Post-COVID syndrome (PCS) is a complex condition that can emerge after recovery from SARS-CoV-2 infection, even in young, healthy individuals with mild acute illness. While the underlying mechanisms remain unclear, viral persistence and immune dysregulation are considered key contributors. This study investigates whether the persistence of viral proteins in gut-associated lymphoid tissue (GALT) is linked to PCS and how it may influence immune cell populations in the terminal ileum (TI). Peripheral blood (PB) and TI biopsies were obtained 15 to 22 months after acute SARS-CoV-2 infection from 43 SARS-CoV-2 convalescent patients (20 with (PCS+) and 23 without PCS symptoms (PCS-)). Mononuclear cells were isolated from PB and TI for flow cytometric and histological analysis. PCS+ individuals exhibited a distinct immune profile characterized by increased mast cell activity, and elevated zonulin levels, indicating compromised gut barrier function alongside with elevated SARS-CoV-2 nucleocapsid protein expression in the TI. Additional findings included expansion of plasmacytoid dendritic cells, alterations in NK cell subsets, and higher proportions of central memory T-cells with low PD-1 expression in TI. Elevated MMP-9 levels further indicated localized gut inflammation and tissue remodeling. These results highlight the gut-immune interface as potential driver of PCS and support therapeutic strategies targeting viral persistence and intestinal immune homeostasis.

Background and Aims: Hepatitis C virus (HCV) infections were previously treated with interferon (IFN) but today direct acting antivirals (DAAs) with cure rates >95% are available. DAA treatment failure is primarily attributed to resistance associated mutations (RAMs), often imposing a fitness cost. Interferon treatment outcome was shown to be associated with the interferon sensitivity determining region (ISDR), which is part of the replication enhancing domain (ReED) in non-structural protein (NS) 5A. We found that accumulation of mutations in the ReED was indicative of elevated viral genome replication fitness. This study investigates the impact of HCV replication fitness on antiviral treatment outcomes. Methods: We utilized chimeric HCV subgenomic replicons containing RAMs and ReED sequences from patients after interferon treatment or DAA failure to assess replication fitness of patient isolates in presence and absence of inhibitors. Results: Replication fitness did not impact on IFN sensitivity in cell culture but resulted in higher remaining antigen levels for highly replicating variants at a given IFN concentration. Furthermore, we identified ReED variants substantially increasing HCV replication in several patients who failed DAA therapy across different genotypes. High replicator ReEDs rescued the fitness loss caused by RAMs like Y93C/H (NS5A) and S282T (NS5B). While high replication fitness did not intrinsically increase drug sensitivity (IC50), it allowed the virus to sustain robust replication despite antiviral pressure. Conclusions: Elevated replication fitness might support interferon treatment due to increased antigen presentation, facilitating adaptive immune responses. Furthermore, ReED mediated increase in replication fitness could contribute to DAA treatment failure by preserving higher replication upon treatment and compensating for RAM associated fitness costs. Thus, patients failing DAA treatment should be monitored for RAMs and ReED mutations. ### Competing Interest Statement The authors have declared no competing interest. Deutsche Forschungsgemeinschaft, https://ror.org/018mejw64, 519777725, 272983813 – TRR 179 Deutsches Zentrum für Infektionsforschung (DZIF), DZIF academy stipend, TTU Hepatitis 05.821

Chimeric antigen receptor (CAR) T cells and bispecific T cell engagers have become integral components in the treatment of relapsed/refractory multiple myeloma. We report a 63-year-old male who received ciltacabtagene autoleucel CAR T cells and the GPRC5D × CD3 bispecific talquetamab for early relapse of his multiple myeloma. Nine months after CAR T therapy, he developed a symptomatic leukemic peripheral T cell lymphoma with cutaneous and intestinal involvement. Longitudinal single-cell RNA and T cell receptor sequencing of peripheral blood and bone marrow revealed two hyperexpanded CAR-carrying T cell clones. These expanded clones exhibited an exhausted effector-memory T cell transcriptional signature, and the neoplasm itself was sensitive to dexamethasone treatment. The immunophenotypic and transcriptional alterations of these abnormal T cells resembled those of T-large granular lymphocytic leukemia. Spatial transcriptomes of skin lesions confirmed the aberrant CAR-expressing T cells. Whole-genome sequencing revealed three distinct integration sites, within the introns of ZGPAT, KPNA4 and polycomb-associated noncoding RNAs. Before and after CAR T whole-genome analyses implicated clonal outgrowth of a TET2-mutated precursor propelled by additional subclone-specific loss of heterozygosity and other secondary mechanisms. This case highlights the evolution of a CAR-carrying peripheral T cell lymphoma following CAR T cell and bispecific T cell engager therapy, offering critical insights into the clonal evolution from a predisposed hematopoietic precursor to a mature neoplasm.

