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Background: Despite viral suppression, antiretroviral therapy (ART) does not restore CD4(+) T-cell counts in many patients infected with human immunodeficiency virus type 1 (HIV-1).Methods: In a single-arm pilot trial involving ART recipients with suppressed plasma levels of HIV-1 RNA for at least 48 weeks and stable suboptimal CD4(+) T-cell recovery, subjects added maraviroc, a CCR5 antagonist, to their existing ART for 24 weeks. After stopping maraviroc, they were followed for an additional 24 weeks. A Wilcoxon signed-rank test was used to evaluate whether maraviroc was associated with an increase of at least 20 cells/µL in the CD4(+) T-cell count.Results: A total of 34 subjects were enrolled. The median age was 50 years, and the median baseline CD4(+) T-cell count was 153 cells/µL. The median increase in CD4(+) T-cell count from baseline to week 22/24 was 12 cells/µL (90% confidence interval, 1-22). A CD4(+) T-cell count increase of at least 20 cells/µL was not detected (P = .97). Markers of immune activation and apoptosis decreased during maraviroc intensification; this decline partially reversed after discontinuing maraviroc.Conclusions: Adding maraviroc to suppressive ART for 24 weeks was not associated with an increase in CD4(+) T-cell counts of at least 20 cells/µL. Further studies of CCR5 antagonists in the dampening of immune activation associated with HIV infection are warranted. Clinical Trials Registration. NCT 00709111. [ABSTRACT FROM AUTHOR]

It seems likely that type 1 and type 2 diabetes lie at different points of the same spectrum, separated by the misunderstanding that one belongs to childhood and the other to adulthood. The spectrum is that of tempo - the rate at which beta cell function is lost over time. A combination of beta cell upߚregulation (insulin demand, largely determined by obesity) and the geneticallyߚdetermined immune response to it ('autoimmunity') determines tempo, ranging from slow to fast with every variant in between. There is good evidence that people who go on to develop type 1 (fast) diabetes are, like those who develop type 2 (slow diabetes), insulin resistant, and overwhelming evidence that body mass plays a key role. The prevention of type 1 diabetes may lie in weight restriction from an early age. [ABSTRACT FROM AUTHOR]

Objective: Insulin resistance (IR) is associated with diabetes. IR is higher during puberty in both sexes, with some studies showing the increase to be independent of changes in adiposity. Few longitudinal studies have reported on children, and it remains unclear when the rise in IR that is often attributed to puberty really begins. We sought to establish from longitudinal data its relationship to pubertal onset, and interactions with age, sex, adiposity, and IGF-1.Research Design and Methods: The EarlyBird Diabetes study is a longitudinal prospective cohort study of healthy children aged 5-14 years. Homeostasis model assessment (HOMA-IR), skinfolds (SSF), adiposity (percent fat, measured by dual-energy X-ray absorptiometry), serum leptin, and IGF-1 were measured annually in 235 children (134 boys). Pubertal onset was adduced from Tanner stage (TS) and from the age at which luteinizing hormone (LH) first became serially detectable (≥0.2 international units/L).Results: IR rose progressively from age 7 years, 3-4 years before TS2 was reached or LH became detectable. Rising adiposity and IGF-1 together explained 34% of the variance in IR in boys and 35% in girls (both P < 0.001) over the 3 years preceding pubertal onset. The contribution of IGF-1 to IR was greater in boys, despite their comparatively lower IGF-1 levels.Conclusions: IR starts to rise in mid-childhood, some years before puberty. Its emergence relates more to the age of the child than to pubertal onset. More than 60% of the variation in IR prior to puberty was unexplained. The demography of childhood diabetes is changing, and prepubertal IR may be important. [ABSTRACT FROM AUTHOR]

Objective To establish in children whether inactivity is the cause of fatness or fatness the cause of inactivity. Design A non-intervention prospective cohort study examining children annually from 7 to 10 years. Baseline versus change to follow-up associations were used to examine the direction of causality. Setting Plymouth, England. Participants 202 children (53% boys, 25% overweight/obese) recruited from 40 Plymouth primary schools as part of the EarlyBird study. Main outcome measures Physical activity (PA) was measured using Actigraph accelerometers. The children wore the accelerometers for 7 consecutive days at each annual time point. Two components of PA were analysed: the total volume of PA and the time spent at moderate and vigorous intensities. Body fat per cent (BF%) was measured annually by dual energy x ray absorptiometry. Results BF% was predictive of changes in PA over the following 3 years, but PA levels were not predictive of subsequent changes in BF% over the same follow-up period. Accordingly, a 10% higher BF% at age 7 years predicted a relative decrease in daily moderate and vigorous intensities of 4 min from age 7 to 10 years (r=-0.17, p=0.02), yet more PA at 7 years did not predict a relative decrease in BF% between 7 and 10 years (r=-0.01, p=0.8). Conclusions Physical inactivity appears to be the result of fatness rather than its cause. This reverse causality may explain why attempts to tackle childhood obesity by promoting PA have been largely unsuccessful. [ABSTRACT FROM AUTHOR]

