Analyzing the Interplay between COVID-19 Viral Load, Inflammatory Markers, and Lymphocyte Subpopulations on the Development of Long COVID.

The global impact of the SARS-CoV-2 infection has been substantial, affecting millions of people. Long COVID, characterized by persistent or recurrent symptoms after acute infection, has been reported in over 40% of patients. Risk factors include age and female gender, and various mechanisms, including chronic inflammation and viral persistence, have been implicated in long COVID's pathogenesis. However, there are scarce studies in which multiple inflammatory markers and viral load are analyzed simultaneously in acute infection to determine how they predict for long COVID at long-term follow-up. This study explores the association between long COVID and inflammatory markers, viral load, and lymphocyte subpopulation during acute infection in hospitalized patients to better understand the risk factors of this disease. This longitudinal retrospective study was conducted in patients hospitalized with COVID-19 in northern Mexico. Inflammatory parameters, viral load, and lymphocyte subpopulation during the acute infection phase were analyzed, and long COVID symptoms were followed up depending on severity and persistence (weekly or monthly) and assessed 1.5 years after the acute infection. This study analyzed 79 patients, among them, 41.8% presented long COVID symptoms, with fatigue being the most common (45.5%). Patients with long COVID had higher lymphocyte levels during hospitalization, and NK cell subpopulation levels were also associated with long COVID. ICU admission during acute COVID-19 was also linked to the development of long COVID symptoms.

Viral load and its relationship with the inflammatory response and clinical outcomes in hospitalization of patients with COVID-19.

Background: The values of viral load in COVID-19 disease have gained relevance, seeking to understand its prognostic value and its behavior in the course of the disease, although there have been no conclusive results. In this study we sought to analyze serum viral load as a predictor of clinical outcome of the disease, as well as its association with inflammatory markers. Methods: An observational and retrospective study in a private hospital in North Mexico, patients with SARS-COV-2 infection confirmed by reverse transcriptase polymerase chain reaction (RT-PCR) were followed through clinical outcome, viral load measurement, quantification of inflammatory markers and lymphocyte subpopulations. For the analysis, multiple regression models were performed. Results: We studied 105 patients [47 (SD 1.46) years old, 68.6% men]. After analysis with multiple regression models, there was an association between viral load at admission and vaccination schedule (ß-value=-0.279, p= 0.007), age (ß-value= 0.010, p = 0.050), mechanical ventilation (ß-value= 0.872, p = 0.007), lactate dehydrogenase (ß-value= 1.712, p= 0.004), D-dimer values at admission (ß-value= 0.847, p= 0.013) and subpopulation of B lymphocytes at admission (ß-value= -0.527, p= 0.042). There was no association with days of hospitalization, use of nasal prongs or high flux mask. Peak viral load (10 days after symptoms onset) was associated with peak IL-6 (ß-value= 0.470, p= 0.011). Peak viral load matched with peak procalcitonin and minimal lymphocyte values. C-reactive protein peak was before the peak of viral load. The minimum value viral load was documented on day 12 after symptom onset; it matched with the minimum values of IL-6 and ferritin, and the peak of D-dimer. Conclusions: SARS-COV-2 admission viral load is associated with vaccination status, mechanical ventilation, and different inflammatory markers.

[Hematologic and molecular response with dasatinib as second-line treatment in chronic myeloid leukemia (CML) with treatment failure]. / Respuesta hematológica y molecular en leucemia mieloide crónica (LMC) con falla a tratamiento con dasatinib como fármaco de segunda línea.

BACKGROUND: Chronic myeloid leukemia is a myeloproliferative disease characterized by the Philadelphia chromosome and with this, the chimeric protein BCR-ABL. The first-line treatment is imatinib, a tyrosine kinase inhibitor, that has showed good results, but with a significant percentage of treatment failure. This failure has led to second-generation tyrosine kinase inhibitors as second-line treatment such as dasatinib. OBJECTIVES: The objective of the study was to evaluate the efficacy of dasatinib as second-line treatment. MATERIAL AND METHODS: Observational, longitudinal, and retrospective study. Patients with diagnosis of chronic myeloid leukemia that presented failure to first-line treatment were included in the present study; the hematologic response was evaluated at 3, 6, and 12 months, and molecular response at 12 months of follow-up after dasatinib treatment was started. RESULTS: Of a total of 14 patients that were included in the study, a response in the white cell count of 84.6% with a mean response at 4.7 months of follow-up was observed; also 84.6% platelet response with a mean response at 4.7 months of follow-up. Molecular response was also evaluated at a 12-month follow-up, achieving a 50% response with a mean response at 11.08 months of follow-up. A survival rate of 80% at a 12-month follow-up was observed. CONCLUSIONS: The use of dasatinib as a second-line treatment is effective in achieving a sustained hematologic response of 84.6% and a molecular response in 50%, also finding a hematologic response without achieving a total molecular response.