To quantify virologic failure (VF), identify predictors, characterize resistance patterns at failure, and evaluate time to resuppression in the RESINA cohort. ART-naïve adults initiating ART in 2001–2024 were followed. VF was defined as at least one HIV-1 RNA > 200 copies/mL after suppression or ≥ 0.5-log₁₀ rebound. Participants were grouped by treatment era (2001–2007, 2008–2013, ≥ 2014), reflecting availability of drug classes. Genotypes at baseline and VF were interpreted using the HIV-GRADE algorithm. Predictors of VF were assessed with logistic regression; time to resuppression (< 50 copies/mL) after first VF with Cox models and Kaplan–Meier plots. Among 5136 participants, 139 (2.7

BACKGROUND:Immunocompromised individuals, hemato-oncologic diseases or post-transplantation included, are, due to impaired immune response, at increased risk for severe and prolonged COVID-19. Observational Studies showed that SARS-CoV-2 RNAemia has been associated with poorer prognosis and higher disease severity. OBJECTIVE:The aim of this study was to investigate the occurrence of RNAemia and its association with anti-SARS-CoV-2 antibodies in immunocompromised COVID-19 patients. Risk factors for RNAemia were included in the analysis. STUDY DESIGN:A retrospective study was conducted in 55 immunocompromised patients tested positive for SARS-CoV-2, who received treatment with monoclonal antibodies (mAb) between December 2021 and March 2022. Serological and virological tests were performed before mAb administration and clinical data were collected from electronic health records. RESULTS:Out of 55 patients, 35 % showed SARS-CoV-2 RNAemia. RNAemia was present in the 2 reported fatal cases. It was associated with negative testing for anti-receptor binding domain (RBD) IgG, anti-S2 domain of spike protein (S2) IgG and a lower leukocyte count. No association was found between previous COVID-19 vaccinations and the risk for RNAemia in immunocompromised patients. CONCLUSION:The study underscores the importance of humoral response in controlling SARS-CoV-2 replication. RNAemia can serve as a potential biomarker for disease severity in immunocompromised individuals. Therefore, it should be considered in clinical settings for appropriate therapy decisions. Further research is needed to evaluate the pathophysiology and implications of RNAemia in immunodeficient patients with COVID-19.

Background: Gastrointestinal mucosal damage due to human immunodeficiency virus (HIV) infection leads to microbial translocation and immune activation, contributing to the development of non-infectious comorbidities (NICM) in people living with HIV (PLWH). Additionally, persistent proviral HIV-1 in the gut-associated lymphatic tissue (GALT) can trigger immunological changes in the epithelial environment, impacting the mucosal barrier. However, the role of zonulin, a modulator of epithelial tight junctions in GALT during HIV infection, remains poorly understood. Methods: We measured zonulin in serum and intestinal tissue sections from five treatment-naive (HIV+NAIVE) and 10 cART-treated (HIV+cART) HIV+ individuals, along with 11 controls (CTRL). We compared zonulin levels with clinical characteristics, inflammatory markers (IFN-α, CXCR3, and PD-1), and the viral reservoir in peripheral blood (PB) and terminal ileum (TI). Results: Upon HIV infection, TI was found to harbor more HIV DNA than PB. Circulating zonulin levels were highest in HIV+NAIVE compared to HIV+cART or CTRL. Surprisingly, in the gut tissue sections, zonulin levels were higher in CTRL than in HIV+ individuals. Elevated circulating zonulin levels were found to be correlated with CD4+T-cell depletion in PB and TI, and with intestinal IFN-α. Conclusions: The findings of this study indicate a shift in zonulin levels from the gut to the bloodstream in response to HIV infection. Furthermore, elevated systemic zonulin levels are associated with the depletion of intestinal CD4+ T cells and increased gut inflammation, suggesting a potential link between systemic zonulin and intestinal damage. Gaining insight into the regulation of gut tight junctions during HIV infection could offer valuable understanding for preventing NICM in PLWH.

