Dataset Information

Clinical Outcomes and Inflammatory Markers by HIV Serostatus and Viral Suppression in a Large Cohort of Patients Hospitalized With COVID-19.

ABSTRACT:

Background

Limited data exist about clinical outcomes and levels of inflammatory and immune markers among people hospitalized with COVID-19 by HIV serostatus and by HIV viral suppression.

Setting

Large tertiary care health system in the Bronx, NY, USA.

Methods

We conducted a retrospective cohort study of 4613 SARS-CoV-2 PCR-positive patients admitted between March 10, 2020, and May 11, 2020. We examined in-hospital intubation, acute kidney injury (AKI), hospitalization length, and in-hospital mortality by HIV serostatus, and by HIV-viral suppression and CD4 counts among people living with HIV (PLWH) using adjusted competing risks regression. We also compared immune and inflammatory marker levels by HIV serostatus and viral suppression.

Results

Most patients were either non-Hispanic Black (36%) or Hispanic (37%); 100/4613 (2.2%) were PLWH, among whom 15 had detectable HIV viral load. PLWH compared to patients without HIV had increased intubation rates (adjusted hazard ratio 1.73 [95% CI: 1.12 to 2.67], P = 0.01). Both groups had similar rates of AKI, length of hospitalization, and death. No (0%) virally unsuppressed PLWH were intubated or died, versus 21/81 (26%, P = 0.04) and 22/81 (27%, P = 0.02) of virally suppressed PLWH, respectively. Among PLWH, higher CD4 T-cell counts were associated with increased intubation rates. C-reactive protein, IL-6, neutrophil counts, and ferritin levels were similar between virally suppressed PLWH and patients without HIV, but significantly lower for unsuppressed PLWH (all P < 0.05).

Conclusions

PLWH had increased risk of intubation but similarly frequent rates of AKI and in-hospital death as those without HIV. Findings of no intubations or deaths among PLWH with unsuppressed HIV viral load warrant further investigation.

SUBMITTER: Patel VV

PROVIDER: S-EPMC8720497 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BACKGROUND:Tuberculosis (TB) and AIDS are the leading causes of infectious disease death worldwide. In some TB-HIV co-infected individuals treated for both diseases simultaneously, a pathological inflammatory reaction termed immune reconstitution inflammatory syndrome (IRIS) may occur. The risk factors for IRIS are not fully defined. We investigated the association of HLA-B, HLA-C, and KIR genotypes with TB, HIV-1 infection, and IRIS onset. METHODS:Patients were divided into four groups: Group 1- TB+/HIV+ (n?=?88; 11 of them with IRIS), Group 2- HIV+ (n?=?24), Group 3- TB+ (n?=?24) and Group 4- healthy volunteers (n?=?26). Patients were followed up at INI/FIOCRUZ and HGNI (Rio de Janeiro/Brazil) from 2006 to 2016. The HLA-B and HLA-C loci were typed using SBT, NGS, and KIR genes by PCR-SSP. Unconditional logistic regression models were performed for Protection/risk estimation. RESULTS:Among the individuals with TB as the outcome, KIR2DS2 was associated with increased risk for TB onset (aOR?=?2.39, P?=?0.04), whereas HLA-B*08 and female gender were associated with protection against TB onset (aOR?=?0.23, P?=?0.03, and aOR?=?0.33, P?=?0.01, respectively). Not carrying KIR2DL3 (aOR?=?0.18, P?=?0.03) and carrying HLA-C*07 (aOR?=?0.32, P?=?0.04) were associated with protection against TB onset among HIV-infected patients. An increased risk for IRIS onset was associated with having a CD8 count ?500 cells/mm3 (aOR?=?18.23, P?=?0.016); carrying the KIR2DS2 gene (aOR?=?27.22, P?=?0.032), the HLA-B*41 allele (aOR?=?68.84, P?=?0.033), the KIR2DS1?+?HLA-C2 pair (aOR?=?28.58, P?=?0.024); and not carrying the KIR2DL3?+?HLA-C1/C2 pair (aOR?=?43.04, P?=?0.034), and the KIR2DL1?+?HLA-C1/C2 pair (aOR?=?43.04, P?=?0.034), CONCLUSIONS: These results suggest the participation of these genes in the immunopathogenic mechanisms related to the conditions studied. This is the first study demonstrating an association of HLA-B*41, KIR2DS2, and KIR + HLA-C pairs with IRIS onset among TB-HIV co-infected individuals.

