Quality of life and depressive symptoms among Peruvian university students during the COVID-19 pandemic (preprint)

ObjectivesCharacterize the quality of life and depressive symptoms of university students in Peru during the COVID-19 pandemic and to determine the associated factors. MethodsMulti-centre study in 1634 university students recruited by convenience sampling. Quality of life (QoL) was assessed with the European Quality of Life-5 Dimensions at three levels (EQ-5D-3L) and depressive symptoms with the Patient Health Questionarie-9 (PHQ-9). To evaluate factors associated with QoL and depressive symptoms, linear and adjusted regressions were used, with robust variance reporting coefficients ({beta}). ResultsThe percentage of participants most affected by QoL dimension was: anxiety/depression (47.2%) and pain/discomfort (35.6%). Regarding the Visual Analog Scale (EQ-VAS) of QoL, the score was 76.0 + 25.6. Those who had family economic decline during quarantine ({beta}=-3.4, IC95%=-6.5 to -0.3) or family with chronic diseases ({beta}=-3.7, IC95%=-6.1 to -1.4) presented significantly lower scores in their QoL. Regarding depressive symptomatology, the university students reported a moderate to severe level (28.9%). A higher risk of depressive symptoms was found in residents of Ayacucho ({beta}=0.8, IC95%=0.1 to 1.5), those who were released from quarantine ({beta}=0.7, IC95%=0.2 to 1.2) and those who had a family member with chronic disease ({beta}=1.5, IC95%=1.0 to 2.1). ConclusionsAlmost half and one third of participants reported anxiety/depression, and pain/discomfort in their QoL respectively. Nearly a third presented moderate and severe depressive symptoms. The deterioration of QoL was worse in those who had a decrease in income and a family member with chronic illness. The presence of depressive symptoms was found in students in Ayacucho, those who left home during quarantine and those who had a family member with chronic diseases.

Elevated temperature inhibits SARS-CoV-2 replication in respiratory epithelium independently of the induction of IFN-mediated innate immune defences (preprint)

The pandemic spread of SARS-CoV-2, the etiological agent of COVID-19, represents a significant and ongoing international health crisis. A key symptom of SARS-CoV-2 infection is the onset of fever, with a hyperthermic temperature range of 38 to 41{degrees}C. Fever is an evolutionarily conserved host response to microbial infection and inflammation that can influence the outcome of viral pathogenicity and regulation of host innate and adaptive immune responses. However, it remains to be determined what effect elevated temperature has on SARS-CoV-2 tropism and replication. Utilizing a 3D air-liquid interface (ALI) model that closely mimics the natural tissue physiology and cellular tropism of SARS-CoV-2 infection in the respiratory airway, we identify tissue temperature to play an important role in the regulation of SARS-CoV-2 infection. We show that temperature elevation induces wide-spread transcriptome changes that impact upon the regulation of multiple pathways, including epigenetic regulation and lncRNA expression, without disruption of general cellular transcription or the induction of interferon (IFN)-mediated antiviral immune defences. Respiratory tissue incubated at temperatures >37{degrees}C remained permissive to SARS-CoV-2 infection but severely restricted the initiation of viral transcription, leading to significantly reduced levels of intraepithelial viral RNA accumulation and apical shedding of infectious virus. To our knowledge, we present the first evidence that febrile temperatures associated with COVID-19 inhibit SARS-CoV-2 replication. Our data identify an important role for temperature elevation in the epithelial restriction of SARS-CoV-2 that occurs independently of the induction of canonical IFN-mediated antiviral immune defences and interferon-stimulated gene (ISG) expression.

Evaluating the effects of SARS-CoV-2 Spike mutation D614G on transmissibility and pathogenicity (preprint)

Global dispersal and increasing frequency of the SARS-CoV-2 Spike protein variant D614G are suggestive of a selective advantage but may also be due to a random founder effect. We investigate the hypothesis for positive selection of Spike D614G in the United Kingdom using more than 25,000 whole genome SARS-CoV-2 sequences. Despite the availability of a large data set, well represented by both Spike 614 variants, not all approaches showed a conclusive signal of positive selection. Population genetic analysis indicates that 614G increases in frequency relative to 614D in a manner consistent with a selective advantage. We do not find any indication that patients infected with the Spike 614G variant have higher COVID-19 mortality or clinical severity, but 614G is associated with higher viral load and younger age of patients. Significant differences in growth and size of 614G phylogenetic clusters indicate a need for continued study of this variant.