Journal of Medical VirologyVolume 96, Issue 1 e29353 LETTER TO THE EDITOR Lack of monkeypox virus (MPXV) transmission despite occupational exposure of a large number of health care workers Wolfgang A. Wetsch, Corresponding Author Wolfgang A. Wetsch [email protected] orcid.org/0000-0001-5800-6665 Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany Correspondence Wolfgang A. Wetsch, Department of Anaesthesiology and Intensive Care Medicine, University Hospital Cologne, Kerpener Str. 62, 50937 Cologne, Germany. Email: [email protected]Search for more papers by this authorEva Heger, Eva Heger orcid.org/0000-0001-7625-5139 Institute of Virology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorHendrik Drinhaus, Hendrik Drinhaus Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorBernd W. Böttiger, Bernd W. Böttiger orcid.org/0000-0001-8000-8931 Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorRemco Overbeek, Remco Overbeek orcid.org/0000-0002-4046-0234 Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorClara Lehmann, Clara Lehmann orcid.org/0000-0002-7042-1578 Department I of Internal Medicine, University Hospital Cologne, Faculty of Medicine, University of Cologne, German Center for Infection Research Partner Side Köln-Bonn, University of Cologne, Cologne, GermanySearch for more papers by this authorGerd Fätkenheuer, Gerd Fätkenheuer Department I of Internal Medicine, University Hospital Cologne, Faculty of Medicine, University of Cologne, German Center for Infection Research Partner Side Köln-Bonn, University of Cologne, Cologne, GermanySearch for more papers by this authorNorma Jung, Norma Jung orcid.org/0000-0002-5740-0772 Department I of Internal Medicine, University Hospital Cologne, Faculty of Medicine, University of Cologne, German Center for Infection Research Partner Side Köln-Bonn, University of Cologne, Cologne, GermanySearch for more papers by this authorJulia Fischer, Julia Fischer orcid.org/0000-0001-6138-7454 Department I of Internal Medicine, University Hospital Cologne, Faculty of Medicine, University of Cologne, German Center for Infection Research Partner Side Köln-Bonn, University of Cologne, Cologne, GermanySearch for more papers by this authorJens Kneifel, Jens Kneifel Department of Hospital Hygiene and Infection Control, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorJanine Zweigner, Janine Zweigner orcid.org/0000-0002-0360-434X Department of Hospital Hygiene and Infection Control, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorFlorian Klein, Florian Klein orcid.org/0000-0003-1376-1792 Institute of Virology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorUlrike Wieland, Ulrike Wieland orcid.org/0000-0003-3480-4413 Institute of Virology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this author Wolfgang A. Wetsch, Corresponding Author Wolfgang A. Wetsch [email protected] orcid.org/0000-0001-5800-6665 Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, Germany Correspondence Wolfgang A. Wetsch, Department of Anaesthesiology and Intensive Care Medicine, University Hospital Cologne, Kerpener Str. 62, 50937 Cologne, Germany. Email: [email protected]Search for more papers by this authorEva Heger, Eva Heger orcid.org/0000-0001-7625-5139 Institute of Virology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorHendrik Drinhaus, Hendrik Drinhaus Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorBernd W. Böttiger, Bernd W. Böttiger orcid.org/0000-0001-8000-8931 Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorRemco Overbeek, Remco Overbeek orcid.org/0000-0002-4046-0234 Department of Anaesthesiology and Intensive Care Medicine, University Hospital of Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorClara Lehmann, Clara Lehmann orcid.org/0000-0002-7042-1578 Department I of Internal Medicine, University Hospital Cologne, Faculty of Medicine, University of Cologne, German Center for