scholarly journals A Case Report: Genetically Distinct Severe Acute Respiratory Syndrome Coronavirus-2 Variant Causing Reinfection

2021 ◽  
Vol 12 ◽  
Author(s):  
Mohammad Enayet Hossain ◽  
Md. Mahfuzur Rahman ◽  
Md. Shaheen Alam ◽  
Monira Sarmin ◽  
Yeasir Karim ◽  
...  

Background: The emergence of novel variants has been a great deal of international concern since the recently published data suggest that previous infections with SARS-CoV-2 may not protect an individual from new variants. We report a patient had two distinct episodes of COVID-19 with different variants of SARS-CoV-2.Methods: The nasopharyngeal samples collected from the two episodes were subjected to whole-genome sequencing and comparative genome analysis.Results: The first infection presented with mild symptoms, while the second infection presented with severe outcomes which occurred 74 days after the patient recovered from the first episode. He had elevated C-reactive protein, ferritin, and bilateral consolidation as a sign of acute infection. Genome analysis revealed that the strains from the first and second episodes belonged to two distinct Nexstrain clades 20B and 20I and Pangolin lineages B.1.1.25 and B.1.1.7, respectively. A total of 36 mutations were observed in the episode-2 strain when compared with the reference strain Wuhan-Hu-1. Among them, eight mutations were identified in the receptor-binding domain (RBD).Conclusion: Our findings concern whether the immunity acquired by natural infection or mass vaccination could confer adequate protection against the constantly evolving SARS-CoV-2. Therefore, continuous monitoring of genetic variations of SARS-CoV-2 strains is crucial for interventions such as vaccine and drug designs, treatment using monoclonal antibodies, and patient management.

2018 ◽  
Vol 29 (11) ◽  
pp. 1089-1097 ◽  
Author(s):  
M Duro ◽  
MC Manso ◽  
S Barreira ◽  
I Rebelo ◽  
R Medeiros ◽  
...  

The objective of this study was to investigate the factors underlying the development of metabolic syndrome (MetS) in HIV-infected patients. Two hundred and sixty-six clinical cases were selected for a retrospective study. The sample was classified using the Adult Treatment Panel III guidelines and the identification of risk or protective factors associated with MetS evaluated via multivariate logistic or multinomial regressions. HIV-infected individuals diagnosed with MetS tend to be older, overweight, or obese (85% have a BMI ≥ 25), with a waist circumference > 90 cm (96.5 [88.8–105.5] cm, median [interquartile range]). Blood testing these individuals revealed high fasting levels of insulin (8.1 [5.8–21.6] pg/ml), glucose (98.0 [84.0–116.0] mg/dl), triglycerides (201.0 [142.0–267.3] mg/dl), and high-density lipoprotein cholesterol (36.5 [29.8–43.3] mg/dl) in addition with higher levels of inflammatory mediators such as high-sensitivity C-reactive protein (2.5 [1.0–4.9] mg/dl) and interleukin-6 (3.4 [2.8–3.8] pg/ml). The likelihood of HIV-infected individuals who are virally suppressed developing MetS is about 60% higher than those with acute infection. Treatment with nucleoside reverse transcriptase inhibitors (NRTIs) and protease inhibitors (PIs) increases the chance of developing MetS by around 2.4 times. Individuals with a lower antioxidant capacity (total antioxidant status [TAS] <1.33) have a 2.6 times higher risk of developing MetS. HIV-related chronic inflammation, a low TAS, and treatment with NRTIs in association with PIs are additional MetS risk factors.


Author(s):  
Johann Steiner ◽  
Thomas Frodl ◽  
Kolja Schiltz ◽  
Henrik Dobrowolny ◽  
Roland Jacobs ◽  
...  

Abstract Innate immunity has been linked to initiation of Alzheimer’s disease and multiple sclerosis. Moreover, risk of first-episode psychosis (FEP) and schizophrenia (Sz) is increased after various infections in predisposed individuals. Thus, we hypothesized an analogous role of innate immunity with increased C-reactive protein (CRP) in non-affective psychosis. Differential blood count, CRP, neutrophil and monocyte–macrophage activation markers, cortisol and psychotic symptoms (Positive and Negative Syndrome Scale [PANSS]) were assessed in controls (n = 294) and acutely ill unmedicated FEP (n = 129) and Sz (n = 124) patients at baseline and after 6 weeks treatment. Neutrophils, monocytes, and CRP were increased in patients vs controls at baseline (P < .001), and neutrophil and monocyte counts correlated positively with activation markers. Eosinophils were lower at baseline in FEP (P < .001) and Sz (P = .021) vs controls. Differences in neutrophils (P = .023), eosinophils (P < .001), and CRP (P < .001) were also present when controlling for smoking and cortisol, and partially remitted after antipsychotic treatment. FEP patients with high neutrophils (P = .048) or monocytes (P = .021) had higher PANSS-P scores at baseline but similar disease course. CRP correlated with PANSS-P at baseline (ρ = 0.204, P = .012). Improvement of positive symptoms after treatment correlated with declining neutrophils (ρ = 0.186, P = .015) or CRP (ρ = 0.237, P = .002) and rising eosinophils (ρ = −0.161, P = .036). In FEP, normalization of neutrophils (ρ = −0.231, P = .029) and eosinophils (ρ = 0.209, P = .048) correlated with drug dosage. In conclusion, innate immune system activation correlated with PANSS-P, supporting the immune hypothesis of psychosis. Neutrophil and monocyte counts and CRP levels may be useful markers of disease acuity, severity, and treatment response.


