Monkeypox (MPX) transmission outside non-endemic countries has been reported since May 2022, rapidly evolving into a multi-country outbreak. A potential role of sexual contact in transmission dynamics, as well as a predominance of anogenital lesions, are remarkable features of current cases. Screening for sexually transmitted infections (STIs) plays an important role in the evaluation of patients with suspected MPX infection. Herein we report the first case of a patient diagnosed with both MPX and acute HIV infection in Latin America. He had no major complications during his clinical course, and antiretroviral therapy was promptly initiated. Diagnosis of acute HIV requires a high level of suspicion and appropriate laboratory investigation. Health practitioners need to consider this diagnosis while evaluating patients with suspected MPX with a recent unprotected sexual contact.

COVID-19 has a broad spectrum of clinical manifestations. We assessed the impact of single nucleotide polymorphisms (SNPs) of inflammasome genesas risk factors for progression toCOVID-19 critical outcomes, such as mechanical ventilation support (MVS) or death.The study included 451 hospitalized individuals followed up at the INI/FIOCRUZ, Rio de Janeiro, Brazil, from 06/2020 to 03/2021. SNPs genotyping was determined by Real-Time PCR. We analyzed risk factors for progression to MVS (n = 174[38.6 %]) or death (n = 175[38.8 %])as a result of COVID-19 by Cox proportional hazardmodels.Slower progression toMVSwas associated with allele G (aHR = 0.66;P = 0.005) or the genotype G/G (aHR = 0.391;P = 0.006) in the NLRP3 rs10754558 or the allele G (aHR = 0.309;P = 0.004) in the IL1βrs1143634, while C allele in the NLRP3 rs4612666 (aHR = 2.342;P = 0.006) or in the rs10754558 (aHR = 2.957;P = 0.005) were associated with faster progression to death. Slower progression to death was associated to allele G (aHR = 0.563;P = 0.006) or the genotype A/G (aHR = 0.537;P = 0.005) in the CARD8 rs6509365; the genotype A/C in the IFI16 rs1101996 (aHR = 0.569;P = 0.011); the genotype T/T (aHR = 0.394;P = 0.004) or allele T (aHR = 0.68;P = 0.006) in the NLRP3 rs4612666, and the genotype G/G (aHR = 0.326;P = 0.005) or allele G (aHR = 0,68;P = 0.014) in the NLRP3 rs10754558. Our results suggest that inflammasome genetic variations might influence the critical clinical course of COVID-19.

Objectives: The risk of major venous thromboembolism (VTE) among patients with COVID‐19 is high but varies with disease severity. Estimate the incidence of lower extremity deep venous thrombosis (DVT) in critically ill hospitalized patients with COVID‐19, validate the Wells score for DVT diagnosis, and determine patients' prognosis. Methods: This was an observational follow‐up study in the context of the diagnosis and prognosis of DVT. All patients were hospitalized in the intensive care unit (ICU) of the Evandro Chagas National Institute of Infectious Diseases. Participants with COVID‐19 pneumonia were included. Lower‐limb Doppler to assess DVT was performed at admission and follow‐up. Prognosis outcomes were death, length of stay, need for mechanical ventilation, vasopressor use, and hemodialysis. Wells' score sensitivity and specificity were estimated at admission. Survival curves were estimated for patients with DVT and adjusted for the SAPS 3 score. Results: Between June 2020 and January 2021, 186 patients were included. The DVT incidence was 0.097. A Wells score of 2 or higher had a sensitivity and specificity of 1.00 and 0.94, respectively. Mortality and mechanical ventilation support were higher in participants with DVT. For these outcomes, after SAPS 3 adjustment, participants with DVT had twice the hazard of those without DVT. A web calculator ( https://pedrobrasil.shinyapps.io/INDWELL/ ) is available for predictions. Conclusions: One can use the Wells score to accurately diagnose DVT in critically ill patients with COVID‐19. DVT increases the severity of COVID‐19, which highlights the importance of its early diagnosis, treatment, and prophylaxis in the ICU setting.