Infection Research Partner Side Köln-Bonn, University of Cologne, Cologne, GermanySearch for more papers by this authorGerd Fätkenheuer, Gerd Fätkenheuer Department I of Internal Medicine, University Hospital Cologne, Faculty of Medicine, University of Cologne, German Center for Infection Research Partner Side Köln-Bonn, University of Cologne, Cologne, GermanySearch for more papers by this authorNorma Jung, Norma Jung orcid.org/0000-0002-5740-0772 Department I of Internal Medicine, University Hospital Cologne, Faculty of Medicine, University of Cologne, German Center for Infection Research Partner Side Köln-Bonn, University of Cologne, Cologne, GermanySearch for more papers by this authorJulia Fischer, Julia Fischer orcid.org/0000-0001-6138-7454 Department I of Internal Medicine, University Hospital Cologne, Faculty of Medicine, University of Cologne, German Center for Infection Research Partner Side Köln-Bonn, University of Cologne, Cologne, GermanySearch for more papers by this authorJens Kneifel, Jens Kneifel Department of Hospital Hygiene and Infection Control, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorJanine Zweigner, Janine Zweigner orcid.org/0000-0002-0360-434X Department of Hospital Hygiene and Infection Control, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorFlorian Klein, Florian Klein orcid.org/0000-0003-1376-1792 Institute of Virology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this authorUlrike Wieland, Ulrike Wieland orcid.org/0000-0003-3480-4413 Institute of Virology, University Hospital Cologne, Faculty of Medicine, University of Cologne, Cologne, GermanySearch for more papers by this author First published: 04 January 2024 https://doi.org/10.1002/jmv.29353Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Supporting Information Filename Description jmv29353-sup-0001-Suppl_figure2_final.tiff2.1 MB Supplementary Figure: Phylogenetic analysis of the patient's MPXV strain. Maximum likelihood phylogeny of 69 MPXV isolates based on complete genome sequences. Respective sequences of the outgroup, clade I (formerly "Central African" or "Congo Basin" clade) and clade II (formerly "West African" clade) are highlighted by different colors: outgroup (grey), clade I (green), clade II of previous outbreaks before 2022 (dark blue), clade II of the current outbreak (light blue) and index patient (red). The final phylogeny was generated using Mega11 version 11.0.11. Genomes of six MPXV strains (including the strain of the index patient) were sequenced with the Illumina MiSeq system and aligned with 69 additional MPXV genomes available at NCBI and GISAID using MAFFT v7.490 (2021/Oct/30). The 69 sequences included two other poxvirus genomes (cowpox virus, X94355, and horsepox virus, DQ792504, grey), eight genomes of clade I (green) and six genomes of clade II (dark blue) as outgroup and reference sequences, respectively. The resulting alignment was then used to construct a maximum likelihood phylogenetic tree with 100 bootstrap replicates using the "Tamura-Nei" model of Mega11.0.11. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article. REFERENCES 1 World Health Organization. 2022-23 Mpox (Monkeypox) outbreak: global trends. Produced on 20 November 2023. Accessed on November 20, 2023. https://worldhealthorg.shinyapps.io/mpx_global/ Google Scholar 2Choudhary OP, Chopra H, Shafaati M, et al. Reverse zoonosis and its relevance to the monkeypox outbreak 2022. New Microbes New Infect. 2022; 49-50:101049. 10.1016/j.nmni.2022.101049 PubMedWeb of Science®Google Scholar 3Thornhill JP, Barkati S, Walmsley S, et al. Monkeypox virus infection in humans across 16 countries—April−June 2022. N Engl J Med. 2022; 387(8): 679-691. 10.1056/NEJMoa2207323 CASPubMedWeb of Science®Google Scholar 4Mitjà O, Ogoina D, Titanji BK, et al. Monkeypox. Lancet. 2023; 401(10370): 60-74. 