Summary: Background & aims: In adults, adjustments in resting energy expenditure (REE) are used to defend energy balance against disturbance caused by over-and under-nutrition, and may be linked to changes in insulin resistance and leptin. Little is known of these associations in children. Our aim was to test the hypothesis that long-term weight gain in children is met with adaptive changes in resting energy expenditure, mediated by insulin resistance and/or leptin. Methods: REE by indirect calorimetry, anthropometry, body composition by DEXA, insulin resistance (HOMA-IR) and serum leptin were measured annually in 232 children from the age of 7–10 y. Results: REE rose from 7 to 10 y, and the rise exceeded that predicted by the concurrent rise in fat and fat-free mass by 184 kcal/day in the boys and by 160 kcal/day in the girls. However, there were no significant relationships in either gender between this ‘excess’ rise in REE and change in body composition (r ≤ 0.08, p ≥ 0.42). The rise in both boys and girls was associated with, but not explained by, a rise in insulin resistance (p ≤ 0.002). There was no association with serum leptin (p ≥ 0.32). Conclusions: The data do not support the hypothesis of adaptive changes in REE in pre-pubertal children, and insulin resistance explains very little of the pre-pubertal rise in REE. The rise in REE beyond that explained by changes in body composition may reflect an increase in energy requirements prior to puberty. [ABSTRACT FROM AUTHOR]

The enhanced-sensitivity Trofile assay (Monogram Biosciences) was used to retest coreceptor use at both study screening and study entry for 118 treatment-experienced subjects in AIDS Clinical Trials Group A5211 who had CCR5-tropic (R5) virus detected by the original Trofile assay at study screening. Among 90 recipients of vicriviroc, a significantly (P< .001) greater mean reduction in HIV-1 RNA was observed in 72 subjects with R5 virus versus 15 subjects reclassified as having dual/mixed-tropic viruses at screening: -1.11 versus -0.09 log(10) copies/mL at day 14 and -1.91 versus -0.57 log(10) copies/mL at week 24, respectively. Results suggest that the enhanced-sensitivity assay is a better screening tool for determining patient eligibility for CCR5 antagonist therapy. [ABSTRACT FROM AUTHOR]

Objective: To look for same-sex (gender assortative) association of body mass index (BMI) in healthy trios (mother, father and child) from a contemporary birth cohort, which might imply shared environment rather than shared genes because selective mother-daughter and father-son gene transmission is not a common Mendelian trait. Design: Prospective (longitudinal) cohort study with four annual time points, from 5 to 8 years. Subjects: 226 healthy trios from a 1995 to 1996 birth cohort randomly selected in the city of Plymouth, UK. Measurements: Average BMI of the two parents and maternal/paternal BMI separately related to the BMI-SDS (standard deviation score) of all offspring and to the BMI-SDS of the sons and the daughters separately. Results: There were big differences in BMI-SDS among the daughters grouped according to mothers' category of BMI (effect size 1.37 SDS), but not their sons (effect size 0.16 SDS, gender interaction P<0.004), and among the sons grouped according to their fathers' BMI (effect size 1.28 SDS), but not their daughters (effect size 0.17, gender interaction P=0.02). Children whose same-sex parents were of normal weight, weighed either close to (girls+0.20 BMI-SDS) or less than (boys,-0.34 BMI-SDS) children of 20 years ago, and did not change from 5 to 8 years. In contrast, the risks of obesity at 8 years were 10-fold greater (girls 41%, P<0.001) or sixfold greater (boys 18%, P<0.05) if the same-sex parent was obese. Longitudinal linear mixed effects (multilevel) modelling showed a marked influence of maternal and paternal BMI on the rate of weight gain, which was unaffected by birth weight of the child. We report perhaps the largest effect sizes so far recorded in childhood obesity. Conclusions: Childhood obesity today seems to be largely confined to those whose same-sex parents are obese, and the link does not seem to be genetic. Parental obesity, like smoking, might be targeted in the interests of the child. [ABSTRACT FROM AUTHOR]

