Since its emergence in December 2019, Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has spread globally and become a major public health burden. Despite its close phylogenetic relationship to SARS-CoV, SARS-CoV-2 exhibits increased human-to-human transmission dynamics, likely due to efficient early replication in the upper respiratory epithelium of infected individuals. Since different temperatures encountered in the human upper and lower respiratory tract (37°C and 33°C, respectively) have been shown to affect the replication kinetics of several respiratory viruses, as well as host immune response dynamics, we investigated the impact of temperatures during SARS-CoV-2 and SARS-CoV infection using the primary human airway epithelial cell culture model. SARS-CoV-2, in contrast to SARS-CoV, replicated to higher titers when infections were performed at 33°C rather than 37°C. Although both viruses were highly sensitive to type I and type III interferon pretreatment, a detailed time-resolved transcriptome analysis revealed temperature-dependent interferon and pro-inflammatory responses specifically induced by SARS-CoV or SARS-CoV-2, which amplitude was inversely proportional to their replication efficiencies at 33°C or 37°C. These data provide crucial insight on pivotal virus–host interaction dynamics and are in line with characteristic clinical features of SARS-CoV-2 and SARS-CoV, as well as their respective transmission efficiencies.

Three outbreaks of respiratory illness associated with human coronavirus HCoV-OC43 infection occurred in geographically unrelated aged-care facilities in Melbourne, Australia during August and September 2002. On clinical and epidemiological grounds the outbreaks were first thought to be caused by influenza virus. HCoV-OC43 was detected by RT-PCR in 16 out of 27 (59%) specimens and was the only virus detected at the time of sampling. Common clinical manifestations were cough (74%), rhinorrhoea (59%) and sore throat (53%). Attack rates and symptoms were similar in residents and staff across the facilities. HCoV-OC43 was also detected in surveillance and diagnostic respiratory samples in the same months. These outbreaks establish this virus as a cause of morbidity in aged-care facilities and add to increasing evidence of the significance of coronavirus infections.

The SARS-CoV-2 pandemic has presented new challenges to food manufacturers. During the early phase of the pandemic, several large outbreaks of coronavirus disease 2019 (COVID-19) occurred in food manufacturing plants resulting in deaths and economic loss, with approximately 15% of personnel diagnosed as asymptomatic for COVID-19. Spread by asymptomatic and presymptomatic individuals has been implicated in large outbreaks of COVID-19. In March 2020, we assisted in implementation of environmental monitoring programs for SARS-CoV-2 in zones 3 and 4 of 116 food production facilities. All participating facilities had already implemented measures to prevent symptomatic personnel from coming to work. During the study period, from 17 March to 3 September 2020, 1.23% of the 22,643 environmental samples tested positive for SARS-CoV-2, suggesting that infected individuals were actively shedding virus. Virus contamination was commonly found on frequently touched surfaces such as doorknobs, handles, table surfaces, and sanitizer dispensers. Most processing plants managed to control their environmental contamination when they became aware of the positive findings. Comparisons of positive test results for plant personnel and environmental surfaces in one plant revealed a close correlation. Our work illustrates that environmental monitoring for SARS-CoV-2 can be used as a surrogate for identifying the presence of asymptomatic and presymptomatic personnel in workplaces and may aid in controlling infection spread. HIGHLIGHTS

To examine the relationship between obesity, Type 2 diabetes, and periodontal disease in Vietnamese patients. The sample included 712 patients aged 18 years or older who first visited the Institute of Traditional Medicine, Ho Chi Minh City. All participants completed a questionnaire and underwent anthropometric index measurements for obesity (height, weight, waist, and hip circumferences) and had their body fat percentage measured. A full periodontal examination was performed and a fasting glycemic level was determined. Occurrence and risk of periodontal outcomes were compared across 3 different measurements of obesity (body mass index, waist–hip ratio, and body fat percentage). The prevalence of periodontitis in obese group (37.0%, 36.4%, and 24.6% by body mass index, waist–hip ratio, and body fat percentage, respectively) or Type 2 diabetic group (50.7%) was significantly higher than those without these conditions (p < .05). Subjects with obesity or Type 2 diabetes had significantly greater pocket depth and clinical attachment loss than those who are not obese or diabetic (p < .001). Multivariate logistic regression, adjusted for confounding variables, showed that the likelihood (odds ratio, OR) for periodontitis was highest in the obese and Type 2 diabetic group (OR = 4.24, CI [2.29, 7.86]; OR = 4.06, CI [2.24, 7.36]; and OR = 5.44, CI [2.94, 10.03]), followed by the obese and non‐Type 2 diabetic group (OR = 2.28, CI [1.05, 4.95]; OR = 2.02, CI [1.34, 3.56]), and then the nonobese and Type 2 diabetic group (OR = 2.20, CI [1.21, 3.98]; OR = 1.99, CI [0.93, 4.24] and OR = 5.22, CI [2.76, 9.84]) when obesity was defined by body mass index, waist–hip ratio, and body fat percentage, respectively, (p < .05). There was a significant association between obesity, Type 2 diabetes, or those with both systemic conditions and periodontitis in Vietnamese patients.

Aim. The aim of our study was to evaluate whether there was a difference in antimicrobial effect between the PRP of healthy volunteers and that of patients with chronic periodontitis against P. gingivalis, which was fresh cultured from subgingival plaque. Methods. Subgingival plaque of patients with moderate and severe chronic periodontitis was collected to isolate P. gingivalis. The PRP of four individuals with healthy periodontium and four patients with moderate and severe periodontitis were collected with a specific kit using a two-centrifuge procedure, and then, the antibacterial properties against P. gingivalis were tested, through their minimum inhibitory concentration (MIC), adhesion resistance assay, and biofilm susceptibility assay. Results. P. gingivalis was successfully isolated from the subgingival plaque of the 21st patient. The round, smooth, and black colony appeared in the agar disk after 7–10 days of incubation under anaerobic conditions. Bacterial identification was performed by MALDI-TOF and confirmed by PCR. All PRP samples tested showed the ability to inhibit P. gingivalis growth. The MIC value (expressed as fraction of PRP) was 1/2, and PRP prevented P. gingivalis attachment on the disk surface. However, PRP did not have a strong effect on the suppression of P. gingivalis biofilm. Conclusion. PRP of individuals with healthy periodontium and chronic periodontitis patients showed antibacterial properties against P. gingivalis. This material can become an adjunct to periodontal treatment.