Project description:An outbreak of enterovirus D68 (EV-D68) caused severe respiratory illness in 2014. The disease spectrum of EV-D68 infections in children with underlying medical conditions other than asthma, the role of EV-D68 loads on clinical illness, and the variation of EV-D68 strains within the same institution over time have not been described. We sought to define the association between EV-D68 loads and sequence variation, and the clinical characteristic in hospitalized children at our institution from 2011 to 2014.May through November 2014, and August to September 2011 to 2013, a convenience sample of nasopharyngeal specimens from children with rhinovirus (RV)/EV respiratory infections were tested for EV-D68 by RT-PCR. Clinical data were compared between children with RV/EV-non-EV-D68 and EV-D68 infections, and among children with EV-D68 infections categorized as healthy, asthmatics, and chronic medical conditions. EV-D68 loads were analyzed in relation to disease severity parameters and sequence variability characterized over time.In 2014, 44% (192/438) of samples tested positive for EV-D68 vs. 10% (13/130) in 2011-13 (p<0.0001). PICU admissions (p<0.0001) and non-invasive ventilation (p<0.0001) were more common in children with EV-D68 vs. RV/EV-non-EV-D68 infections. Asthmatic EV-D68+ children, required supplemental oxygen administration (p = 0.03) and PICU admissions (p <0.001) more frequently than healthy children or those with chronic medical conditions; however oxygen duration (p<0.0001), and both PICU and total hospital stay (p<0.01) were greater in children with underlying medical conditions, irrespective of viral burden. By phylogenetic analysis, the 2014 EV-D68 strains clustered into a new sublineage within clade B.This is one of the largest pediatric cohorts described from the EV-D68 outbreak. Irrespective of viral loads, EV-D68 was associated with high morbidity in children with asthma and co-morbidities. While EV-D68 circulated before 2014, the outbreak isolates clustered differently than those from prior years.

Project description:Achieving the UNAIDS 95% sustained viral suppression (VS) rate requires considerable global efforts, particularly among adolescents living with HIV (ALHIV) who are often associated with high rates of virological failure (VF). In this study, we prospectively assessed the rate of VS, and the factors associated with VF in a cohort of adolescents followed up according to the WHO guidelines in Cameroon. A cross-sectional study was carried out in 2021 among adolescents (aged 10-19 years) receiving ART in the national program in Cameroon. Socio-demographic and clinical data were collected using patients' medical files and a brief interview with the participant and/or his guardian. Thereafter, a first viral load test (VL1) was performed using the ABBOTT Platform. For adolescents with VL1 > 1000 copies/ml, adherence-enhancing interventions were routinely performed each month for 3 consecutive months, after which a second viral load (VL2) was measured. Adolescents with VL2 > 1000 copies/ml were considered in VF. Overall, 280 adolescents were enrolled, of whom 89.3% (250/280) acquired HIV infection via mother-to-child transmission. The median age was 16.0 (IQR: 13.0-18.0) years and the median duration on ART was 9.8 (IQR: 5.1-12.8) years. Females and males were almost equally represented, as 52.1% (146/280) were female, while 47.9% (134/280) were males (p = 0.47). The VS rate was 88.2% (CI: 83.8-91.7%) overall; 89.0% (CI: 82.0-93.1%) and 88.7% (CI: 81.2-93.0%) in females and males, respectively. Being on second or third-line ART, self-declared suboptimal adherence, and a history of past VF were independently associated with VF. The high rate of VS we report in this study is welcome in the era of the 95/95/95 UNAIDS goals, and indicates that improving treatment outcomes in this specific and fragile population that represent adolescents in Sub-Saharan Africa is achievable. 20/10/2020 NCT04593979 ( https://clinicaltrials.gov/ct2/show/NCT04593979 ).