Objective: Recent evidence suggests that, in children, traditional markers of metabolic disturbance are related only weakly to physical activity. We therefore sought to establish the corresponding relationships with newer metabolic markers.Research Design and Methods: This was a nonintervention longitudinal study of 213 healthy children recruited from 54 schools in Plymouth, U.K. MTI accelerometers were used to make objective 7-day recordings of physical activity at ages 5 +/- 0.3 (mean +/- SD), 6, 7, and 8 years. Overall physical activity was taken as the average of the four annual time points. The metabolic markers at 8 years were adiponectin, leptin, high-sensitivity C-reactive protein (hsCRP), and insulin resistance (homeostasis model assessment). Potential confounders included percent body fat measured by dual-energy X-ray absorptiometry and diet measured by food frequency questionnaire.Results: Whereas physical activity did not correlate with insulin resistance (r = -0.01), leptin (r = +0.04), or hsCRP (r = +0.01) independently of percent body fat, it did correlate with adiponectin, but inversely (r = -0.18, P = 0.02). This unexpected inverse relationship was strongest among the less active children (physical activity < median: r = -0.30, P = 0.01) but negligible in the more active children (physical activity > median: r = +0.04, P = 0.76). Adiponectin was significantly higher (0.52 SD, P < 0.01) in the least active tertile compared with the other two tertiles. Insulin resistance, however, did not differ across the physical activity tertiles (P = 0.62).Conclusions: Adiponectin levels in children are highest among those who are least active, but their insulin resistance is no different. Adiponectin has a known insulin-sensitizing effect, and our findings are consistent with a selective effect at low levels of physical activity. [ABSTRACT FROM AUTHOR]

BACKGROUND: In the UK and USA, government guidelines for childhood physical activity have been set (> or =60 min/day at > or =3 metabolic equivalents of thermogenesis (METs)), and body mass index (BMI) chosen as the outcome measure. AIM: To determine the extent to which physical activity at the government-recommended intensity is associated with change in body mass/fat and metabolic health in pre-pubertal children. METHODS: Non-intervention longitudinal study of 113 boys and 99 girls (born 1995/96) recruited from 54 schools. Physical activity (Actigraph accelerometers), changes in body mass (raw and age/gender-standardised BMI), fatness (skin-fold thickness and waist circumference) and metabolic status (insulin resistance, triglycerides, cholesterol/HDL ratio and blood pressure - separately and as a composite metabolic z score) were measured on four annual occasions (5, 6, 7 and 8 years). RESULTS: Mean physical activity did not change over time in either sex. Averaging the 7-day recordings from four time points rather than one increased the reliability of characterising a child's activity from 71% to 90%. Some 42% of boys and 11% of girls met the guideline. There were no associations between physical activity and changes in any measurement of body mass or fatness over time in either sex (eg, BMI standard deviation scores: r = -0.02, p = 0.76). However, there was a small to moderate inverse association between physical activity and change in composite metabolic score (r = -0.19, p<0.01). Mixed effects modelling showed that the improvement in metabolic score among the more active compared to the less active children was linear with time (-0.08 z scores/year, p = 0.001). CONCLUSIONS: In children, physical activity above the government-recommended intensity of 3 METs is associated with a progressive improvement in metabolic health but not with a change in BMI or fatness. Girls habitually undertake less physical activity than boys, questioning whether girls in particular should be encouraged to do more, or the recommendations adjusted for girls. [ABSTRACT FROM AUTHOR]

