The latest medical research on Public Health

The World Mental Health Qatar (WMHQ) study, the first national general population mental health survey in Qatar, was conducted as part of the World Health Organization (WHO) World Mental Health (WMH) Survey Initiative. It was one of the few WMH survey conducted during the COVID-19 pandemic. This paper presents the methodological advances and challenges encountered while conducting the survey by telephone during the pandemic.

Disproportionate stratified sampling using a national-level cellular telephone frame selected a representative sample of Arabic-speaking adults. Participants were initially contacted via Short Message Service text, followed by telephone interviews. WMH training materials supported a comprehensive training program, and data quality was ensured through a quality control indicator system and extensive monitoring.

Over 234 days, 5195 interviews in Arabic were completed, averaging 77 min each. In line with Qatar's population, the majority of participants were non-Qatari residents living in Qatar (72.2%).

A distributed remote Computer Assisted Telephone Interviewing system facilitated centralized quality monitoring and data security. However, the pandemic intensified challenges such as remote management of interviewer productivity, low response rates, and rising survey costs. The findings will inform Qatar's mental health policymakers, and the strategies used to address these challenges offer valuable insights for researchers worldwide.

We investigated the feasibility of replacing face-to-face with telephone interviews conducted as part of the World Mental Health Qatar (WMHQ) survey and discuss the main methodological changes across the two pilots that were subsequently implemented in the full-scale WMHQ telephone survey.

We assessed the net mode effect by comparing the lifetime prevalence estimates of the main mental disorder classes (mood and anxiety disorders) and a number of disorders across the two survey pilots conducted prior to and post-pandemic.

The main differences in terms of methodology for both pilots stemmed from differences in the survey mode, including questionnaire length, study recruitment method, and fielding team size and structure. These factors influenced response rates and costs. However, the lifetime prevalence estimates and other key indicators of survey results did not differ across modes.

Our findings confirm the comparability of data collected via telephone and face-to-face modes, supporting the adoption of telephone surveys for future mental health studies, particularly in the context of pandemics. They also confirm the feasibility of changing or mixing modes depending on field conditions in future psychiatric epidemiological research.

SARS-Co-V2 infection can induce ER stress-associated activation of unfolded protein response (UPR) in host cells, which may contribute to the pathogenesis of COVID-19. To understand the complex interplay between SARS-Co-V2 infection and UPR signaling, we examined the effects of acute pre-existing ER stress on SARS-Co-V2 infectivity.

Huh-7 cells were treated with Tunicamycin (TUN) and Thapsigargin (THA) prior to SARS-CoV-2pp transduction (48 h p.i.) to induce ER stress. Pseudo-typed particles (SARS-CoV-2pp) entry into host cells was measured by Bright GloTM luciferase assay. Cell viability was assessed by cell titer Glo® luminescent assay. The mRNA and protein expression was evaluated by RT-qPCR and Western Blot.

TUN (5 µg/mL) and THA (1 µM) efficiently inhibited the entry of SARS-CoV-2pp into host cells without any cytotoxic effect. TUN and THA's attenuation of virus entry was associated with differential modulation of ACE2 expression. Both TUN and THA significantly reduced the expression of stress-inducible ER chaperone GRP78/BiP in transduced cells. In contrast, the IRE1-XBP1s and PERK-eIF2α-ATF4-CHOP signaling pathways were downregulated with THA treatment, but not TUN in transduced cells. Insulin-mediated glucose uptake and phosphorylation of Ser307 IRS-1 and downstream p-AKT were enhanced with THA in transduced cells. Furthermore, TUN and THA differentially affected lipid metabolism and apoptotic signaling pathways.

These findings suggest that short-term pre-existing ER stress prior to virus infection induces a specific UPR response in host cells capable of counteracting stress-inducible elements signaling, thereby depriving SARS-Co-V2 of essential components for entry and replication. Pharmacological manipulation of ER stress in host cells might provide new therapeutic strategies to alleviate SARS-CoV-2 infection.