± 53.69 ng/ml and a significant increase in Ferritin level in males 525.6 ± 69.55 μg/L compared to females 254.1 ± 33.73 μg/L. However, no other significant change is seen in the other parameters (CRP, LDH, and WBCs, L, and N) although all of these parameters are abnormal, compared to the normal reference values.
Conclusion: This study concludes that there is a significant increase in the D-dimer and Ferritin concentrations in male patients compared to female patients, who were infected with COVID-19. Also there are no significant differences in other parameters (CRP, LDH, WBCs, L, and N) between male and female patients.
{"title":"Comparison of some hematological parameters between male and female patients infected with COVID-19.","authors":"Hayder H Abed, Ahmed Ghdhban Al-Ziaydi, Ihab Abbas Taher, Ahmed K Al Dulaimi","doi":"10.3233/HAB-220006","DOIUrl":"https://doi.org/10.3233/HAB-220006","url":null,"abstract":"<p><strong>Background: </strong>COVID-19 is a highly contagious virus that is rapidly spreading across the world. As the number of COVID-19 patients is quickly rising, and certain nations and areas, such as the third world countries, lack the medical resources, it is critical to track and monitor a patient's status using blood parameters on regular testing. The aim of this study is to compare the serum D-dimer levels, Ferritin, CRP, WBCs, Lymphocytes, and Neutrophils in male and female patients infected with COVID-19.</p><p><strong>Objective and methods: </strong>The study procedure includes evaluating the D-dimer level, Ferritin, CRP, WBCs, lymphocytes, and neutrophils in 116 patients infected with COVID-19 (48 Females and 68 Males).</p><p><strong>Result: </strong>The result of this study shows a significant increase in the D-dimer level in males 1618 ± 247.7 ng/ml compared to females 684.5 ± 53.69 ng/ml and a significant increase in Ferritin level in males 525.6 ± 69.55 μg/L compared to females 254.1 ± 33.73 μg/L. However, no other significant change is seen in the other parameters (CRP, LDH, and WBCs, L, and N) although all of these parameters are abnormal, compared to the normal reference values.</p><p><strong>Conclusion: </strong>This study concludes that there is a significant increase in the D-dimer and Ferritin concentrations in male patients compared to female patients, who were infected with COVID-19. Also there are no significant differences in other parameters (CRP, LDH, WBCs, L, and N) between male and female patients.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":" ","pages":"151-155"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40470317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Soad Ghabeshi, Ali Najafi, Batol Zamani, Mozhdeh Soltani, Amanuel Godana Arero, Shim Izadi, Ahmad Piroozmand
Background: Considerable evidence supports that SLE could be related to apoptotic cells and EBV infection.
Objective: The aim of this study was to identify the transcriptional signature of EBV infection in SLE patients for survey of the molecular apoptosis signaling pathways.
Methods: The PBMCs gene expression profiles of healthy control and SLE patients were obtained from GEO. Functional annotation and signaling pathway enrichment were carried out using DAVID, KEGG. To validate bioinformatics analysis the changes in genes expression of some of obtained genes, Real time PCR was performed on PBMCs from 28 SLE patients and 18 controls.
Results: We found that mean viral load was 6013 ± 390.1 copy/μg DNA from PBMCs in all patients. QRT-PCR results showed that the expression of the DUSP1 and LAMP3 genes which had most changes in the logFC among 4 candidate genes, increased significantly in comparison with control. The consistent expression of LMP2 as viral latency gene involve in apoptosis signaling pathways was detected in SLE patients with EBV viral load and some controls.
Conclusions: The study indicated that some cellular genes may have an important role in pathogenesis of SLE through apoptosis signaling pathways. Beside, EBV infection as an environmental risk factor for SLE may affect the dysfunction of apoptosis.