BACKGROUND: Rising obesity has been observed in all age groups. Anthropometric cut-points have been used to predict metabolic risk in children, although they are not based on known outcomes. AIM: We examined the trends, associations and predictions of metabolic health from anthropometry in prepubertal children. METHOD: Three hundred and seven healthy children were examined annually between 5 and 8 yr. Measures: height, weight, body mass index (BMI), sum of skinfold thickness at five sites (SSF) and waist circumference (WC). Outcome measures: homeostasis model assessment of insulin resistance (HOMA-IR), high-density lipoprotein cholesterol (HDL-C) and triglycerides (TG). RESULTS: Two hundred and thirty-one [131 boys (B) and 100 girls (G)] children had complete data sets at all four time points. (i) All measures of adiposity rose from 5 to 8 yr (BMI - B: +3.4%, G: +5.7%; WC - B: +10.4%, G: +11.8%; SSF - B: +23.3%, G: +30.7%, all p < 0.001). HOMA-IR unexpectedly fell (B: -16.6%, p = 0.01; G: -32.5%, p < 0.001). This fall was significant between 5 and 6 yr in both genders (5-6 yr - B: -17.8%, p < 0.001; G: -20.0%, p = 0.002) and between 6 and 7 yr in girls only (6-7 yr - B: -10.8%, p = 0.12; G: -19.2%, p = 0.001). HDL-C rose (B: +17.8%, G: +17.1%, both p < 0.001) and TG fell (B: -4.8%, p = 0.16; G: -11.6%, p = 0.006). (ii) Correlations between insulin resistance (IR) and anthropometry were poor at 5 yr but strengthened by 8 yr (BMI - B: r = 0.20/0.38, G: r = 0.28/0.49; WC - B: r = 0.25/0.40, G: r = 0.32/0.58; SSF - B: r = 0.11/0.36, G: r = 0.18/0.53). (iii) In girls, but not boys, adiposity at 5 yr predicted IR better at 8 yr (BMI - r(2 )= 0.17; WC - r(2 )= 0.28; SSF - r(2 )= 0.17, all p < 0.001) than it did at 5 yr (BMI - r(2 )= 0.08, p < 0.01; WC - r(2 )= 0.10, p < 0.01; SSF - r(2 )= 0.03, p = 0.07). CONCLUSIONS: Cross-sectional association cannot indicate direction of trend or predict the future. Predicting metabolic health from anthropometric measures in prepubertal children requires longitudinal data, tracking variables from childhood into adulthood. Until the data set reaches adulthood, it is probably not safe to make recommendations on which children to 'target' or whether early intervention would be of benefit. [ABSTRACT FROM AUTHOR]

Rare mutations in the glucokinase (GCK) gene cause fasting hyperglycemia and considerably influence birth weight when present in a mother or her offspring. The role of common variation of GCK is uncertain. A polymorphism at position -30 of the GCK beta-cell-specific promoter, present in 30% of the population, has been variably associated with type 2 diabetes and diabetes-related quantitative traits. Using 1,763 U.K. Caucasian normoglycemic adult subjects, we demonstrated that the A allele at GCK(-30) is associated with a 0.06-mmol/l increase in fasting plasma glucose (FPG) (P = 0.003). The A allele was also associated with an increase in FPG in 755 women who were 28 weeks pregnant (0.075 mmol/l, P = 0.003). We then went on to analyze the effect of GCK(-30) on birth weight using 2,689 mother/child pairs. The presence of the A allele in the mother was associated with a 64-g (25-102 g) increase in offspring birth weight (P = 0.001). We did not detect a fetal genotype effect. The increase in offspring birth weight in the 30% of mothers carrying an A allele at GCK(-30) is likely to reflect an elevated FPG during pregnancy. This study establishes that common genetic variation, in addition to rare mutations and environmental factors, can affect both FPG and birth weight. [ABSTRACT FROM AUTHOR]

BACKGROUND: Insulin resistance is believed to be the process underlying type 2 diabetes and premature cardiovascular disease. We have established that a relation between body mass and insulin resistance calculated by homeostasis model assessment (HOMA-IR) exists by 5 y of age in contemporary UK children. Resting energy expenditure (REE) is variable among individuals and is one of many factors controlling body mass. OBJECTIVE: The objective was to investigate the relations between REE, body mass, and HOMA-IR in young children. DESIGN: EarlyBird is a nonintervention prospective cohort study of 307 healthy 5-y-olds that asks the question: Which children develop insulin resistance and why? REE by indirect calorimetry and HOMA-IR were measured in addition to total body mass, fat-free mass (FFM) by bioimpedance, body mass index (BMI; in kg/m(2)), and skinfold thickness when the mean age of the cohort was 5.9 +/- 0.2 y. RESULTS: Whereas the BMI of the boys was lower than that of the girls (x +/- SD: boys, 15.9 +/- 1.9; girls, 16.5 +/- 1.9; P = 0.03), their REE was higher by 6% (x +/- SD: 4724 +/- 615 compared with 4469 +/- 531 kJ/d; P = 0.002). This difference persisted after adjustment for FFM and other anthropometric variables (P = 0.04). In boys, there was a weak, although significant, inverse correlation between REE and HOMA-IR, independent of fat mass and FFM (boys: r = -0.21, P = 0.03; girls: r = 0.12, P = 0.34). CONCLUSION: There is a sex difference in REE at 6 y of age that cannot be explained by body composition. The difference appears to be intrinsic, and its contribution to sex differences in adiposity and HOMA-IR in children merits further exploration. Copyright © 2004 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