2019 ◽  
Vol 6 (Supplement_2) ◽  
pp. S629-S629
Author(s):  
Supavit Chesdachai ◽  
Nicole Engen ◽  
Joshua Rhein ◽  
Lillian Tugume ◽  
Tadeo kiiza. Kandole ◽  
...  

Abstract Background C-reactive protein (CRP) is an acute-phase protein produced by the liver in response to systemic inflammation. CRP is a helpful surrogate biomarker widely used in various infections, particularly for following the progression and resolution of infection. We aimed to determine the association between baseline CRP level and cryptococcal meningitis outcome. Methods We reviewed 168 prospectively enrolled HIV-infected Ugandans with confirmed first-episode cryptococcal meningitis. Baseline serum samples collected within 5 days from diagnosis had CRP levels measured and categorized into quartiles. We compared baseline serum CRP with 18-week survival using unadjusted time-to-event analysis. Results Of 168 participants, the first quartile of baseline serum CRP was 83.6 mg/L. Baseline CD4 count, HIV viral load, and cerebrospinal fluid results did not differ by quartile. Participants with CRP > 49.5 mg/L more likely presented with Glasgow Coma Scale <15 (P = 0.03). The 18-week mortality rate was 54.8% (46/84) in the highest two quartile CRP groups (49.5 mg/L), 40.5% (17/42) in the mid-range CRP group (29–49.5 mg/L), and 14.3% (6/42) in the low CRP group (<29 mg/L) (P < 0.001) (Figure 1). Conclusion Higher baseline serum CRP is associated with increased mortality in HIV-infected individuals with first-episode cryptococcal meningitis. The serum CRP could be a surrogate marker for undiagnosed co-infections or may reflect immune dysregulation leading to worse outcomes in persons with advanced AIDS and concomitant cryptococcal meningitis. Additional studies investigating more specific inflammatory biomarkers and the longitudinal trend in CRP with effective therapy would be informative. Disclosures All authors: No reported disclosures.


2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Oliver Zimmermann ◽  
Kefei Li ◽  
Myron Zaczkiewicz ◽  
Matthias Graf ◽  
Zhongmin Liu ◽  
...  

The role of C-reactive protein (CRP) in atherosclerosis is controversially discussed. Whereas initial experimental studies suggested a pathogenic role for CRP in atherogenesis, more recent genetic data from Mendelian randomization trials failed to provide evidence for a causative role of CRP in cardiovascular disease. Also, experimental results from laboratories all over the world were indeed contradictory, partly because of species differences in CRP biology and partly because data were not accurately evaluated. Here we summarize the published data from experimental work with mainly human material in order to avoid confusion based on species differences in CRP biology. Experimental work needs to be reevaluated after reconsideration of some traditional rules in research: (1) in order to understand a molecule’s role in disease it may be helpful to be aware of its role in physiology; (2) it is necessary to define the disease entity that experimental CRP research deals with; (3) the scientific consensus is as follows: do not try to prove your hypothesis. Specific CRP inhibition followed by use of CRP inhibitors in controlled clinical trials may be the only way to prove or disprove a causative role for CRP in cardiovascular disease.


2013 ◽  
Vol 33 (3) ◽  
pp. 273-279 ◽  
Author(s):  
Jie Dong ◽  
Yuan Chen ◽  
Suping Luo ◽  
Rong Xu ◽  
Ying Xu

BackgroundWhether peritoneal protein leakage predicts risk for peritonitis in patients on peritoneal dialysis (PD) is unknown. In this observational cohort study, we aimed to determine that association and, further, to explore if it might be explained by systemic inflammation.MethodsWe prospectively followed 305 incident PD patients to first-episode peritonitis, censoring, or the end of the study. Demographics, comorbidity score, biochemistry, and peritoneal protein clearance (PrC) were collected at baseline. The predictors of first-episode peritonitis were analyzed prospectively.ResultsDuring follow-up, 14 868 patient months and 251 episodes of peritonitis were observed. The baseline PrC was 73.2 mL/day (range: 53.2 – 102 mL/day). Patients with a high PrC were prone to be older and malnourished. They also had a higher comorbidity score and higher C-reactive protein values. In 132 first episodes of peritonitis, baseline PrC was shown to be a significant independent predictor after adjustment for age, sex, body mass index, diabetes, residual renal function, hemoglobin, and peritoneal transport rate. Systemic inflammatory markers such as serum albumin, C-reactive protein, and interleukin-6 could not explain the association of PrC and high risk for peritonitis.ConclusionsBaseline peritoneal protein leakage was able to independently predict risk for peritonitis, which is not explained by systemic inflammation. The underlying mechanisms should be explored in future.


