Background and Objectives: The neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) are novel biomarkers that provide insight into systemic inflammation and how the immune system responds to stress or infection. These ratios have been associated with predicting clinical outcomes in various diseases, including COVID-19. This study aims to evaluate the prognostic value of NLR and PLR in anticipating ICU admission, acute respiratory failure, and disease severity in COVID-19 patients. Materials and Methods: We conducted a retrospective, observational study that included 536 patients diagnosed with COVID-19. We analyzed the NLR and PLR values at admission and correlated them with ICU admission, the onset of acute respiratory failure, and clinical outcomes. Results: Statistical correlations were identified between elevated NLR and PLR values and the development of complications during hospitalization (p = 0.04 and p = 0.00), acute hypoxemic respiratory failure (p = 0.00), and admission to the intensive care unit (ICU) (p = 0.04). No correlations were found between the values of these ratios and mortality (p = 0.46 and p = 0.32) nor with the development of hepatic cytolysis (p = 0.79 and p = 0.87). Conclusions: NLR and PLR are reliable, easily obtainable biomarkers that can aid in the early prediction of ICU admission and disease severity in COVID-19 patients, offering valuable insights for risk stratification and clinical management. Further prospective studies are needed to validate these biomarkers as part of a broader predictive model for critical care in COVID-19.

Objectives: This study aimed to evaluate the risk of hepatitis B virus reactivation (HBVr) in COVID-19 patients receiving immunosuppressive treatment, which has been insufficiently studied to date. Secondarily, we aimed to evaluate the seroprevalence of HBV infection in COVID-19 patients. Methods: We performed HBV screening on all Romanian adults hospitalized in four COVID-19 wards between October 2021 and September 2022. We enrolled patients with positive hepatitis B core antibody (anti-HBc) without protective hepatitis B surface antibody (anti-HBs), HBV treatment, or baseline immunosuppressive conditions, and we conducted a virological follow-up on these patients at 3 months. Results: We identified 333/835 (39.9%) anti-HBc-positive patients. Follow-up was performed for 13 patients with positive hepatitis B surface antigen (HBsAg) and 19 HBsAg-negative/anti-HBc-positive patients. Among those who received immunosuppressants, 4/23 (17.4%) patients experienced HBVr: 1 out of 8 (12.5%) HBsAg-positive patients (with 1.99 log increase in HBV DNA level) and 3 out of 15 (20%) HBsAg-negative/anti-HBc-positive patients (with a de novo detectable HBV DNA level). Conclusions: Administration of COVID-19 immunosuppressants may result in a significant risk of HBVr in co-infected patients. We recommend performing an HBV triple screen panel (HBsAg, anti-HBs, anti-HBc) for all COVID-19 patients receiving immunosuppressive treatment. HBV prophylaxis may be indicated in certain patients. Larger studies are needed in order to establish appropriate and cost-effective management for these patients.

Background: Human herpesvirus 6 (HHV-6) is considered a ubiquitous virus, with many countries reporting a seroprevalence of more than 80–90% among the general population. However, this virus is unique among herpesviruses in its ability to integrate into the genetic material of the host’s cells. Thus, there are three ways by which HHV-6 can cause an active infection–primary infection, reactivation of a latent acquired infection, or activation of iciHHV-6 (inherited chromosomally integrated HHV-6). Whole blood quantitative polymerase chain reaction (qPCR) is very useful in distinguishing between iciHHV-6 and primary infection/reactivation. Our aim is to assess the role of HHV-6 in the aetiology of central nervous system (CNS) infections in adults and children, to describe all HHV-6-positive cases in an attempt to determine the susceptible population and to identify potential risk factors that can be linked to HHV-6 meningoencephalitis. Methods: We performed a retrospective study involving patients that were admitted to Prof. Dr. Matei Bals National Institute of Infectious Diseases, Bucharest, Romania, with a diagnosis of meningitis or encephalitis. We only selected the clinical records of patients that had a multiplex PCR Biofire^® FilmArray^® meningitis/encephalitis panel. Results: We report a 5% HHV-6 positivity in the cerebrospinal fluid (CSF) of patients with CNS infections tested with a commercial multiplex PCR M/E (meningitis/encephalitis) panel. Additionally, 2% to 4% of the total study population (n = 100) had active HHV-6 infections, which denotes 40 to 80% of the HHV-6-positive samples. We did not observe any statistically significant correlation between HHV-6 positivity in the CSF and variables such as age, sex, or comorbidities, including obesity, diabetes, hypertension, immunosuppression, or oncologic disease. Therefore, no risk factors could be linked with HHV-6 positivity in the CSF. Conclusions: although multiplex qualitative PCR is highly useful for providing rapid results and identifying nearly every pathogen that can cause meningitis/encephalitis, we have to be aware of this type of test’s limitations. All patients with HHV-6 detectable in their CSF via a multiplex PCR test should also undergo qPCR testing from both CSF and blood to prevent over-diagnosing HHV-6 CNS infections, to avoid unnecessary antiviral treatments, and ensure the accurate identification of the true diagnosis.

