The persistence of HIV reservoirs, including latently infected, resting CD4⁺ T cells, is the major obstacle to cure HIV infection. CD32a expression was recently reported to mark CD4⁺ T cells harboring a replication-competent HIV reservoir during antiretroviral therapy (ART) suppression. We aimed to determine whether CD32 expression marks HIV latently or transcriptionally active infected CD4⁺ T cells. Using peripheral blood and lymphoid tissue of ART-treated HIV⁺ or SIV⁺ subjects, we found that most of the circulating memory CD32⁺ CD4⁺ T cells expressed markers of activation, including CD69, HLA-DR, CD25, CD38, and Ki67, and bore a T_H2 phenotype as defined by CXCR3, CCR4, and CCR6. CD32 expression did not selectively enrich for HIV- or SIV-infected CD4⁺ T cells in peripheral blood or lymphoid tissue; isolated CD32⁺ resting CD4⁺ T cells accounted for less than 3% of the total HIV DNA in CD4⁺ T cells. Cell-associated HIV DNA and RNA loads in CD4⁺ T cells positively correlated with the frequency of CD32⁺ CD69⁺ CD4⁺ T cells but not with CD32 expression on resting CD4⁺ T cells. Using RNA fluorescence in situ hybridization, CD32 coexpression with HIV RNA or p24 was detected after in vitro HIV infection (peripheral blood mononuclear cell and tissue) and in vivo within lymph node tissue from HIV-infected individuals. Together, these results indicate that CD32 is not a marker of resting CD4⁺ T cells or of enriched HIV DNA–positive cells after ART; rather, CD32 is predominately expressed on a subset of activated CD4⁺ T cells enriched for transcriptionally active HIV after long-term ART.

Introduction: Some patients with COVID-19 pneumonia present systemic disease involving multiple systems. There is limited information about the clinical characteristics and events leading to acute kidney injury (AKI). We described the factors associated with the development of AKI and explored the relation of AKI and mortality in Mexican population with severe COVID-19. Methods: We retrospectively reviewed the medical records of individuals with severe pneumonia caused by SARS-CoV-2 hospitalized at the largest third-level reference institution for COVID-19 care in Mexico between March and April 2020. Demographic information, comorbidities, clinical and laboratory data, dates of invasive mechanical ventilation (IMV) and hospitalization, mechanical-ventilator settings and use of vasoactive drugs were recorded. Results: Of 99 patients studied, 58 developed AKI (58.6%). The risk factors for AKI were older age (OR = 1.07, 95% CI = 1.01–1.13, p = 0.024); obesity (OR = 6.58, 95% CI = 1.8–24.05, p = 0.040); and the need for IMV (OR = 6.18, CI = 1.29–29.58, p = 0.023). The risk factors for mortality were obesity (OR = 5.57, 95% CI = 1.48–20.93, p = 0.011); requirement of vasoactive drugs on admission (OR = 5.35, 95% CI = 1.16–24.61, p = 0.031); and AKI (OR = 8.61, 95% CI = 2.24–33.1, p = 0.002). In-hospital mortality was significantly higher in patients with AKI stage 3 (79.3%) and AKI stage 2 (68.7%) compared with those with AKI stage 1 (25%; p = 0.004). Fifty-three patients underwent the furosemide stress test (FST) to predict progression to AKI stage 3. Of those, 12 progressed to AKI stage 3 (22%). The ROC curve for the FST had an AUC of 0.681 (p = 0.009); a sensitivity of 81.6% and a specificity of 54.5%. Conclusions: AKI was common in our cohort of patients with severe pneumonia caused by SARS-CoV-2 infection. The risk factors for AKI were older age, obesity and the need for of IMV on admission. The risk factors for mortality were obesity, requirement of vasoactive drugs on admission and AKI. Mortality was more frequent in patients with AKI stages 2–3. The FST had an acceptable predictive capacity to identify patients progressing to AKI stage 3.