10.1016/S0140-6736(22)02075-X PubMedWeb of Science®Google Scholar 5Peiró-Mestres A, Fuertes I, Camprubí-Ferrer D, et al. Frequent detection of monkeypox virus DNA in saliva, semen, and other clinical samples from 12 patients, Barcelona, Spain, May to June 2022. Euro Surveill. 2022; 27(28):2200503. 10.2807/1560-7917.ES.2022.27.28.2200503 CASPubMedGoogle Scholar 6Nörz D, Brehm TT, Tang HT, et al. Clinical characteristics and comparison of longitudinal qPCR results from different specimen types in a cohort of ambulatory and hospitalized patients infected with monkeypox virus. J Clin Virol. 2022; 155:105254. 10.1016/j.jcv.2022.105254 PubMedWeb of Science®Google Scholar 7Brosius I, Van Dijck C, Coppens J, et al. Presymptomatic viral shedding in high-risk mpox contacts: a prospective cohort study. J Med Virol. 2023; 95(5):e28769. 10.1002/jmv.28769 CASPubMedWeb of Science®Google Scholar 8Meister TL, Brüggemann Y, Todt D, et al. Stability and inactivation of monkeypox virus on inanimate surfaces. J Infect Dis. 2023; 2:jiad127. Google Scholar 9Nörz D, Pfefferle S, Brehm TT, et al. Evidence of surface contamination in hospital rooms occupied by patients infected with monkeypox, Germany, June 2022. Euro Surveill. 2022; 27(26):2200477. 10.2807/1560-7917.ES.2022.27.26.2200477 PubMedGoogle Scholar 10Marshall KE, Barton M, Nichols J, et al. Health care personnel exposures to subsequently Laboratory-Confirmed monkeypox patients—Colorado, 2022. MMWR Morb Mortal Wkly Rep. 2022; 71(38): 1216-1219. 10.15585/mmwr.mm7138e2 PubMedWeb of Science®Google Scholar 11Zachary KC, Philpotts LL, Shenoy ES. Mpox exposure and transmission in healthcare settings during the 2022 global outbreak. Curr Opin Infect Dis. 2023; 36(4): 257-262. 10.1097/QCO.0000000000000933 CASPubMedWeb of Science®Google Scholar 12Choi Y, Jeon E, Kim T, et al. Case report and literature review of occupational transmission of monkeypox virus to healthcare workers, South Korea. Emerging Infect Dis. 2023; 29(5): 997-1001. 10.3201/eid2905.230028 PubMedWeb of Science®Google Scholar 13Safir A, Safir M, Henig O, et al. Nosocomial transmission of MPOX virus to health care workers—an emerging occupational hazard: a case report and review of the literature. Am J Infect Control. 2023; 51(9): 1072-1076. 10.1016/j.ajic.2023.01.006 CASPubMedWeb of Science®Google Scholar 14Choudhary OP, Fahrni ML, Saied AA, Chopra H. Ring vaccination for monkeypox containment: strategic implementation and challenges. Int J Surg. 2022; 105:106873. 10.1016/j.ijsu.2022.106873 PubMedWeb of Science®Google Scholar Volume96, Issue1January 2024e29353 ReferencesRelatedInformation

Quantification of hepatitis C virus (HCV)-RNA in serum or plasma samples is an essential parameter in HCV diagnostics. Here, the NeuMoDx™Molecular System (Qiagen) was tested for the most common HCV genotypes and compared to the cobas c6800 system (Roche).HCV-RNA from 131 plasma/serum samples from chronically infected patients was determined in parallel on the NeuMoDx and c6800 systems. Linearity was analysed using the four most common HCV genotypes (1-4) in our cohort. The coefficient of variation (CV) within (intra-assay) and between (inter-assay) runs was calculated based on HCV-RNA concentration. Quantitative HCV-RNA results were highly correlated on both test systems (R2=0.7947; y=0.94x+0.37). On average, the NeuMoDx and c6800 HCV RNA levels showed a mean difference of only 0.05 log10 IU/mL but with a broad distribution (±1.2 2xSD). The NeuMoDx demonstrated very good linearity across all HCV genotypes tested at concentrations between 1.7 and 6.2 log10 IU/mL (R2 range: 0.9257-0.9991) with the highest mean coefficient of determination for genotype 1 (R2=0.9909). The mean intra- and inter-assay CV for both serum and plasma samples was <5%. The NeuMoDx HCV-RNA Assay demonstrates high subtype-independent comparability, linearity, and reproducibility for the quantification of HCV-RNA in serum and plasma samples from chronically infected patients.

