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Amniotic fluid was collected through an intrauterine catheter from 52 women with clinical intraamniotic infection and from 52 uninfected matched control women. The amniotic fluid was cultured quantitatively for anaerobes and aerobes. Patients with intraamniotic infection were matched with the control women on the basis of gestational age, interval from membrane rupture to specimen collection, and interval from membrane rupture to delivery. The patients with intraamniotic infection had a significantly higher mean temperature (38.4 vs. 37.1 C) and a higher mean leukocyte count (15,740 vs. 11,740 cells/mm3). In 80.6% of specimens from the women with intraamniotic infection and 30.8% of those from the control subjects, greater than or equal to 10(2) colony-forming units (cfu)/ml were isolated from the amniotic fluid (P less than 0.001). Also, in 69.2% of the former and 7.7% of the latter, there were greater than or equal to 10(2) cfu of isolates considered to be "high-virulence" isolates/ml (P less than 0.001). [ABSTRACT FROM AUTHOR]

In children and younger adults up to 39 years of age, SARS-CoV-2 usually elicits mild symptoms that resemble the common cold. Disease severity increases with age starting at 30 and reaches astounding mortality rates that are ~330 fold higher in persons above 85 years of age compared to those 18-39 years old. To understand age-specific immune pathobiology of COVID-19, we have analyzed soluble mediators, cellular phenotypes, and transcriptome from over 80 COVID-19 patients of varying ages and disease severity, carefully controlling for age as a variable. We found that reticulocyte numbers and peripheral blood transcriptional signatures robustly correlated with disease severity. By contrast, decreased numbers and proportion of naïve T-cells, reported previously as a COVID-19 severity risk factor, were found to be general features of aging and not of COVID-19 severity, as they readily occurred in older participants experiencing only mild or no disease at all. Single-cell transcriptional signatures across age and severity groups showed that severe but not moderate/mild COVID-19 causes cell stress response in different T-cell populations, and some of that stress was unique to old severe participants, suggesting that in severe disease of older adults, these defenders of the organism may be disabled from performing immune protection. These findings shed new light on interactions between age and disease severity in COVID-19., (© 2023. The Author(s), under exclusive licence to American Aging Association.)

HIV-positive patients whose viral loads are successfully controlled by active antiretroviral therapy (ART) show no clinical signs of AIDS. However, their lifespan is shorter compared with individuals with no HIV infection and they prematurely exhibit a multitude of chronic diseases typically associated with advanced age. It was hypothesized that immune system aging may correlate with, and provide useful biomarkers for, this premature loss of healthspan in HIV-positive subjects. Here, we tested whether the immune correlates of aging, including cell numbers and phenotypes, inflammatory status, and control of human cytomegalovirus (hCMV) in HIV-positive subjects on long-term successful ART (HIV+) may reveal increased "immunological age" compared with HIV-negative, age-matched cohort (HIV-) in participants between 50 and 69 years of age. Specifically, we expected that younger HIV+ subjects may immunologically resemble older individuals without HIV. We found no evidence to support this hypothesis. While T cells from HIV+ participants displayed differential expression in several differentiation and/or inhibitory/exhaustion markers in different T cell subpopulations, aging by a decade did not pronounce these changes. Similarly, while the HIV+ participants exhibited higher T cell responses and elevated inflammatory marker levels in plasma, indicative of chronic inflammation, this trait was not age-sensitive. We did find differences in immune control of hCMV, and, more importantly, a sustained elevation of sCD14 and of proinflammatory CD4 and CD8 T cell responses across age groups, pointing towards uncontrolled inflammation as a factor in reduced healthspan in successfully treated older HIV+ patients., (© 2022 The Authors. Aging Cell published by Anatomical Society and John Wiley & Sons Ltd.)

We conducted a serological study to define correlates of immunity against SARS-CoV-2. Compared to those with mild coronavirus disease 2019 (COVID-19) cases, individuals with severe disease exhibited elevated virus-neutralizing titers and antibodies against the nucleocapsid (N) and the receptor binding domain (RBD) of the spike protein. Age and sex played lesser roles. All cases, including asymptomatic individuals, seroconverted by 2 weeks after PCR confirmation. Spike RBD and S2 and neutralizing antibodies remained detectable through 5-7 months after onset, whereas α-N titers diminished. Testing 5,882 members of the local community revealed only 1 sample with seroreactivity to both RBD and S2 that lacked neutralizing antibodies. This fidelity could not be achieved with either RBD or S2 alone. Thus, inclusion of multiple independent assays improved the accuracy of antibody tests in low-seroprevalence communities and revealed differences in antibody kinetics depending on the antigen. We conclude that neutralizing antibodies are stably produced for at least 5-7 months after SARS-CoV-2 infection., Competing Interests: Declaration of Interests Unrelated intellectual property of D.B. and Washington University has been licensed by Sana Biotechnology. J.N.Ž. is on the scientific advisory board of and receives research funding from Young Blood, Inc. R.S. is a founder and chief scientific officer of Geneticure. R.W. is currently an employee of Vir Biotechnology. A provisional patent application related to this work has been filed with the US Patent Office., (Copyright © 2020 Elsevier Inc. All rights reserved.)

Amniotic fluid was collected via a transcervical intrauterine catheter from patients with clinical evidence of intrauterine infection and from uninfected comparison patients. The amniotic fluid was cultured for Mycoplasma hominis and Ureaplasma urealyticum, as well as for aerobic and anaerobic bacteria. Two series of patients are reported. In the first, there were 52 patients with intraamniotic infection and 52 matched controls. Eighteen patients (35%) with intraamniotic infection and four control patients (8%) had M. hominis in the amniotic fluid (P less than .001). Twenty-six patients (50%) with intraamniotic infection and 26 control patients (50%) had U. urealyticum in the amniotic fluid. In the second series, samples were collected consecutively. M. hominis was isolated from 32% (19/60) of specimens from patients with signs of infection and from 14% (8/56) of afebrile comparison patients (P less than .02). U. urealyticum was recovered from 43% and 39% of these fluids, respectively; the difference was not significant. When M. hominis was found in amniotic fluids of patients with signs of infection, the amniotic fluid usually contained greater than or equal to 10(2) cfu of a high virulent bacterial isolate per milliliter. Qualitative cultures showed that M. hominis in the amniotic fluid is associated with clinical intrauterine infection.