Zika virus (ZIKV) infection has been linked to the Guillain–Barré syndrome. From November 2015 through March 2016, clusters of cases of the Guillain–Barré syndrome were observed during the outbreak of ZIKV infection in Colombia. We characterized the clinical features of cases of Guillain–Barré syndrome in the context of this ZIKV infection outbreak and investigated their relationship with ZIKV infection.

A 30-year-old Colombian woman with past history of immune thrombocytopenia (ITP) presented to the emergency room with two days of global headache, arthralgia, myalgia, and low level fever and generalized erythematous rash. Platelets dropped to 9 × 10⁹/L (fourth day of symptoms) without hemorrhagic manifestations but recovered to 30 × 10⁹/L in 24 hours (fifth day). Dengue virus infection, as well as other viral infections, was ruled out. Zika virus (ZIKV) was evaluated in serum and urine samples by real-time reverse-transcriptase polymerase chain reaction (genomic regions within E protein and NS2b protein). Urine sample was positive and serum sample negative for ZIKV, confirming a recent ZIKV infection with urinary tract virus excretion at 7^th day after disease onset. To our knowledge this is the first description of a case of severe immune thrombocytopenia exacerbation and antinuclear antibody positivity induced by ZIKV infection.

This study aimed to investigate whether monocyte dysregulation and hyperinflammation serve as predictive markers for mortality in young patients with SARS-CoV-2 severe pneumonia. A prospective cohort study was conducted in a tertiary-level public University Hospital in Colombia. Forty young adults (18–50 years of age) with severe pneumonia and SARS-CoV-2 infection confirmed by qPCR, were enrroled. Serum cytokines and the monocyte phenotype profile, including PDL1/HLA-DR expression, were determined during the first 24 h of hospitalization. Routine laboratory parameters were measured throughout patient follow-up until either death or hospital discharge. We also included a cohort of twenty-five healthy control subjects. Elevated levels of IL-10, IL-8, and IL-6 cytokines emerged as robust predictors of mortality in young adults with severe pneumonia due to SARS-CoV-2 infected. A descriptive analysis revealed a cumulative mortality rate of 30 % in unvaccinated and ICU-admitted patients. Patients who died had significantly lower expression of HLA-DR on their classical monocytes subsets (CD14⁺CD16⁻) than survivors and healthy controls. Lower expression of HLA-DR was associated with greater clinical severity (APACHE≥12) and bacterial coinfection (relative risk 2.5 95%CI [1.18–5.74]). Notably, the expression of HLA-DR in 27.5 % of CD14⁺/CD16^- monocytes was associated with a significantly lower probability of survival. The early reduction in HLA-DR expression within classical monocytes emerged as an independent predictor of mortality, irrespective of comorbidities. Together with PD-L1 expression and cytokine alterations, these findings support the notion that monocyte immunosuppression plays a fundamental role in the pathogenesis and mortality of young patients infected with SARS-CoV-2. These findings hold significant implications for risk assessment and therapeutic strategies in managing critically ill young adults with SARS-CoV-2 infection.

Hutchinson–Gilford progeria syndrome (HGPS) is a rare congenital disease caused by mutations in the LMNA gene. Children with HGPS are phenotypically characterized by lipodystrophy, short height, low body weight, scleroderma, reduced joint mobility, osteolysis, senile facial features, and cardiovascular compromise that usually lead to death. We aimed to describe the case of a patient who reached above-average age expectancy for children with HGPS in Latin America and describe the clinical and molecular characteristics of the patient. A 14-year-old female patient was presented with progeria-compatible phenotypic characteristics. HGPS was confirmed via LMNA gene sequencing that detected a heterozygous c.1824C>T (p.Gly608Gly) mutation. The primary aim is to describe the HGPS case, the molecular gene mutation finding, and make a short review of the limited available treatment options for children with HGPS. Such as the farnesyl transferase inhibitors in conjunction with other pharmacological therapies that have insinuated improvement in health, and survival rate.