Author(s):  
Marwa Awad Mustafa ◽  
Maaly Mohamad Mabrouk ◽  
Sabry Abd Ellatif Abou Saif ◽  
Nadia Muhammad Elwan

Background: Spontaneous bacterial peritonitis (SBP) is an acute infection of ascites with the absence of surgically treatable cause and the gold standard method in its diagnosis is the presence of 250 polymorphonuclear neutrophils (PMN) /mm3 or more by diagnostic paracentesis. Blood neutrophil/lymphocytic ratio (NLR) is an applicable, inexpensive, and simple test for inflammation. C-reactive protein/albumin ratio (CAR) is an inflammatory marker used for the diagnosis and follow-up of many diseases and morbidities. We aimed to evaluate the clinical utility of both blood NLR and CAR as applicable, simple and non-invasive tests for SBP follow-up. Patients and Methods: This study was done on 80 cirrhotic ascitic patients attending the Tropical Medicine Department of Tanta University Hospital. They were subjected to full history taking, clinical examination, laboratory investigations, and ascitic fluid analysis. The patients were divided into two groups according to the results of diagnostic paracentesis into group I: 40 cirrhotic ascitic patients without spontaneous bacterial peritonitis and group II: 40 cirrhotic ascitic patients with spontaneous bacterial peritonitis, and then SBP group were tested after treatment by third-generation cephalosporin for five days for ascitic sample, NLR and CAR. Results: Both blood NLR and CAR were significantly higher in SBP patients. Also, a significant decrease in both ratios was observed post-treatment with significant positive correlations between both NLR and CAR with ascitic neutrophil count after SBP treatment. Conclusion: NLR and CAR can be used as quick, cheap, and applicable markers of the response of treatment in SBP patients.


2020 ◽  
Vol 7 (12) ◽  
Author(s):  
Supavit Chesdachai ◽  
Nicole W Engen ◽  
Joshua Rhein ◽  
Lillian Tugume ◽  
Tadeo Kiiza Kandole ◽  
...  

Abstract Background C-reactive protein (CRP) is an acute phase protein produced by the liver in response to systemic inflammation. CRP is a helpful surrogate biomarker used for following the progression and resolution of infection. We aimed to determine the association of baseline CRP level and the temporal change in CRP over time with cryptococcal meningitis outcome. Methods We reviewed 168 prospectively enrolled HIV-infected Ugandans with confirmed first-episode cryptococcal meningitis. Baseline plasma CRP collected within 5 days of meningitis diagnosis was categorized into quartiles. We compared baseline CRP with 18-week survival using time-to-event analysis. Results Of 168 participants, the baseline first quartile of serum CRP was &lt;29.0 mg/L, second quartile 29.0–49.5 mg/L, third quartile 49.6–83.6 mg/L, and fourth quartile &gt;83.6 mg/L. Baseline CD4 count, HIV viral load, and cerebrospinal fluid results did not differ by CRP quartile. Participants with CRP &gt;49.5 mg/L more likely presented with Glasgow Coma Scale (GCS) &lt;15 (P = .03). The 18-week mortality rate was 55% (46/84) in the highest 2 quartile CRP groups (&gt;49.5 mg/L), 41% (17/42) in the mid-range CRP group (29.0–49.5 mg/L), and 14% (6/42) in the low-CRP group (&lt;29.0 mg/L; P &lt; .001). After adjustment for possible confounding factors including GCS &lt;15, CRP remained significantly associated with mortality (adjusted hazard ratio, 1.084 per 10 mg/L; 95% CI, 1.031–1.139; P = .0016). Conclusions Higher baseline CRP is associated with increased mortality in HIV-infected individuals with first-episode cryptococcal meningitis. CRP could be a surrogate marker for undiagnosed coinfections or may reflect immune dysregulation, leading to worse outcomes in persons with advanced AIDS and concomitant cryptococcal meningitis.


2021 ◽  

Viral persistence following acute COVID infection is increasingly being reported by patients and gradually being recognized as a medical syndrome. Like much about COVID, this so-called Long COVID is perplexing. It is associated with numerous symptoms, foremost among them profound fatigue, and often occurs in a relapsing/remitting pattern. There is one “living” guideline for managing Long COVID and even terminology and definitions of the syndrome are in flux. Long COVID occurs in patients who have recovered from the acute infection and this may be viral persistence, a form of autoimmunity, or the long-term results of organ damage sustained during the acute infection. Symptoms have been reported up to six months after acute infection with no clear association between the severity of the acute infection and the presence or absence of Long COVID. The symptoms of the acute illness do not necessarily align with the symptoms of Long COVID. Disruptions to the autonomic function in Long COVID are particularly puzzling, including orthostatic intolerance syndrome (which may not have occurred during the acute infection). Loss of the sense of smell and taste is one symptom that appears common in both acute and Long COVID; on the other hand, fever is more prevalent in acute than Long COVID. Research is urgently needed to better understand Long COVID, for example: what is the role of elevated biomarkers such as D-dimer and C-reactive protein in Long COVID? Is Long COVID one or more than one syndrome? How can patients with Long COVID be appropriately treated?


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