Background: Severe COVID-19 presents a variety of clinical manifestations associated with inflammatory profiles. People living with HIV (PLWH) could face a higher risk of hospitalization and mortality from COVID-19, depending on their immunosuppression levels. This study describes inflammatory markers in COVID-19 clinical outcomes with and without HIV infection. Methods: We analyzed 112 inpatients of the Hospital Center for COVID-19 (INI/FIOCRUZ), including 22 cases of COVID-19 in PLWH (COVID/PLWH group). Plasma samples were tested for a panel of 15 cytokines by Luminex. Sociodemographic, clinical, and laboratory data were collected from patients’ clinical records. Results: COVID-19 individuals were stratified according to the WHO clinical severity profiles at hospitalization. Significant differences in clinical scores, symptoms (coughs), and the occurrence of HIV infection were found among the groups. Clinical blood parameters and plasma cytokines were analyzed among COVID-19 groups with distinct severity profiles. Critical COVID-19 cases showed higher levels of inflammatory markers (Bilirubin, D-dimer, PCR, and urea, as well as IL-8, IL-10, TNF-α, INF-α, IL-1β, IL-17A, IL-23, IL-6) than moderate and severe groups. The COVID/PLWH group had lower CD4 counts (64 cells/mm³) and cytokine levels than other COVID-19 patients. Conclusions: Overall, critically ill COVID-19 patients exhibited heightened inflammatory responses, while COVID/PLWH demonstrated unique immunological characteristics without increased mortality risk.

COVID-19 perturbs the renin-angiotensin system (RAAS) and inflammatory pathways, shaping disease severity. Soluble ACE2 (sACE2) and angiotensin II (Ang II) are central regulators of vascular and immune homeostasis. We profiled plasma from COVID-19 patients and controls using ELISA, together with 48 cytokine profiling and clinical data. Both sACE2 and Ang II were significantly elevated in patients. Increased Ang II was associated with oxygen supplementation and dyspnea, and negatively correlated with IL-3, whereas sACE2 correlated with IL-13 and FGF. Comorbidities modulated cytokine expression: diabetes mellitus was linked to reduced LIF and MCP-1, hypertension to decreased LIF and increased IP-10, and obesity to elevated IL-12p70. Age correlated with TNF and HGF, and reduced oxygen saturation was associated with lower LIF. These findings reveal that acute COVID-19 disrupts RAAS and amplifies immune dysregulation, with Ang II emerging as a pivotal mediator of respiratory compromise and inflammatory imbalance, underscoring its potential as a biomarker and therapeutic relevance.

This study aimed to identify the distinct intrinsic response potential of γδ T cells from COVID-19 patients with different illness severities, to better understand the implication of these cells in COVID-19 disease. Forty-four COVID patients were enrolled at hospitalization and classified as: moderate without oxygen support (MWO₂; N = 15), moderate with oxygen support (MO₂; N = 15), or severe disease requiring mechanical ventilation (SD; N = 14). γδ T cells were characterized ex vivo, isolated from peripheral blood cells, stimulated in vitro with OKT3 and K562 cells, and evaluated for functional markers by flow cytometry. Ex vivo analysis identified 16.21% of total γδ T cells as Vδ1⁻Vδ2⁻. SD patients presented a lower frequency of TRAIL⁺ and of IL-17-producing Vδ2 cells, as well as lower value of fluorescence intensity values for TNF-α in Vδ2 cells, than MWO₂ patients (p < 0.05). In addition, paired analyses showed a lower frequency of IL-17-producing than CD161⁺ Vδ2 cells in SD patients (p < 0.05). These observations suggest a more restricted response potential of the Vδ2 subset in severe disease, show the impact of general immune dysregulation on these cells, or even suggest some role for IL-17-producing Vδ2 cells in preventing critical symptoms.