Since its outbreak in December 2019, the coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), led to an enormous rise in scientific response with an excess of COVID-19-related studies on the pathogenesis and potential therapeutic approaches. Solid organ transplant (SOT) recipients are a heterogeneous population with long-lasting immunosuppression as a joining element. Immunocompromised patients are a vulnerable population with a high risk of severe infections and an increased infection-related mortality rate. It was postulated that the hyperinflammatory state due to cytokine release syndrome during severe COVID-19 could be alleviated by immunosuppressive therapy in SOT patients. On the other hand, it was previously established that T cell-mediated immunity, which is significantly weakened in SOT recipients, is the main component of antiviral immune responses. In this paper, we present the current state of science on COVID-19 immunology in relation to solid organ transplantation with prospective therapeutic and vaccination strategies in this population.

The Immunology of SARS-CoV-2 Infection and Vaccines in Solid Organ Transplant Recipients.

Coronavirus disease 2019 (COVID-19) is reported to have long-term effects on cardiovascular health and physical functioning, even in the nonhospitalized population. The physiological mechanisms underlying these long-term consequences are however less well described. We compared cardiovascular risk factors, arterial stiffness, and physical functioning in nonhospitalized patients with COVID-19, at a median of 6 mo postinfection, versus age- and sex-matched controls. Cardiovascular risk was assessed using blood pressure and biomarker concentrations (amino-terminal pro-B-type-natriuretic-peptide, high-sensitive cardiac troponin I, C-reactive protein), and arterial stiffness was assessed using carotid-femoral pulse wave velocity. Physical functioning was evaluated using accelerometry, handgrip strength, gait speed and questionnaires on fatigue, perceived general health status, and health-related quality of life (hrQoL). We included 101 former patients with COVID-19 (aged 59 [interquartile range, 55–65] yr, 58% male) and 101 controls. At 175 [126–235] days postinfection, 32% of the COVID-19 group reported residual symptoms, notably fatigue, and 7% required post-COVID-19 care. We found no differences in blood pressure, biomarker concentrations, or arterial stiffness between both groups. Former patients with COVID-19 showed a higher handgrip strength (43 [33–52] vs. 38 [30–48] kg, P = 0.004) and less sleeping time (8.8 [7.7–9.4] vs. 9.8 [8.9–10.3] h/day, P < 0.001) and reported fatigue more often than controls. Accelerometry-based habitual physical activity levels, gait speed, perception of general health status, and hrQoL were not different between groups. In conclusion, one in three nonhospitalized patients with COVID-19 reports residual symptoms at a median of 6 mo postinfection, but we were unable to relate these symptoms to increases in cardiovascular risk factors, arterial stiffness, or physical dysfunction. NEW & NOTEWORTHY We examined cardiovascular and physical functioning outcomes in nonhospitalized patients with COVID-19, at a median of 6 mo postinfection. When compared with matched controls, minor differences in physical functioning were found, but objective measures of cardiovascular risk and arterial stiffness did not differ between groups. However, one in three former patients with COVID-19 reported residual symptoms, notably fatigue. Follow-up studies should investigate the origins of residual symptoms and their long-term consequences in former, nonhospitalized patients with COVID-19.

Long-term cardiovascular health status and physical functioning of nonhospitalized patients with COVID-19 compared with non-COVID-19 controls

The absence of effective drugs for COVID-19 prevention and treatment requires the search for new candidates among approved medicines. Fundamental studies and clinical observations allow us to approach an understanding of the mechanisms of damage and protection from exposure to SARS-CoV-2, to identify possible points of application for pharmacological interventions. In this review we presented studies on the anti-inflammatory, antioxidant, and immunotropic properties of melatonin. We have attempted to present scientifically proven mechanisms of action for the potential therapeutic use of melatonin during SARS-CoV-2 infection. A wide range of pharmacological properties allows its inclusion as an effective addition to the methods of prevention and treatment of COVID-19.

