Correlation between Platelet to Lymphocyte Ratio with C-Reactive Protein in COVID-19 Patients

Author(s):  
Novianti Anggie Lestari ◽  
Dwi Retnoningrum

Coronavirus 2019 (COVID-19) is an infectious disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Inflammation occurs when the body is infected with the virus. Platelets play a role in immune response and immunomodulation by activating P-Selectin Glycoprotein (PSGL) to the site of inflammation. Lymphocytes play a role through CD4 T-cells, B-cells producing specific viral antibodies, and CD8 cytotoxic T-cells by directly killing the virus in infected cells. This study aimed to prove the correlation between PLR and CRP as inflammation markers in COVID-19 patients. This study was a retrospective observational study with the cross-sectional approach at Dr. Kariadi Hospital, Semarang, for the period March-August 2020. Spearman test performed for analyzing data with p<0.05 was significant. Thirty-three confirmed COVID-19 patients with median value of PLR 218 (103-1609) and CRP 15.94 (1.24-200) mg/L were tested for correlation with a value of p=0.013 and r=0.427. The increase of PLR and CRP in COVID-19 patients was caused by an inflammatory process mediated by the immune response. High values in the blood were associated with disease severity and poor prognosis. There was a statistically significant moderate positive correlation between PLR and CRP in COVID-19 patients.

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Alexandra J. Spencer ◽  
Paul F. McKay ◽  
Sandra Belij-Rammerstorfer ◽  
Marta Ulaszewska ◽  
Cameron D. Bissett ◽  
...  

AbstractSeveral vaccines have demonstrated efficacy against SARS-CoV-2 mediated disease, yet there is limited data on the immune response induced by heterologous vaccination regimens using alternate vaccine modalities. Here, we present a detailed description of the immune response, in mice, following vaccination with a self-amplifying RNA (saRNA) vaccine and an adenoviral vectored vaccine (ChAdOx1 nCoV-19/AZD1222) against SARS-CoV-2. We demonstrate that antibody responses are higher in two-dose heterologous vaccination regimens than single-dose regimens. Neutralising titres after heterologous prime-boost were at least comparable or higher than the titres measured after homologous prime boost vaccination with viral vectors. Importantly, the cellular immune response after a heterologous regimen is dominated by cytotoxic T cells and Th1+ CD4 T cells, which is superior to the response induced in homologous vaccination regimens in mice. These results underpin the need for clinical trials to investigate the immunogenicity of heterologous regimens with alternate vaccine technologies.


2021 ◽  
Author(s):  
Emily Stephenson ◽  
◽  
Gary Reynolds ◽  
Rachel A. Botting ◽  
Fernando J. Calero-Nieto ◽  
...  

AbstractAnalysis of human blood immune cells provides insights into the coordinated response to viral infections such as severe acute respiratory syndrome coronavirus 2, which causes coronavirus disease 2019 (COVID-19). We performed single-cell transcriptome, surface proteome and T and B lymphocyte antigen receptor analyses of over 780,000 peripheral blood mononuclear cells from a cross-sectional cohort of 130 patients with varying severities of COVID-19. We identified expansion of nonclassical monocytes expressing complement transcripts (CD16+C1QA/B/C+) that sequester platelets and were predicted to replenish the alveolar macrophage pool in COVID-19. Early, uncommitted CD34+ hematopoietic stem/progenitor cells were primed toward megakaryopoiesis, accompanied by expanded megakaryocyte-committed progenitors and increased platelet activation. Clonally expanded CD8+ T cells and an increased ratio of CD8+ effector T cells to effector memory T cells characterized severe disease, while circulating follicular helper T cells accompanied mild disease. We observed a relative loss of IgA2 in symptomatic disease despite an overall expansion of plasmablasts and plasma cells. Our study highlights the coordinated immune response that contributes to COVID-19 pathogenesis and reveals discrete cellular components that can be targeted for therapy.