背景:大量证据支持SLE可能与细胞凋亡和EBV感染有关。目的:本研究的目的是鉴定EBV感染SLE患者的转录特征,以调查分子凋亡信号通路。方法:从GEO获取健康对照和SLE患者的PBMCs基因表达谱。使用DAVID、KEGG进行功能注释和信号通路富集。为了验证生物信息学分析中部分基因表达变化的有效性,我们对28例SLE患者和18例对照组的pbmc进行了Real time PCR检测。结果:所有患者外周血单核细胞的平均病毒载量为6013±390.1拷贝/μg DNA。QRT-PCR结果显示,4个候选基因中logFC变化最大的DUSP1和LAMP3基因的表达量较对照显著升高。LMP2作为参与细胞凋亡信号通路的病毒潜伏期基因,在EBV病毒载量的SLE患者和部分对照组中表达一致。结论:本研究提示一些细胞基因可能通过凋亡信号通路在SLE发病中起重要作用。此外,EBV感染作为SLE的环境危险因素可能影响细胞凋亡功能障碍。
{"title":"Evaluation of molecular apoptosis signaling pathways and its correlation with EBV viral load in SLE patients using systems biology approach.","authors":"Soad Ghabeshi, Ali Najafi, Batol Zamani, Mozhdeh Soltani, Amanuel Godana Arero, Shim Izadi, Ahmad Piroozmand","doi":"10.3233/HAB-211505","DOIUrl":"https://doi.org/10.3233/HAB-211505","url":null,"abstract":"<p><strong>Background: </strong>Considerable evidence supports that SLE could be related to apoptotic cells and EBV infection.</p><p><strong>Objective: </strong>The aim of this study was to identify the transcriptional signature of EBV infection in SLE patients for survey of the molecular apoptosis signaling pathways.</p><p><strong>Methods: </strong>The PBMCs gene expression profiles of healthy control and SLE patients were obtained from GEO. Functional annotation and signaling pathway enrichment were carried out using DAVID, KEGG. To validate bioinformatics analysis the changes in genes expression of some of obtained genes, Real time PCR was performed on PBMCs from 28 SLE patients and 18 controls.</p><p><strong>Results: </strong>We found that mean viral load was 6013 ± 390.1 copy/μg DNA from PBMCs in all patients. QRT-PCR results showed that the expression of the DUSP1 and LAMP3 genes which had most changes in the logFC among 4 candidate genes, increased significantly in comparison with control. The consistent expression of LMP2 as viral latency gene involve in apoptosis signaling pathways was detected in SLE patients with EBV viral load and some controls.</p><p><strong>Conclusions: </strong>The study indicated that some cellular genes may have an important role in pathogenesis of SLE through apoptosis signaling pathways. Beside, EBV infection as an environmental risk factor for SLE may affect the dysfunction of apoptosis.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":"30 1","pages":"37-46"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39960017","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Imtiaz Mahmood Tahir, Abdur Rauf, Huma Mehboob, Samia Sadaf, Muhammad Shaiful Alam, Fadia Kalsoom, Abdelhakim Bouyahya, Aicha El Allam, Nasreddine El Omari, Saad Bakrim, Muhammad Akram, Syed Kashif Raza, Talha Bin Emran, Yahia N Mabkhot, Gokhan Zengin, Marina Derkho, Suray Natalya, Mohammad Ali Shariati
In numerous studies related to tumor prognosis, programmed death-ligand 1 (PD-L1) has been identified as a biomarker. This work aimed to determine the prognostic importance of PD-L1 in breast cancer. We searched electronic databases such as PubMed, Google scholar, home pages of publishing groups, medical, clinical, and pharmaceutical sciences journals, as well as other relevant sources to discover the importance of PD-1 and PD-L1 expression in breast cancer therapies and also recurrence. The keywords used in this search were autoimmunity, programmed cell death, PD-L1 or PD-1, and breast cancer. Our inclusion criteria included studies showing the synergy between the expression of PD-L1 and PD-1 in primary breast cancers as prognostic markers and this research was limited to humans only. We included review articles, original research, letters to the editor, case reports, and short communications in our study, published in English. We focused our work on PD-L1 mRNA expression in breast cancer cell lines. PD-L1 expression has been decisively demonstrated to be a high-risk factor for breast cancer with a bad prognosis.
{"title":"Prognostic significance of programmed death-1 and programmed death ligand-1 proteins in breast cancer.","authors":"Imtiaz Mahmood Tahir, Abdur Rauf, Huma Mehboob, Samia Sadaf, Muhammad Shaiful Alam, Fadia Kalsoom, Abdelhakim Bouyahya, Aicha El Allam, Nasreddine El Omari, Saad Bakrim, Muhammad Akram, Syed Kashif Raza, Talha Bin Emran, Yahia N Mabkhot, Gokhan Zengin, Marina Derkho, Suray Natalya, Mohammad Ali Shariati","doi":"10.3233/HAB-220001","DOIUrl":"https://doi.org/10.3233/HAB-220001","url":null,"abstract":"<p><p>In numerous studies related to tumor prognosis, programmed death-ligand 1 (PD-L1) has been identified as a biomarker. This work aimed to determine the prognostic importance of PD-L1 in breast cancer. We searched electronic databases such as PubMed, Google scholar, home pages of publishing groups, medical, clinical, and pharmaceutical sciences journals, as well as other relevant sources to discover the importance of PD-1 and PD-L1 expression in breast cancer therapies and also recurrence. The keywords used in this search were autoimmunity, programmed cell death, PD-L1 or PD-1, and breast cancer. Our inclusion criteria included studies showing the synergy between the expression of PD-L1 and PD-1 in primary breast cancers as prognostic markers and this research was limited to humans only. We included review articles, original research, letters to the editor, case reports, and short communications in our study, published in English. We focused our work on PD-L1 mRNA expression in breast cancer cell lines. PD-L1 expression has been decisively demonstrated to be a high-risk factor for breast cancer with a bad prognosis.</p>","PeriodicalId":53564,"journal":{"name":"Human Antibodies","volume":" ","pages":"131-150"},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40593062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}