For more than a decade, the fetal programming hypothesis has taught that insulin resistance and its associated metabolic disturbances result from poor gestational environment, for which low birth weight is a surrogate. Low birth weight, however, is now uncommon in industrialized societies. We have investigated the relevance of birth weight, "catch-up" weight, and current weight to insulin resistance in 300 contemporary British children. Insulin resistance at 5 years was not related to birth weight but was correlated with current weight and weight catch-up in both sexes, more strongly so in girls (r = 0.33, P < 0.001 vs. r = 0.18, P = 0.03), who were intrinsically more insulin-resistant than boys. Weight change merely co-correlated with current weight (r = 0.67, P < 0.01 in both sexes) and did not improve on the prediction of insulin resistance. Most important, insulin resistance at 5 years was the same in children of heavier birth weight, whose weight SD score had not changed, as in those of lighter birth weight, matched for current weight, who had experienced so-called catch-up (boys 0.89 and 0.88 units, respectively, P = 0.96; girls 1.26 and 1.13 units, P = 0.41). Insulin resistance in contemporary children seems to be a function of excess current weight rather than of low birth weight or change in weight. [ABSTRACT FROM AUTHOR]

When participants enrolled in an HIV prevention trial hold a preventive misconception (PM) - expectations that experimental interventions will confer protection from HIV infection - they may engage in behaviors that increase their risk of acquiring HIV. This can raise ethical concerns about whether those enrolled in the trial understand the nature of participation and their safety. Consequently, we systematically evaluated the prevalence of PM and its association with risk behaviors in a trial examining three candidate regimens for oral HIV pre-exposure prophylaxis in which all participants received at least one antiretroviral agent. Overall, trial participants exhibited relatively high preventive expectations that may be associated with an increase in risk behaviors among men who have sex with men. In addition, we identified substantial site variability in PM that necessitates future research to uncover its source. This will allow appropriate measures to be taken to mitigate PM and help ensure that participants have an accurate understanding of the potential risks and benefits of trial participation throughout the course of a trial.

Clinical severity scores facilitate comparisons to understand risk factors for severe illness. For the 2022 multinational monkeypox clade IIb virus outbreak, we developed a 7-item Mpox Severity Scoring System (MPOX-SSS) with initial variables refined by data availability and parameter correlation. Application of MPOX-SSS to the first 200 patients diagnosed with mpox revealed higher scores in those treated with tecovirimat, presenting >3 days after symptom onset, and with CD4 counts <200 cells/mm3. For individuals evaluated repeatedly, serial scores were concordant with clinical observations. The pilot MPOX-SSS demonstrated good discrimination, distinguished change over time, and identified higher scores in expected groups., Competing Interests: Potential conflicts of interest. J. Z., W. F., T. J. W. are part of the NIH funded study of tecovirimat for mpox (STOMP) leadership team. All authors have submitted the ICMJE Form for Disclosure of Potential Conflicts of Interest., (© The Author(s) 2023. Published by Oxford University Press on behalf of Infectious Diseases Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Purpose: To determine whether treatment of anal high-grade squamous intraepithelial lesions (HSIL), vs active monitoring, is effective in reducing incidence of anal cancer in persons living with HIV, the US National Cancer Institute funded the Phase III ANal Cancer/HSIL Outcomes Research (ANCHOR) clinical trial. As no established patient-reported outcomes (PRO) tool exists for persons with anal HSIL, we sought to estimate the construct validity and responsiveness of the ANCHOR Health-Related Symptom Index (A-HRSI)., Methods: The construct validity phase enrolled ANCHOR participants who were within two weeks of randomization to complete A-HRSI and legacy PRO questionnaires at a single time point. The responsiveness phase enrolled a separate cohort of ANCHOR participants who were not yet randomized to complete A-HRSI at three time points: prior to randomization (T1), 14-70 (T2), and 71-112 (T3) days following randomization., Results: Confirmatory factor analysis techniques established a three-factor model (i.e., physical symptoms, impact on physical functioning, impact on psychological functioning), with moderate evidence of convergent validity and strong evidence of discriminant validity in the construct validity phase (n = 303). We observed a significant moderate effect for changes in A-HRSI impact on physical functioning (standardized response mean = 0.52) and psychological symptoms (standardized response mean = 0.60) from T2 (n = 86) to T3 (n = 92), providing evidence of responsiveness., Conclusion: A-HRSI is a brief PRO index that captures health-related symptoms and impacts related to anal HSIL. This instrument may have broad applicability in other contexts assessing individuals with anal HSIL, which may ultimately help improve clinical care and assist providers and patients with medical decision-making., (© 2023. The Author(s), under exclusive licence to Springer Nature Switzerland AG.)