Objectives: This study aimed to evaluate the risk of hepatitis B virus reactivation (HBVr) in COVID-19 patients receiving immunosuppressive treatment, which has been insufficiently studied to date. Secondarily, we aimed to evaluate the seroprevalence of HBV infection in COVID-19 patients. Methods: We performed an HBV screening in all Romanian adults hospitalized in 4 COVID-19 wards between October 2021 and September 2022. We enrolled patients with positive hepatitis B core antibody (anti-HBc) without protective hepatitis B surface antibody (anti-HBs), HBV treatment or immunosuppressive conditions, whom we followed virologically at 3 months. Results: We identified 333/835 (39.9%) anti-HBc-positive patients. Follow-up was performed in 13 patients with positive hepatitis B surface antigen (HbsAg) and 19 HBsAg-negative/anti-HBc-positive patients. Among those who received immunosuppressants, 4/23 (17.4%) patients experienced HBVr: 1 out of 8 (12.5%) HBsAg-positive patients (with 1.99 log increase in HBV DNA level) and 3 out of 15 (20%) HBsAg-negative/anti-HBc-positive patients (with de novo detectable HBV DNA level). Conclusions: Administration of COVID-19 immunosuppressants may result in a significant risk of HBVr in co-infected patients. We recommend performing an HBV triple screen panel (HBsAg, anti-HBs, anti-HBc) in all COVID-19 patients receiving immunosuppressive treatment. HBV prophylaxis may be indicated in certain patients. Larger studies are needed in order to establish an appropriate and cost-effective management in these patients.

Background: COVID-19 has largely become an endemic disease in many regions, with sporadic outbreaks, with some areas where the disease shows a seasonal pattern like the influenza virus. The focus has shifted towards managing mild and moderate forms of disease through outpatient care, aiming to prevent healthcare system overload. Consequently, identifying markers that could be used in stratifying the risk and the prognostic assessment has become crucial. Cardiovascular implications of COVID-19 are a critical area of research due to their significant impact on disease severity, mortality, and morbidity. Methods: We conducted a retrospective, observational study and included 472 patients, diagnosed with COVID-19, all of whom were admitted to Prof. Dr. Matei Bals National Institute of Infectious Disease, Bucharest, Romania. Levels of cardiac biomarkers like creatine kinase (CK), creatine kinase-myocardial band (CKMB), myoglobin, troponins, and NT-pro-BNP were measured and analyzed in relation to clinical presentation and outcomes. Results: We combined CKMB, myoglobin, and troponin I to predict hospital length of stay (LOS). Our model significantly predicted LOS (F = 12.537, p = 0.0001), with higher levels associated with prolonged stays (β = 0.166, p = 0.000). Logistic regression demonstrated that the combination of elevated CKMB and myoglobin levels significantly increased the odds of a longer LOS (OR = 1.679, p = 0.000). Furthermore, we found significant correlations with acute respiratory failure (p = 0.001), severe forms of disease (p = 0.000), and the development of complications during hospitalization (p = 0.027). Conclusions: These findings emphasize the value of combining cardiac biomarkers to stratify risk and predict hospital outcomes in COVID-19 patients. Routine cardiac monitoring and targeted management strategies could decrease the risk of complications, reducing the LOS. Our findings highlight the potential of cardiac biomarkers as prognostic tools to stratify risk, guide clinical interventions, and improve outcomes in COVID-19 patients.

Abnormal liver function tests are frequently reported in patients with COVID-19. This study aimed to identify potential treatment-associated hepatocellular injury in COVID-19 patients by dynamically assessing circulating miR-122, a biomarker with high hepatic specificity and sensitivity. An exploratory approach was additionally used, given the limited evidence regarding factors influencing miR-122 expression in this setting. We performed a prospective cohort study including 96 adult participants enrolled at a tertiary hospital in Bucharest, Romania, between March 2022 and July 2023: 78 COVID-19 patients (57 with baseline and follow-up miR-122 assessment after 5 days of treatment and 21 with a single measurement) and 18 non-COVID-19 participants included for comparison. Plasma miR-122 levels were measured using quantitative polymerase chain reaction, normalized to U6 small nuclear RNA, and expressed as log₁₀(2^−ΔCt). No associations were observed between miR-122 expression and remdesivir administered for standard treatment durations (3–5 days) or other COVID-19–specific therapies. However, a duration-dependent relationship with remdesivir cannot be excluded. Moreover, therapeutic paracetamol use prior to presentation was positively associated with miR-122 expression at follow-up and remained significant after adjustment. Additionally, bivariate analyses revealed inverse correlations between baseline miR-122 and inflammatory biomarkers, with multivariable analysis showing an independent positive association with lymphocyte count.