Chronic kidney disease (CKD) patients have an increased risk of morbidity and mortality following SARS-CoV-2 infection. Vaccination in these patients is prioritized, and monitoring of the immune response is paramount to define further vaccination strategies. This prospective study included a cohort of 100 adult CKD patients: 48 with kidney transplant (KT) and 52 on hemodialysis without prior COVID-19. The patients were assessed for humoral and cellular immune responses after four months of an anti-SARS-CoV-2 primary two-dose vaccination scheme (CoronaVac or BNT162b2) and one month after a booster third dose of BNT162b2 vaccine. We identified poor cellular and humoral immune responses in the CKD patients after a primary vaccination scheme, and these responses were improved by a booster. Robust polyfunctional CD4⁺ T cell responses were observed in the KT patients after a booster, and this could be attributed to a higher proportion of the patients having been vaccinated with homologous BNT162b2 schemes. However, even after the booster, the KT patients exhibited lower neutralizing antibodies, attributable to specific immunosuppressive treatments. Four patients suffered severe COVID-19 despite three-dose vaccination, and all had low polyfunctional T-cell responses, underscoring the importance of this functional subset in viral protection. In conclusion, a booster dose of SARS-CoV-2 mRNA vaccine in CKD patients improves the impaired humoral and cellular immune responses observed after a primary vaccination scheme.

• Serum from 110 people from a randomized population-based sample was studied. • In the same individuals NAbs titer levels are higher for Wuhan compared to Omicron. • NAbs seropositivity showed a substantial decrease in individuals over 70 years old. • For both types of viruses, the number of vaccine boosters influences the NAbs titer. • Omicrons seropositivity was higher in people with a history of COVID-19 infection.

Hantavirus cardiopulmonary syndrome (HCPS) caused by Andes Orthohantavirus (ANDV) carries case-fatality rates up to 40%; however, the innate immune determinants of disease severity remain poorly defined. Natural killer (NK) cells are central mediators of early antiviral immunity, but their landscape during the earliest phase of ANDV infection has not been characterized. Using multiparameter flow cytometry and unsupervised UMAP-based clustering in PBMCs from 13 HCPS patients stratified by severity and nine healthy donors, we show that severe HCPS is characterized by a coordinated disruption of the CD56dim NK cell compartment, encompassing reduced subset frequencies, specific reduction in the terminally differentiated NKG2C+CD57+ adaptive-like pool, and intrinsic impairment of IFN-γ production and degranulation, deficits that were absent in mild patients and persisted in part beyond clinical recovery. Furthermore, CD56dimCD16+ NK cell frequencies correlated negatively with viral load across all acute patients, independent of clinical severity. These findings establish severe HCPS not merely as a state of NK cell depletion, but as one of selective functional impairment of the most cytotoxically competent NK cell population during the critical early acute phase of ANDV infection.