Introduction: Long COVID (LC) affects approximately 10% of individuals post-SARS-CoV-2 infection, with symptoms persisting beyond 12 weeks. The underlying mechanisms remain unclear, and current models often focus on pre-existing comorbidities.Methods: This cohort study aimed to identify robust biomarkers and clarify LC pathogenesis through a comprehensive analysis performed in 32 LC individuals 26 months post-infection compared with 35 fully recovered individuals recruited between March and July 2022. Blood and fecal samples were collected, and multiple parameters associated with immune dysfunction, endothelial damage, bacterial translocation, and coagulation alterations, alongside signs of viral persistence and sociodemographic and clinical features, were analyzed.Results: Although viral RNA was undetected on blood or stool, elevated plasma IgG against the nucleocapsid may indicate frequent reinfections, greater infection severity, or delayed immune normalization. Increased levels of prothrombin, thrombin, fibrinogen, sEPCR, and CRP pointed to persistent endothelial dysfunction and coagulation imbalance. Lower levels of the bactericidal protein REG3A suggest potential disruptions in mucosal immune response. We found no major differences in traditional comorbidities, highlighting that LC may stem from distinct pathogenic mechanisms beyond pre-existing conditions. Importantly, our study revealed impaired humoral immunity and identified an association between vaccine heterogeneity and increased LC risk, emphasizing the relevance of consistent vaccination strategies. A Random Forest model using the measured biomarkers achieved 100% accuracy in classifying LC individuals, reinforcing their diagnostic potential.Discussion: These findings support a multifactorial model of LC involving immune dysregulation and persistent endothelial damage that led to coagulation abnormalities and a pro-thrombotic profile, supporting that LC is more closely related to a sustained, uncontrolled inflammatory response rather than immunodeficiency, and underscoring the value of multidimensional biomarker profiling for guiding clinical management and prevention strategies.

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In May 2022, a large outbreak of monkeypox virus (MPXV) occurred in several non‐endemic regions worldwide. Another outbreak in 2024 raised global concerns, particularly for immunocompromised individuals like people with HIV (PWH). Since the latent HIV‐1 reservoir remains a major barrier to a cure, we investigated how past mpox infection affected reservoir dynamics in this population. PWH who had mpox at an average of 9 months before sampling showed a significantly smaller HIV‐1 reservoir than MPXV‐unexposed PWH. This reduction was accompanied by enhanced antigen‐driven proviral reactivation in CD4+ T cells, especially central memory cells (TCM), and increased expression of T‐cell activation and proliferation markers like CD32 and Ki67. Mpox also induced sustained immune stress, as reflected by a prolonged decrease in CD4+ T naïve (TN) cells, increased expression of immune senescence and exhaustion markers like PD‐1, LAG‐3, and CD57, as well as metabolic dysfunction in CD4+ TN and TCM cells, which showed impaired glucose uptake and reduced proliferative capacity. These findings suggest that MPXV‐induced immune activation leads to long‐lasting changes in T‐cell homeostasis and reprograms the HIV‐1 reservoir, which may have implications for monitoring immune competence and vaccine responses in this population. Understanding the interplay between HIV‐1/MPXV co‐infection, T‐cell dynamics, and HIV‐1 reservoir modulation provides novel insights into how controlled proviral reactivation may inform the design of cure‐oriented strategies.

The high morbimortality due to SARS-CoV-2 infection in oncohematological diseases (OHD) and hematopoietic stem cell transplant (HSCT) recipients in the pre-vaccine era has made vaccination a priority in this group. After HSCT, the immune responses against common vaccines such as tetanus, varicella, rubella, and polio may be lost. However, the loss of immunity developed by COVID-19 vaccination after HSCT has not been completely defined. In this study, both humoral and cellular immunity against SARS-CoV-2 were analyzed in 29 individuals with OHD who were vaccinated before receiving allogeneic (n = 11) or autologous (n = 18) HSCT. All participants had low but protective levels of neutralizing IgGs against SARS-CoV-2 after HSCT despite B-cell lymphopenia and immaturity. Although antibody-dependent cellular cytotoxicity was impaired, direct cellular cytotoxicity was similar to healthy donors in participants with autologous-HSCT, in contrast to individuals with allogeneic–HSCT, which severely deteriorated. No significant changes were observed in the immune response before and after HSCT. During follow-up, all reported post-HSCT SARS-CoV-2 infections were mild. This data emphasizes that COVID-19 vaccination is effective, necessary, and safe for individuals with OHD and also supports the persistence of some degree of immune protection after HSCT, at least in the short term, when patients cannot yet be revaccinated.

Chronic lymphocytic leukaemia (CLL) is a lymphoproliferative disorder of abnormal B-lymphocytes. Due to immune deregulation and therapy-related factors, CLL individuals face increased infection risks, making vaccination a priority. Although COVID-19 is no longer a global emergency, understanding vaccine responses in this vulnerable population, especially those undergoing active cancer treatments, remains critical for broader infectious disease prevention strategies. We have characterized the humoral and cellular immune response of SARS-CoV-2 vaccination elicited by CLL individuals under standard-of-care treatment and watch and wait (W&W) strategy compared with healthy subjects who received a three-dose regimen six months ago. Seroconversion rates varied between 81.8% and 71.4% in individuals under W&W and dropped to 28.6%-22.2% in those under treatment, with antibody titres and neutralizing activity following the same pattern, highlighting the impact of active therapies on vaccine immunogenicity. Analysis of B-cell dynamics revealed that individuals under W&W maintained the highest levels of total B cells (CD19+) throughout the study (up to 3.5-fold higher than healthy donors, p<0.0001). Basal naïve B cells were markedly reduced across CLL groups (up to 4.3-fold lower in treated vs. W&W, p<0.0001), while memory subsets expanded over time, particularly in the W&W cohort after booster vaccination. Additionally, we found that the actively treated CLL group exhibited higher levels of cytotoxic cells (including CD8+ T cells and NK cells) when compared to the W&W or the healthy population groups. However, none of these cell populations demonstrated an increased activation capacity. Moreover, the direct cytotoxic capacity of peripheral blood mononuclear cells (PBMCs) from CLL persons was also more efficient in the W&W group. Through our comprehensive characterization of both humoral and cellular immune responses in CLL individuals, this study provides insight into the complex immunological landscape following SARS-CoV-2 vaccination. Our detailed analysis supports the current vaccination strategy against SARS-CoV-2 for CLL patients, confirming its effectiveness and underscoring the importance of close monitoring and representing a significant advancement in our understanding of immune responses in hematological malignancies.