BACKGROUND:Cytomegalovirus (CMV) infections are a common complication after kidney transplantation (KTx) and negatively affecting patient outcome. Valganciclovir (VGC) prophylaxis is often limited by drug-induced side effects and dose reduction due to decline in kidney function.METHOD:In the present study, episodes of CMV viremia in the first year after KTx in a cohort of 316 recipients were analyzed retrospectively to identify risk factors linked to persistent infections.RESULTS:In the studied cohort, 18.7% of patients showed a high-risk (HR) constellation (D+/R-) for CMV infections. CMV viremia affected 22% of our cohort, with HR patients being the most affected cohort (44.1%). Within this group, most viremic events (65.3%) occurred while patients were still on prophylactic therapy, showing significantly higher viral loads and a longer duration compared to seropositive recipients.CONCLUSION:The analysis at hand revealed that detection of viremia under ongoing antiviral prophylaxis bears an increased risk for sustained viral replication and antiviral drug resistance in HR patients. We identified low estimated glomerular filtration rate (eGFR) and lower dose VGC prophylaxis post-KTx as a risk factor for breakthrough infections in HR patients in our single center cohort. These patients might benefit from a closer CMV monitoring or novel prophylactic agents as letermovir.

BACKGROUND AND OBJECTIVES Test-to-stay concepts apply serial testing of children in daycare after exposure to SARS-CoV-2 without use of quarantine. This study aims to assess the safety of a test-to-stay screening in daycare facilities. METHODS 714 daycare facilities and approximately 50 000 children ≤6 years in Cologne, Germany participated in a SARS-CoV-2 Pool-polymerase chain reaction (PCR) screening from March 2021 to April 2022. The screening initially comprised post-exposure quarantine and was adapted to a test-to-stay approach during its course. To assess safety of the test-to-stay approach, we explored potential changes in frequencies of infections among children after the adaptation to the test-to-stay approach by applying regression discontinuity in time (RDiT) analyses. To this end, PCR-test data were linked with routinely collected data on reported infections in children and analyzed using ordinary least squares regressions. RESULTS 219 885 Pool-PCRs and 352 305 Single-PCRs were performed. 6440 (2.93%) Pool-PCRs tested positive, and 17 208 infections in children were reported. We estimated that during a period of 30 weeks, the test-to-stay concept avoided between 7 and 20 days of quarantine per eligible daycare child. RDiT revealed a 26% reduction (Exp. Coef: 0.74, confidence interval 0.52–1.06) in infection frequency among children and indicated no significant increase attributable to the test-to-stay approach. This result was not sensitive to adjustments for 7-day incidence, season, SARS-CoV-2 variant, and socioeconomic status. CONCLUSIONS Our analyses provide evidence that suggest safety of the test-to-stay approach compared with quarantine measures. This approach offers a promising option to avoid use of quarantine after exposure to respiratory pathogens in daycare settings.

BACKGROUND:Torque teno virus (TTV) is part of the human virome. TTV load was related to the immune status in patients after organ transplantation. We hypothesize that TTV load could be an additional marker for immune function in people living with HIV (PLWH). METHODS:In this analysis, serum samples of PLWH from the RESINA multicenter cohort were reanalyzed for TTV. Investigated clinical and epidemiological parameters included human pegivirus load, patient age and sex, HIV load, CD4+ T-cell count (Centers for Disease Control and Prevention [CDC] stage 1, 2, or 3), and CDC clinical stage (1993 CDC classification system; stage A, B, or C) before initiation of antiretroviral therapy. Regression analysis was used to detect possible associations among parameters. RESULTS:Our analysis confirmed TTV as a strong predictor of CD4+ T-cell count and CDC class 3. This relationship was used to propose a first classification of TTV load with regard to clinical stage. We found no association with clinical CDC stages A-C. The human pegivirus load was inversely correlated with HIV load but not TTV load. CONCLUSIONS:TTV load was associated with immunodeficiency in PLWH. Neither TTV nor HIV load were predictive for the clinical categories of HIV infection.