COVID-19 Outbreak in a Military Unit in Korea.

OBJECTIVES: This study presents the response of a military unit to the COVID-19 outbreak in Gyeonggi Province. As soon as two soldiers were identified as index cases, the infectious disease investigators of the Gyeonggi Provincial Government, Korea Disease Control and Prevention Agency and the Armed Forces Epidemiologic Investigation Center, discussed the investigation and response plan for an imminent massive outbreak. METHODS: The joint immediate response team (IRT) conducted interviews with confirmed patients with COVID-19, reviewed medical records, performed contact tracing using global positioning system (GPS), and undertook a field investigation. For risk assessment, the joint IRT visited all eight sites of the military units and the army chaplain's church to evaluate the transmission risk of each site. The evaluation items included the size of the site, the use of air conditioning, whether windows were opened, and whether masks were worn. A pooled testing was used for a low-risk population to quickly detect the spread of COVID-19 in the military base. RESULTS: A day before the symptom onset of the index case, the lecturer and >50% of the attendees were infected with COVID-19 while attending a lecture that lasted 2 h and 30 min. Attendees were not wearing masks and were in a poorly ventilated room. CONCLUSION: Since the disease can be spread before symptom onset, contact tracing must be performed to investigate potential exposures prior to symptom onset and manage any exposed persons.

Construction and characterization of an Actinobacillus pleuropneumoniae serotype 2 mutant lacking the Apx toxin secretion protein genes apxIIIB and apxIIID.

Apx toxins have been identified as important virulence factors of Actinobacillus pleuropneumoniae, the etiologic agent of porcine pleuropneumonia. In some A. pleuropneumoniae serotypes, Apx toxins are secreted by the cell membrane proteins encoded by apxIIIB and apxIIID genes. In an effort to develop a live vaccine strain against A. pleuropneumoniae, we inactivated the apxIIIB and apxIIID genes in A. pleuropneumoniae 1536, a serotype 2 strain, resulting in the DeltaapxIIIB/DapxIIID mutant strain (1536DeltaBDeltaD). Immunization of pigs with live 1536DeltaBDeltaD A. pleuropneumoniae conferred protection against homologous challenge with wild-type A. pleuropneumoniae 1536. Thus, impaired Apx toxin secretion may decrease the virulence of A. pleuropneumoniae and may be an effective strategy for the development of a live-attenuated A. pleuropneumoniae vaccine.

Association of the G134A and G184C Polymorphisms in the CYP1A1 Gene with Lung Cancer Incidence.

The G184C and G134A single nucleotide polymorphisms (SNPs) of the CYP1A1 gene result in Ala62Pro and Gly45Asp substitutions, respectively. Here, we tested whether these SNPs are associated with an alteration in lung cancer incidence. We examined 80 Korean subjects with lung cancer and 240 age- and sex-matched controls. For each subject, the CYP1A1 gene was PCR amplified and sequenced. We observed that the odds ratio (OR) for lung cancer was 3.37 higher in subjects with the G184C polymorphism than in controls (95% confidence interval (CI), 0.89~12.73, P = 0.07). In contrast, the OR for lung cancer was 1.23 in subjects with the G134A polymorphism compared to controls (95% CI, 0.68~2.20, P = 0.49). The G184C polymorphism exacerbated the effects of smoking on lung cancer development. Gene-smoking interaction analyses revealed that past or present smokers with the G184C polymorphism had a higher incidence of lung cancer (OR, 24.72; 95% CI, 4.48~136.31; P < 0.01) than control smokers (OR, 6.65; 95% CI, 2.72~16.28; P < 0.01). However, there was only a slight difference in the ORs for lung cancer between control smokers and smokers with the G134A polymorphism. These findings suggest that the G184C polymorphism, but not the G134A polymorphism, is associated with an increased risk of lung cancer.

Arsenic-induced toxicity and the protective role of ascorbic acid in mouse testis.

Oxidative stress has been suggested to be a major cause of male reproductive failure. Here, we investigated whether arsenic, which impairs male reproductive functions in rodent models, acts by inducing oxidative stress. Male 8-week-old ICR mice were given drinking water containing 20 or 40 mg/l sodium arsenite with or without 0.75 or 1.5 g/l of the antioxidant ascorbic acid for 5 weeks. The arsenic-treated mice showed decreased epididymidal sperm counts and testicular weights compared to untreated mice. These effects were reversed in mice that were co-treated with ascorbic acid. Similarly, arsenic treatment lowered the activities of testicular 3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD, which play important roles in steroidogenesis, and this was reversed by co-treatment with ascorbic acid. The testicles of arsenic-treated mice had decreased glutathione (GSH) levels (which correlate inversely with the degree of cellular oxidative stress) and elevated levels of protein carbonyl (a marker of oxidative damage to tissue proteins). Ascorbic acid co-treatment reversed both of these effects. Thus, ascorbic acid blocks both the adverse effects of arsenic on male reproductive functions and the arsenic-induced testicular oxidative changes. These observations support the notion that arsenic impairs male reproductive function by inducing oxidative stress.