2016 ◽  
Vol 90 (16) ◽  
pp. 7066-7083 ◽  
Author(s):  
Saikrishna Gadhamsetty ◽  
Tim Coorens ◽  
Rob J. de Boer

ABSTRACTSeveral experiments suggest that in the chronic phase of human immunodeficiency virus type 1 (HIV-1) infection, CD8+cytotoxic T lymphocytes (CTL) contribute very little to the death of productively infected cells. First, the expected life span of productively infected cells is fairly long, i.e., about 1 day. Second, this life span is hardly affected by the depletion of CD8+T cells. Third, the rate at which mutants escaping a CTL response take over the viral population tends to be slow. Our main result is that all these observations are perfectly compatible with killing rates that are much faster than one per day once we invoke the fact that infected cells proceed through an eclipse phase of about 1 day before they start producing virus. Assuming that the major protective effect of CTL is cytolytic, we demonstrate that mathematical models with an eclipse phase account for the data when the killing is fast and when it varies over the life cycle of infected cells. Considering the steady state corresponding to the chronic phase of the infection, we find that the rate of immune escape and the rate at which the viral load increases following CD8+T cell depletion should reflect the viral replication rate, ρ. A meta-analysis of previous data shows that viral replication rates during chronic infection vary between 0.5 ≤ ρ ≤ 1 day−1. Balancing such fast viral replication requires killing rates that are several times larger than ρ, implying that most productively infected cells would die by cytolytic effects.IMPORTANCEMost current data suggest that cytotoxic T cells (CTL) mediate their control of human immunodeficiency virus type 1 (HIV-1) infection by nonlytic mechanisms; i.e., the data suggest that CTL hardly kill. This interpretation of these data has been based upon the general mathematical model for HIV infection. Because this model ignores the eclipse phase between the infection of a target cell and the start of viral production by that cell, we reanalyze the same data sets with novel models that do account for the eclipse phase. We find that the data are perfectly consistent with lytic control by CTL and predict that most productively infected cells are killed by CTL. Because the killing rate should balance the viral replication rate, we estimate both parameters from a large set of published experiments in which CD8+T cells were depleted in simian immunodeficiency virus (SIV)-infected monkeys. This confirms that the killing rate can be much faster than is currently appreciated.


Author(s):  
Faiza Naseer ◽  
Tahir Ahmad ◽  
Kousain Kousar ◽  
Salik Kakar ◽  
Rabia Gul

Among the leading causes of cancer mortality, prostatic adenocarcinoma (PaC) is at second to lung carcinoma, but it is the most commonly happening non-cutaneous malignancy in elderly men in the world. Therapeutic options for PaC depend on age, growth &amp; stage of malignancy, the desired outcomes and shortcomings of available treatment, estimated cost and patient compliance. Patients older than 60 years with a sluggish localized tumor may be placed on active surveillance, otherwise go with transurethral resection of the prostate (TURP), prostate artery embolization (PAE) and pelvic lymphadenectomy with/without radiation therapy. For metastatic PC androgen-deprivation therapy is an option with or without surgery. These agents decline the body&rsquo;s testosterone production or block its activity by gonadotropin- releasing hormone (GnRH) analogues including leuprolide acetate and goserelin acetate implant. The hormone&rsquo;s activity can be stopped by androgens antagonist such as flutamide, bicalutamide and nilutamide along with chemotherapeutic agents, such as taxanes (e.g., docetaxel, paclitaxel) but after all the disease relapses in 20-30% of patients. So, new immunological or vaccine-based therapeutic moieties have been investigated to meet the objective of providing selectivity to cancerous cells and desired therapeutic outcomes with less/no harmful effects to normal cells. The chimeric version, oncolytic poliovirus and human rhinovirus i.e. PVSRIPO is most promising feature in cancer therapeutics and activate innate immunity by neutrophils infiltration via PAMP &amp; DAMP pathways while Sipuleucel-T expresses major histocompatibility complex (MHC) which can stimulate CD4+ helper T-cells and CD8+ cytotoxic T-cells and ultimately activate the acquired immunity against cancer cells. In this article, we have discussed the role of genetic predisposition and chemotherapeutic approaches including oncolytic poliovirus for the treatment of PaC in order to better understanding of tumor biology and mechanisms involved in chemotherapeutic drugs based resistance.


2021 ◽  
Vol 17 (13) ◽  
pp. 1683-1694
Author(s):  
Daniel J Craig ◽  
Nisha S Nanavaty ◽  
Monika Devanaboyina ◽  
Laura Stanbery ◽  
Danae Hamouda ◽  
...  

