[Epidemiological and virus molecular characterization of dengue fever outbreak in Hunan province, 2018].

Objective: To analyze the epidemiological and etiological characteristics of a dengue fever outbreak in Hunan province in 2018. Methods: Real-time PCR assay was performed for the laboratory diagnosis of 8 suspected dengue fever cases. Etiological surveillance was performed in 186 suspected dengue fever cases and fever cases who had close contacts with dengue fever patients. C6/36 cells was used for the virus isolation from acute phase serum. By sequencing the full length of E genes of 15 dengue virus strains, phylogenetic analysis was performed based on the sequences obtained, including reference sequences from the NCBI GenBank database, the serotypes and gene subtypes of the virus were analyzed to trace the possible source of transmission. An emergency monitoring of vector density and a retrospective survey of sero-epidemiology in healthy population were conducted in the epidemic area. Results: In the serum samples of 8 suspected patients, 6 were dengue virus RNA positive, and 4 were NS1 antigen positive. In 186 suspected patients, 96 were dengue virus nucleic acid, NS1 antigen or antibody positive in etiological test. A total of 64 dengue virus strains were isolated. The phylogenetic analysis showed that all the dengue virus strains belonged to type 2, which might be from Guangdong or Zhejiang provinces. The Bretub index was up to 65, indicating an extremely high risk of transmission. The positive rate of the dengue virus IgG antibody was 0.53%(2/377) in retrospective survey of 377 healthy people. Conclusion: The field epidemiologic and the molecular genetics analyses showed the outbreak of dengue fever in Hunan in 2018 was caused by imported cases and dengue virus 2.

[Strategy for prevention and control of imported infectious disease].

The process of globalization increases the risk of global transmission of infectious diseases, resulting in pressure for country's prevention and control of imported infectious disease. Based on the risk assessment of disease importation and local transmission, a strategy that conducting importation prevention and routine prevention and control before the importation of disease and taking emergency control measures after the importation of disease was developed. In addition, it is important to take part in global infectious disease response action, aid the countries with outbreak or epidemic to actively decrease the risk of disease importation.

Environmental variability and the transmission of haemorrhagic fever with renal syndrome in Changsha, People's Republic of China.

The transmission of haemorrhagic fever with renal syndrome (HFRS) is influenced by climatic, reservoir and environmental variables. The epidemiology of the disease was studied over a 6-year period in Changsha. Variables relating to climate, environment, rodent host distribution and disease occurrence were collected monthly and analysed using a time-series adjusted Poisson regression model. It was found that the density of the rodent host and multivariate El Niño Southern Oscillation index had the greatest effect on the transmission of HFRS with lags of 2­6 months. However, a number of climatic and environmental factors played important roles in affecting the density and transmission potential of the rodent host population. It was concluded that the measurement of a number of these variables could be used in disease surveillance to give useful advance warning of potential disease epidemics.

[Study of the mechanism of cultured neuron injury mediated by nitric oxide during hypoxia and oxidative stress].

OBJECTIVE: To study the mechanisms of cultured neurons injury mediated by nitric oxide and free oxygen radical during hypoxia and oxidative stress. METHODS: The cultured newborn rat neurons were treated with hypoxia, H2O2 and pretreated superoxide dismutase (SOD) respectively. We examined the content of NO, malonaldehyde (MDA), lactate dehydrogenase (LDH) and SOD in cultured supernatant. RESULTS: Comparing with that of control group, the content of NO, LDH, MDA increased and the content of SOD decreased in hypoxia group and H2O2 group. The content between NO and SOD showed the negative correlation. Administration of 200 U/ml SOD before oxidative stress could efficiently decrease the release of NO, LDH and MDA in neurons. The content of NO, LDH and MDA manifested in positive correlation in each group. CONCLUSION: Hypoxia and oxidative stress increased NO production which strengthen neurons injury induced by free radical. SOD played an important role in elimination of free oxygen radicals and protecting neurons from injury by NO.