/pdf/potential-and-possible-therapeutic-effects-of-melatonin-on-1h56mf8b.pdf

Potential and Possible Therapeutic Effects of Melatonin on SARS-CoV-2 Infection

For coronavirus disease 2019 (COVID-19), a pandemic disease characterized by strong immune dysregulation in severe patients, convenient and efficient monitoring of the host immune response is critical. Human hosts respond to viral and bacterial infections in different ways, the former is characterized by the activation of interferon stimulated genes (ISGs) such as IFI27, while the latter is characterized by the activation of anti-bacterial associated genes (ABGs) such as S100A12. This two-tiered innate immune response has not been examined in COVID-19. In this study, the activation patterns of this two-tiered innate immune response represented by IFI27 and S100A12 were explored based on 1421 samples from 17 transcriptome datasets derived from the blood of COVID-19 patients and relevant controls. It was found that IFI27 activation occurred in most of the symptomatic patients and displayed no correlation with disease severity, while S100A12 activation was more restricted to patients under severe and critical conditions with a stepwise activation pattern. In addition, most of the S100A12 activation was accompanied by IFI27 activation. Furthermore, the activation of IFI27 was most pronounced within the first week of symptom onset, but generally waned after 2–3 weeks. On the other hand, the activation of S100A12 displayed no apparent correlation with disease duration and could last for several months in certain patients. These features of the two-tiered innate immune response can further our understanding on the disease mechanism of COVID-19 and may have implications to the clinical triage. Development of a convenient two-gene protocol for the routine serial monitoring of this two-tiered immune response will be a valuable addition to the existing laboratory tests.

/pdf/a-two-gene-marker-for-the-two-tiered-innate-immune-response-1o7fm6eq.pdf

A two-gene marker for the two-tiered innate immune response in COVID-19 patients

Abstract This large-scale study aimed to investigate the trend of laboratory tests of patients with COVID-19. Hospitalized confirmed and probable COVID-19 patients in three general hospitals were examined from March 20, 2020, to June 18, 2021. The confirmed and probable COVID-19 patients with known outcomes and valid laboratory results were included. The least absolute shrinkage and selection operator (LASSO) and Cox regression were used to select admittance prognostic features. Parallel Pairwise Comparison of mortality versus survival was used to examine the trend of markers. In the final cohort, 11,944 patients were enrolled, with an in-hospital mortality rate of 21.8%, mean age of 59.4 ± 18.0, and a male-to-female ratio of 1.3. Abnormal admittance level of white blood cells, neutrophils, lymphocytes, mean cellular volume, urea, creatinine, bilirubin, creatine kinase-myoglobin binding, lactate dehydrogenase (LDH), Troponin, c-reactive protein (CRP), potassium, and creatinine phosphokinase reduced the survival of COVID-19 inpatients. Moreover, the trend analysis showed lymphocytes, platelet, urea, CRP, alanine transaminase (ALT), and LDH have a dissimilar trend in non-survivors compared to survived patients. This study proposed a novel approach to find serial laboratory markers. Serial examination of platelet count, creatinine, CRP, LDH, and ALT can guide healthcare professionals in finding patients at risk of deterioration. 

On-admission and dynamic trend of laboratory profiles as prognostic biomarkers in COVID-19 inpatients

Early detection of severe forms of COVID-19 is absolutely essential for timely triage of patients. We longitudinally followed-up two well-characterized patient groups, hospitalized moderate to severe (n = 26), and ambulatory mild COVID-19 patients (n = 16) at home quarantine. Human D-dimer, C-reactive protein (CRP), ferritin, cardiac troponin I, interleukin-6 (IL-6) levels were measured on day 1, day 7, day 14 and day 28. All hospitalized patients were SARS-CoV-2 positive on admission, while all ambulatory patients were SARS-CoV-2 positive at recruitment. Hospitalized patients had higher D-dimer, CRP and ferritin, cardiac troponin I and IL-6 levels than ambulatory patients (p < 0.001, p < 0.001, p = 0.016, p = 0.035, p = 0.002 respectively). Hospitalized patients experienced significant decreases in CRP, ferritin and IL-6 levels from admission to recovery (p < 0.001, p = 0.025, and p = 0.001 respectively). Cardiac troponin I levels were high during the acute phase in both hospitalized and ambulatory patients, indicating a potential myocardial injury. In summary, D-dimer, CRP, ferritin, cardiac troponin I, IL-6 are predictive laboratory markers and can largely determine the clinical course of COVID-19, in particular the prognosis of critically ill COVID-19 patients.

/pdf/longitudinal-monitoring-of-laboratory-markers-characterizes-1anojivr86.pdf

Longitudinal monitoring of laboratory markers characterizes hospitalized and ambulatory COVID-19 patients.

A call to caution when hydroxychloroquine is given to elderly patients with COVID-19.

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Longitudinal monitoring of laboratory markers characterizes hospitalized and ambulatory COVID-19 patients.

A call to caution when hydroxychloroquine is given to elderly patients with COVID-19.