title: Hygrothermal environment may cause influenza pandemics through immune suppression.
abstract: Over the past few decades, climate warming has caused profound changes in our living environment, and human diseases, including infectious diseases, have also been influenced by these changes. However, it remains unclear if a warm-wet climate can influence the infectivity of influenza and result in influenza pandemics. This study focused on observations of how the hydrothermal environment influences the infectivity of the influenza virus and the resulting immunoreactions of the infected mice. We used a manual climatic box to establish the following 3 environments with different temperatures and humidity: normal environment (T: 24 ± 1°C, RH: 50% ± 4%), wet environment (T: 24 ± 1 °C, RH: 95% ± 4%) and warm-wet environment (T: 33 ± 1 °C, RH: 95% ± 4%), and the mice were fed and maintained in these 3 different environments. After 14 days, half of the mice were infected with H1N1 (A/FM1/1/47, a lung adapted strain of the flu virus specific for the mouse lung) virus for 4 d After establishing the animal model, we observed the microstructure of the lung tissue, the Th1/Th2 T cell subsets, the Th17/Treg balance, the expression of cytokines in the peripheral blood serum and the expression of the immune recognition RLH signal pathway. The results showed that mice in different environments have different reaction. Results showed that after infection, the proportion of Th1/Th2 and Th17/Treg cells in the spleen was significantly increased, and these proportions were increased the most in the infected group kept in wet-hot conditions. After infection, the mRNA levels and protein expression of the RLH (RIG-1-like helicases) signal pathway components were up-regulated while the uninfected animals in the 3 diverse environments showed no significant change. The infected mice kept in the wet and warm-wet environments showed a slight elevation in the expression of RLH pathway components compared to infected mice maintained in the normal environment. Our study suggested that the warm-wet environment may have interfered with the immune response and balance. The mice kept in the warm-wet environment displayed immune tolerance when they were exposed to the influenza virus, and the body was not able to effectively clear the virus, leading to a persistent infection. A warm-wet climate may thus be a factor that contributes to influenza pandemics, people should focus on the warm-wet climate coming and advance prepare to vaccine manufacture.
authors.affiliation: a Department of Pancreatic Disease Center ; the First Affiliated Hospital of Jinan University ; Guangzhou , China.|b Department of Traditional Chinese Medicine ; Medicine College of Jinan University; Guangzhou , China.
authors.forename: Xian-Lin
authors.initials: XL
authors.lastname: Wu
authors.affiliation: a Department of Pancreatic Disease Center ; the First Affiliated Hospital of Jinan University ; Guangzhou , China.|c Department of Hepatobiliary Surgery ; the First Affiliated Hospital of Jinan University; Guangzhou , China.
authors.forename: Yu-Hong
authors.initials: YH
authors.lastname: Luo
authors.affiliation: b Department of Traditional Chinese Medicine ; Medicine College of Jinan University; Guangzhou , China.
authors.forename: Jia
authors.initials: J
authors.lastname: Chen
authors.affiliation: b Department of Traditional Chinese Medicine ; Medicine College of Jinan University; Guangzhou , China.
authors.forename: Bin
authors.initials: B
authors.lastname: Yu
authors.affiliation: d Department of Internal Medicine , Nancheng People's Hospital , Dongguan , China.
authors.forename: Kang-Li
authors.initials: KL
authors.lastname: Liu
authors.affiliation: b Department of Traditional Chinese Medicine ; Medicine College of Jinan University; Guangzhou , China.
authors.forename: Jin-Xiong
authors.initials: JX
authors.lastname: He
authors.affiliation: b Department of Traditional Chinese Medicine ; Medicine College of Jinan University; Guangzhou , China.
authors.forename: Su-Hong
authors.initials: SH
authors.lastname: Lu
authors.affiliation: a Department of Pancreatic Disease Center ; the First Affiliated Hospital of Jinan University ; Guangzhou , China.|c Department of Hepatobiliary Surgery ; the First Affiliated Hospital of Jinan University; Guangzhou , China.
authors.forename: Jie-Xing
authors.initials: JX
authors.lastname: Li
authors.affiliation: e Department of Microbiology and Immunology , Medical College of Jinan University , Guangzhou , China.
authors.forename: Sha
authors.initials: S
authors.lastname: Wu
authors.affiliation: e Department of Microbiology and Immunology , Medical College of Jinan University , Guangzhou , China.
authors.forename: Zhen-You
authors.initials: ZY
authors.lastname: Jiang
authors.affiliation: b Department of Traditional Chinese Medicine ; Medicine College of Jinan University; Guangzhou , China.
authors.forename: Xiao-Yin
authors.initials: XY
authors.lastname: Chen
mesh_terms: D000818:Animals; D016207:Cytokines / Q000097:blood; D004781:Environmental Exposure; D054884:Host-Pathogen Interactions; D006813:Humidity; D053118:Influenza A Virus, H1N1 Subtype / Q000254:growth & development*; D008168:Lung / Q000473:pathology; D051379:Mice; D009976:Orthomyxoviridae Infections / Q000473:pathology* / Q000821:virology; D013154:Spleen / Q000473:pathology; D016176:T-Lymphocyte Subsets / Q000276:immunology; D013696:Temperature
chemical_list: D016207:Cytokines
keywords: FM1; RLH; immunity; influenza; warm-wet climate