Radiation therapy (RT) in some cases results in a systemic anticancer response known as the abscopal effect. Multiple hypotheses support the role of immune activation initiated by RT-induced DNA damage. Optimal radiation dose is necessary to promote the cGAS-STING pathway in response to radiation and initiate an IFN-1 signaling cascade that promotes the maturation and migration of dendritic cells to facilitate antigen presentation and stimulation of cytotoxic T cells. T cells then exert a targeted response throughout the body at areas not subjected to RT. These effects are further augmented through the use of immunotherapeutic drugs resulting in increased T-cell activity. Tumor-infiltrating lymphocyte presence and TREX1, KPNA2 and p53 signal expression are being explored as prognostic biomarkers.


10.17816/cp66 ◽  
2021 ◽  
Vol 2 (1) ◽  
pp. 19-31
Author(s):  
Irina K. Malashenkova ◽  
Sergey A. Krynskiy ◽  
Daniil P. Ogurtsov ◽  
Nikita A. Hailov ◽  
Natalia V. Zakharova ◽  
...  

Introduction. Associations of disturbances in innate and adaptive immunity during the clinical course of schizophrenia have been found in a number of studies. Yet, the relationship of immune parameters and systemic inflammation in relation to the clinical course of the disease and its prognosis, remains poorly understood, which highlights an interesting topic for further research. The goal of this study was to research the immuno-inflammatory changes in patients with clinical continuous and episodic paranoid schizophrenia, to assess the pathogenetic significance of these changes. Methods. Thirty-six patients with paranoid schizophrenia, of which 20 had episodic symptoms and 16 had continuous symptoms, consented to participate in the study, together with 30 healthy volunteers. In the study we assessed the parameters of innate immune response (serum levels of key pro-inflammatory and anti-inflammatory cytokines, C-reactive protein) and the adaptive immune response, including humoral-mediated immunity (serum immunoglobulins IgA, IgM, IgG, circulating immune complexes), as well as the cell link of adaptive immunity (key lymphocyte subpopulations). Positive and negative symptoms were assessed with the positive and negative symptoms scale; frontal dysfunction was assessed by Frontal Assessment Battery (FAB). Results. Both patient groups had higher than normal levels of C-reactive protein and IL-8. There was a significant elevation of circulating immune complexes among patients with continuous symptoms of schizophrenia, compared to patients with episodic symptoms and healthy controls. Levels of CD45+CD3+ lymphocytes (T-cells) differed between clinical groups, with higher values identified among patients with episodic symptoms and lower values among those with continuous symptoms. In addition, patients with episodic symptoms had significantly increased levels of CD45+CD3+CD4+CD25+CD127- regulatory T-cells. Finally, the level of CD45+CD3-CD19+ B-cells was significantly higher among patients with continuous symptoms vs. patients with episodic symptoms and the control groups. Markers of activation of humoral immunity were associated with the severity of frontal disorders in these patients. Discussion. Comprehensive data on the serum level of cytokines and the parameters of adaptive immunity among individuals with continuous schizophrenia, by comparison with patients with episodic schizophrenia, are practically absent in the literature. We have shown that among those with continuous schizophrenia, there are signs of systemic inflammation and chronic activation of the adaptive humoral immune response, while among patients with episodic symptoms of the disease, there are signs of systemic inflammation and certain activation of cell-mediated immunity, without significant changes in the humoral link of adaptive immunity. Conclusion. More studies are needed, but the data obtained in this study are important for subsequent clinical studies of new treatment methods, based on various immunophenotypes of schizophrenia.


2019 ◽  
Vol 21 (Supplement_6) ◽  
pp. vi122-vi122
Author(s):  
Virginia Laspidea ◽  
Montse Puigdelloses ◽  
Ignacio Iñigo-Marco ◽  
Marc Garcia-Moure ◽  
Iker Ausejo ◽  
...  