A high proportion of critically ill patients with COVID-19 develop acute kidney injury (AKI) and die. The early recognition of subclinical AKI could contribute to AKI prevention. Therefore, this study was aimed at exploring the role of the urinary biomarkers NGAL and [TIMP-2] × [IGFBP7] for the early detection of AKI in this population. This prospective, longitudinal cohort study included critically ill COVID-19 patients without AKI at study entry. Urine samples were collected on admission to critical care areas for determination of NGAL and [TIMP-2] × [IGFBP7] concentrations. The demographic information, comorbidities, clinical, and laboratory data were recorded. The study outcomes were the development of AKI and mortality during hospitalization. Of the 51 individuals that were studied, 25 developed AKI during hospitalization (49%). Of those, 12 had persistent AKI (23.5%). The risk factors for AKI were male gender (HR = 7.57, 95% CI: 1.28–44.8; p = 0.026) and [TIMP-2] × [IGFBP7] ≥ 0.2 (ng/mL)²/1000 (HR = 7.23, 95% CI: 0.99–52.4; p = 0.050). Mortality during hospitalization was significantly higher in the group with AKI than in the group without AKI (p = 0.004). Persistent AKI was a risk factor for mortality (HR = 7.42, 95% CI: 1.04–53.04; p = 0.046). AKI was frequent in critically ill COVID-19 patients. The combination of [TIMP-2] × [IGFBP7] together with clinical information, were useful for the identification of subclinical AKI in critically ill COVID-19 patients. The role of additional biomarkers and their possible combinations for detection of AKI in ritically ill COVID-19 patients remains to be explored in large clinical trials.

The integration of HIV DNA into the host genome contributes to lifelong infection in most individuals. Few studies have examined integration in lymphoid tissue, where HIV predominantly persists before and after antiretroviral treatment (ART). Of particular interest is whether integration site distributions differ between infection stages with paired blood and tissue comparisons. Here, we profiled HIV integration site distributions in sorted memory, tissue-resident, and/or follicular helper CD4 ⁺ T cell subsets from paired blood and lymphoid tissue samples from acute, chronic, and ART-treated individuals. We observed minor differences in the frequency of nonintronic and nondistal intergenic sites, varying with tissue and residency phenotypes during ART. Genomic and epigenetic annotations were generally similar. Clonal expansion of cells marked by identical integration sites was detected, with increased detection in chronic and ART-treated individuals. However, overlap between or within CD4 ⁺ T cell subsets or tissue compartments was only observed in 8 unique sites of the 3540 sites studied. Together, these findings suggest that shared integration sites between blood and tissue may, depending on the tissue site, be the exception rather than the rule and indicate that additional studies are necessary to fully understand the heterogeneity of tissue-sequestered HIV reservoirs.

Conclusion: Patients with cochlear implants should be treated no differently than non-implanted patients with similar symptomatology. Objectives: To describe the spectrum of symptomatology, treatment, and long-term follow-up of patients with cochlear implant and vestibular complaints. Methods: This retrospective study included 25 patients with late onset vestibular complaints (more than 1 month post-implantation). Each patient underwent an extensive interrogatory and physical exam with ancillary test to complete a diagnosis. Treatment was given according to this and all patients followed a vestibular rehabilitation program. Results: The total population was 72% male and 28% female, median age was 58 years; minimal follow-up was 9 months (mean = 51, median = 34). Cochleostomy was performed in eight cases and round window insertion was performed in 19 (two patients were removed from each group in the analysis due to their bilateral implantation under a different approach). The mean time from implant to vestibular symptoms was 53 months, median = 32; a Kaplan Meier graphic showed the round window approach has faster onset of symptoms with statistical significance (p = 0.020). The most common complaint was instability in all patients and after both surgical approaches. No difference in symptoms was found with a Kruskall Wallis test except for vertigo spells (more common in the round window approach). In 12 patients the symptomatology was attributed to the implanted side. In the long-term follow-up a relatively high number of patients (20/25) recovered with standard treatment, suggesting the presence of the implant is not associated with poor recovery prognosis.