SARS-CoV-2 seroprevalence in high-risk health care workers in a Belgian general hospital: evolution from the first wave to the second.

Health care workers (HCWs) are at the frontline for combatting the ongoing severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic. To describe recent or past infections, the novel development of serological assays enabled the assessment of the immune response developed in coronavirus disease (COVID-19). Here, we investigate SARS-CoV-2 seroprevalence in high-risk HCWs in a Belgian general hospital after both the first and the second waves. Three different immunoassays were used to determine immune response to SARS-CoV-2 in volunteer HCWs who worked in at least one COVID-19-dedicated ward [emergency department, intensive care unit (ICU) and internal medicine department] in our institution from 8 May 2020 to 19 May 2020 (n = 267) and from 18 January 2021 to 8 February 2021 (n = 189). Risk factors for seropositivity were also assessed using a questionnaire filled out by all participants. We report a steep increase in seroprevalence after the second wave and report a higher seropositivity in HCWs than in the general population. Furthermore, we show that ICU personnel and especially nurses exhibit a proportionally lower SARS-CoV-2 seroprevalence. This study documents the rapid increase in SARS-CoV-2 seroprevalence in highly exposed HCWs in a context of high viral circulation prior to vaccination campaigns. Most importantly, it suggests a lower occupational risk in ICU and illustrates the role of diagnostic labeling and use of personal protective equipment during the COVID-19 pandemic.

Influence of clodronate and compressive force on IL-1ß-stimulated human periodontal ligament fibroblasts.

OBJECTIVES: The aim of this study was to investigate in vitro the effect of clodronate on interleukin-1ß (IL-1ß)-stimulated human periodontal ligament fibroblasts (HPdLFs) with the focus on inflammatory factors of orthodontic tooth movement with and without compressive force. MATERIALS AND METHODS: HPdLFs were incubated with 5 µM clodronate and 10 ng/mL IL-1ß. After 48 h, cells were exposed to 3 h of compressive force using a centrifuge. The gene expression of cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), matrix metalloproteinase 8 (MMP-8), and the tissue inhibitor of MMP (TIMP-1) was analyzed using RT-PCR. Prostaglandin E2 (PGE-2), IL-6, and TIMP-1 protein syntheses were quantified via ELISA. RESULTS: Compressive force and IL-1ß induced an overexpression of COX-2 gene expression (61.8-fold; p < 0.05 compared with control), diminished by clodronate (41.1-fold; p < 0.05 compared with control). Clodronate slowed down the compression and IL-1ß induced IL-6 gene expression (161-fold vs. 85.6-fold; p < 0.05 compared with control). TNF-α was only slightly affected without statistical significance. Clodronate reduced IL-1ß-stimulated MMP-8 expression with and without compressive force. TIMP-1 on gene and protein level was downregulated in all groups. Analyzing the MMP-8/TIMP-1 ratio, the highest ratio was detected in IL-1ß-stimulated HPdLFs with compressive force (21.2-fold; p < 0.05 compared with control). Clodronate diminished IL-1ß-induced upregulation of MMP-8/TIMP-1 ratio with (11.5-fold; p < 0.05 compared with control) and without (12.5-fold; p < 0.05 compared with control) compressive force. CONCLUSION: Our study demonstrates a slightly anti-inflammatory effect by clodronate under compressive force in vitro. Additionally, the periodontal remodeling presented by the MMP-8/TIMP-1 ratio seems to be diminished by clodronate. CLINICAL RELEVANCE: Reduction of pro-inflammatory factors and reduction of periodontal remodeling might explain reduced orthodontic tooth movement under clodronate intake.

Antiretroviral therapy suppresses rectal HIV-RNA shedding despite inflammation in MSM with rectal C. trachomatis and N. gonorrhoeae infections-a cross-sectional, single-center study.

OBJECTIVES: Rectal infections with Chlamydia trachomatis and/or Neisseria gonorrhoeae (CT/NG) are common in men who have sex with men (MSM) and are linked to HIV transmission. However, rectal CT/NG infections are often asymptomatic and it is not known how they contribute to HIV transmission. We assessed clinical and cytological signs of inflammation as well as rectal HIV-RNA in HIV-infected MSM with and without CT/NG infection. METHODS: 112 HIV-positive MSM with or without rectal symptoms and with or without antiretroviral therapy who underwent high-resolution anoscopy (HRA) at the proctological outpatient centre of the University Hospital Essen, Germany, between November 2013 and February 2014 were included in this cross-sectional study. During the examination, rectal swabs for the assessment of CT/NG, HIV-RNA and inflammatory cells (granulocytes, lymphocytes, histiocytes) were collected. 110 patients were assessed according to the study protocol, and no imputation of missing data was performed. RESULTS: Rectal infections with CT or NG were detected in 17 participants, and 4 participants were coinfected. Only symptomatic CT/NG infections (8/17) showed signs of inflammation in HRA. Symptomatic CT/NG infections were also associated with the detection of lymphocytes and histiocytes in rectal cytology (both P<0.001). In contrast, asymptomatic CT/NG infections neither resulted in clinical nor cytological signs of inflammation. Rectal HIV-RNA was undetectable in all participants with rectal CT/NG infections who received combined antiretroviral therapy (ART) when plasma HIV-RNA was below the limit of detection (n=13). Besides rectal CT/NG infections, syphilis (n=4) and HPV-associated lesions (n=37) were frequently detected, and proctological symptoms were associated with simultaneous infection with ≥2 STDs. CONCLUSIONS: Only symptomatic but not asymptomatic rectal infections with CT and/or NG were associated with clinical and cytological signs of inflammation. Rectal HIV shedding was not promoted by CT/NG infections in patients receiving ART with suppressed plasma HIV-RNA. TRIAL REGISTRATION NUMBER: UTN: U1111-1150-4804. German Clinical Trials Register (DRKS): DRKS00005468.