Abstract Diffuse intrinsic pontine glioma (DIPG) is an aggressive brain tumor, being the leading cause of pediatric death caused by cancer. We previously showed that administration of the oncolytic virus Delta-24-RGD to DIPG murine models was safe and led to an increase in the median survival of these animals. However, not all the animals responded, underscoring the need to improve this therapy. In order to increase the antitumoral effect of the virus, we have engineered Delta-24-RGD with the costimulatory ligand 4-1BBL (Delta24-ACT). 4-1BB is a costimulatory receptor that promotes the survival and expansion of activated T cells, and the generation and maintenance of memory CD8+ T cells. In this project, we evaluated the oncolytic effect of Delta24-ACT and the antitumor immune response in DIPG murine models. In vitro, Delta24-ACT was able to infect and induce cell death in a dose-dependent manner in murine DIPG cell lines. In addition, Delta24-ACT was able to replicate in these tumor cells and to express viral proteins. Moreover, infected cells expressed 41BBL in their membranes. Delta24-ACT could induce immunogenic cell death due to an increased secretion of ATP and calreticulin translocation to the membrane of infected cells (in no-infected cells it located in the ER), DAMPs that can trigger the immune response activation. In vivo, Delta24-ACT demonstrated to be safe in all the tested doses and was able to induce a significant increase in the median survival of the treated animals. Moreover, long-term survivors display immunological memory. Delta24-ACT treatment led to antitumoral effect in DIPG murine cell lines in vitro. Of significance, we have demonstrated that in vivo administration of Delta24-ACT is safe and results in an enhanced antitumor effect. Future in vivo studies will explore the underlying immune mechanism of the virus.


2019 ◽  
Vol 1 (1) ◽  
pp. 30-37
Author(s):  
Indri Zaliavani ◽  
Mutiara Anissa ◽  
Fidiariani Sjaaf

In the elderly, environmental stress and decreased cognitive function often cause depression. Depression that is not treated properly can cause an increase in the use of health facilities, a negative influence on the quality of life elderly, and can even cause death. Purpose of this research to know the relationship of cognitive function disorders with depression in the elderly at Posyandu Lansia Ikur Koto working area of the Puskesmas Ikur Koto, Padang. This type of research is correlative analytic with cross-sectional approach. Research has been conducted at posyandu lansia Ikur Koto in February 2019. The samples in this research was elderly who were recorded at the posyandu lansia Ikur Koto there were 51 elderly. Data analysis univariate presented in the form of a frequency distribution table and bivariate analysis using the spearman test using the SPSS program. Result of the 51 respondents, the majority of age was 60-74 years old (70,6%), the highest sex were women (94,1%), the highest education was elementary school (56,9%) ), the most marital status was married (52,9%), the highest health status (58,8%) did not suffer chronic diseases and most medical history does not use drugs (98%),most (72,5%) did not experiencing depression, most (37,3%) had mild cognitive function disorders and there were relationship between cognitive function disorders and depression in the elderly with a value p=0,007<0,05 and r=-0,373. Conclusion is there were significant relationship between cognitive function disorders and depression in the elderly at Posyandu Lansia Ikur Koto working area of the Puskesmas Ikur Koto, Padang.


Author(s):  
Nesrin I. Tarbiah

In December 2019, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a novel coronavirus (COVID-19), materialized in the city of Wuhan and quickly spread to form a global pandemic. An essential role in the immune system is undertaken by lymphocytes, which defend against bacteria, viruses, fungi, and parasites. Previous study found that very severe COVID-19 patients had suppression of the immune response enabling the virus to spread and cause more damage. This was evident by the changes in their white blood cell and lymphocyte count. Early clinical findings suggest that those suffering from severe COVID-19 have reduced numbers of lymphocytes, monocytes, and other granulocytes. One of the most efficient responses for a variety of viral infections is cellular immune response activation, especially via T cells. Viruses can be eliminated by T cytotoxic (CD8+) (Tc) in the host body, these secrete a variety of molecules, including interferons (IFNs), granzyme, and perforin. T helper (CD4+) (Th) cells help by assisting cytotoxic T cells and B cells to eliminate viral infection. CD8+ and CD4+ work together in a coordinated immune response with other constituents to primarily resolve acute viral infections, and after to produce protection against any reinfection. Also, COVID-19 causes dramatic changes in cytokine profiles and serological markers. Therefore, the subsets of immune cells and the level of the pro-inflammatory cytokines are crucial evidence to determine the severity of COVID-19. The disease severity has already been proved to be associated with the disruption in the proinflammatory chemokine response, this eventually leads to a cytokine storm and progression of cytokines release syndrome (CRS). This review aimed to demonstrate a full understanding of the alterations to the immune response by determining the T-cell expression and cytokine levels against the pathological processes of COVID-19, which can be a significant step in early treatment and diagnosis of this disease, in reduction of COVID-19 mortality cases, and to emphasize the most recent and current studies to try to identify new immuno-therapeutics for COVID-19.  


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