Several innovative methods were presented at the 2023 Conference on Retroviruses and Opportunistic Infections (CROI) targeting different aspects of the HIV care continuum to improve testing, linkage to care, and viral suppression. Some of these approaches were directed at more vulnerable groups, such as pregnant women, adolescents, and individuals who inject drugs. In contrast was the devastating impact of the COVID-19 pandemic, with negative outcomes on HIV viral load suppression and retention in care. Data were presented on hepatitis B virus (HBV) suppression showing that tenofovir alafenamide (TAF)/emtricitabine (FTC)/bictegravir (BIC) may be superior to tenofovir disoproxil fumarate/FTC plus dolutegravir in suppressing HBV in HIV/HBV-coinfected individuals. A pilot study examining a 4-week trial of direct-acting antiviral therapy to treat hepatitis C in recently infected individuals showed lower rates of sustained virologic response at 12 weeks than longer courses. Additional data were presented on the use of long-acting cabotegravir/rilpivirine, comparing this regimen with oral TAF/FTC/BIC and the use of long-acting cabotegravir/rilpivirine in those with viremia. Data were presented on a novel strategy of lenacapavir with 2 broadly neutralizing antibodies given every 6 months as maintenance antiretroviral therapy (ART). Data were presented on improving HIV care outcomes in adolescents, interventions to prevent mother-to-child transmission, and HIV reservoirs in children and adolescents. Data were also presented on interactions between ART and hormonal contraception, as well as ART-related weight gain and impact on pregnancy. A study examining BIC pharmacokinetics in pregnancy was presented, as well as retrospective data on outcomes of adolescents receiving TAF/FTC/BIC.

Gay, bisexual, and other men who have sex with men (MSM) and transgender women, particularly those who are living with HIV, are disproportionately affected by human papillomavirus (HPV). For this narrative review of HPV health outcomes and vaccination for gay, bisexual, and other MSM and transgender women in the United States, we highlighted 71 publications regarding 1) burden of HPV infections and related diseases; 2) HPV vaccine efficacy; 3) HPV vaccination recommendations; 4) HPV vaccination coverage; 5) real-world vaccine effectiveness and health impacts; and 6) HPV vaccination acceptability. Vaccination is effective at reducing HPV infections among MSM; in the United States, routine HPV vaccination is recommended for all adolescents at age 11-12 years and for all persons through age 26 years. Efforts are ongoing to increase vaccination coverage and monitor health impacts of vaccination. Increasing vaccination coverage before sexual exposure to HPV is expected to reduce the burden of HPV-related disease.

The 2022 Conference on Retroviruses and Opportunistic Infections provided a rich source of new data and comprehensive reviews on antiviral therapy. For COVID-19, intramuscular sotrovimab was noninferior to intravenous sotrovimab, serostatus did not predict the efficacy of sotrovimab, and molnupiravir appeared safe and modestly effective in decreasing hospitalization rates. Trials from low- and middle-income countries provided data to support transitioning those on first-line therapy with or without virologic suppression and those virologically suppressed on second-line therapy to dolutegravir-based regimens. Additional data supported the use of lenacapavir as a long-acting antiretroviral drug. Data across the United States demonstrate the negative impact of the COVID-19 pandemic on the HIV care continuum, although enhanced outreach efforts and decentralization of antiretroviral therapy delivery were associated with improvements in care engagement outcomes. Researchers described potential mechanisms for the emergence of integrase strand transfer inhibitor resistance. Studies on proviral genotyping high-lighted the limitations of its use in predicting clinically significant resistance. Several studies looked at the epidemiology and treatment of hepatitis C and B and the status of current hepatitis C virus elimination efforts. Data presented on HIV, COVID-19, and maternal and pediatric health included 2-year virologic outcome data of very early antiretroviral therapy in potentially reducing the latent HIV reservoir in infants with HIV. Data presented on COVID-19 and HIV therapeutics in children included SARS-CoV-2-neutralizing monoclonal antibodies in children younger than 12 years of age, remdesivir in hospitalized infants and children, and long-acting therapies for HIV treatment in children.