Articles in press have been peer-reviewed and accepted, which are not yet assigned to volumes /issues, but are citable by Digital Object Identifier (DOI).
Climate and weather significantly influence the duration, timing, and intensity of disease outbreaks, reshaping the global landscape of infectious diseases. Rising temperatures and shifts in precipitation patterns driven by climate change can directly impact the survival and reproduction of pathogens and vector organisms. Moreover, climate change is expected to exacerbate extreme weather events, including floods and droughts, which can disrupt infrastructure and increase the risk of water- and foodborne diseases. There are potential shifts in the temporal and spatial patterns of infectious disease transmission owing to climate change. Furthermore, climate change may alter the epidemiology of vaccine-preventable diseases. These climatic variations not only affect the ecological characteristics of pathogens and vectors but also indirectly influence human behaviors and socioeconomic conditions, further amplifying disease transmission risks. Addressing this challenge requires an interdisciplinary collaboration and comprehensive public health strategies. This review aims to synthesize the current evidence on the impact of climate change on climate-sensitive infectious diseases and elucidate the underlying mechanisms and transmission pathways. Additionally, we explored adaptive policy strategies to mitigate the public health burden of infectious diseases in the context of climate change, offering insights for global health governance and disease control efforts.
In press
, Available online ,
doi: 10.3967/bes2025.100
Cardiovascular diseases (CVD) and their risk factors have an increasingly considerable impact on public health, with their incidence rates continuing to rise globally. This article interprets the essentials of the newly published Annual Report on Cardiovascular Health and Diseases in China (2024), aiming to offer scientific evidence for CVD prevention, treatment, and the formulation of relevant policies.
In press
, Available online ,
doi: 10.3967/bes2025.098
Hypertrophic cardiomyopathy (HCM) is a major contributor to cardiovascular diseases (CVD), the leading cause of death globally. HCM can precipitate heart failure (HF) by causing the cardiac tissue to weaken and stretch, thereby impairing its pumping efficiency. Moreover, HCM increases the risk of atrial fibrillation, which in turn elevates the likelihood of thrombus formation and stroke. Given these significant clinical ramifications, research into the etiology and pathogenesis of HCM is intensifying at multiple levels. In this review, we discuss and synthesize the latest findings on HCM pathogenesis, drawing on key experimental studies conducted both in vitro and in vivo. We also offer our insights and perspectives on these mechanisms, while highlighting the limitations of current research. Advancing fundamental research in this area is essential for developing effective therapeutic interventions and enhancing the clinical management of HCM.
Column
2025, 38(7): 779-780.
doi: 10.3967/bes2025.091
Objectives This study aimed to investigate the impact of foam macrophages (FMs) on the intracellular survival of Mycobacterium tuberculosis (MTB) and identify the molecular mechanisms influencing MTB survival. Methods An in vitro FM model was established using oleic acid induction. Transcriptomic and metabolomic analyses were conducted to identify the key molecular pathways involved in FM-mediated MTB survival. Results Induced FMs effectively restricted MTB survival. Transcriptomic and metabolomic profiling revealed distinct changes in gene and metabolite expression in FMs during MTB infection compared with normal macrophages. Integrated analyses identified significant alterations in the cyclic adenosine monophosphate (cAMP) signaling pathway, indicating that its activation contributes to the FM-mediated restriction of MTB survival. Conclusions FMs inhibit MTB survival. The cAMP signaling pathway is a key contributor. These findings enhance the understanding of the role of FMs in tuberculosis progression, suggest potential targets for host-directed therapies, and offer new directions for developing diagnostic and therapeutic strategies against tuberculosis.
Objective To assess the independent and combined effects of air pollutants, meteorological factors, and greenspace exposure on new tuberculosis (TB) cases. Methods TB case data from Shanghai (2013–2018) were obtained from the Shanghai Center for Disease Control and Prevention. Environmental data on air pollutants, meteorological variables, and greenspace exposure were obtained from the National Tibetan Plateau Data Center. We employed a distributed-lag nonlinear model to assess the effects of these environmental factors on TB cases. Results Increased TB risk was linked to PM2.5, PM10, and rainfall, whereas NO2, SO2, and air pressure were associated with a reduced risk. Specifically, the strongest cumulative effects occurred at various lags: PM2.5 (RR = 1.166, 95% CI: 1.026–1.325) at 0–19 weeks; PM10 (RR = 1.167, 95% CI: 1.028–1.324) at 0–18 weeks; NO2 (RR = 0.968, 95% CI: 0.938–0.999) at 0–1 weeks; SO2 (RR = 0.945, 95% CI: 0.894–0.999) at 0–2 weeks; air pressure (RR = 0.604, 95% CI: 0.447–0.816) at 0–8 weeks; and rainfall (RR = 1.404, 95% CI: 1.076–1.833) at 0–22 weeks. Green space exposure did not significantly impact TB cases. Additionally, low temperatures amplified the effect of PM2.5 on TB. Conclusion Exposure to PM2.5, PM10, and rainfall increased the risk of TB, highlighting the need to address air pollutants for the prevention of TB in Shanghai.
Objective Cigarette smoking exacerbates the progression of pulmonary tuberculosis (TB). The role of tertiary lymphoid structures (TLS) in chronic lung diseases has gained attention; however, it remains unclear whether smoking-exacerbated lung damage in TB is associated with TLS. This study aimed to analyze the characteristics of pulmonary TLS in smokers with TB and to explore the possible role of TLS in smoking-related lung injury in TB. Methods Lung tissues from 36 male patients (18 smokers and 18 non-smokers) who underwent surgical resection for pulmonary TB were included in this study. Pathological and immunohistological analyses were conducted to evaluate the quantity of TLS, and chest computed tomography (CT) was used to assess the severity of lung lesions. The correlation between the TLS quantity and TB lesion severity scores was analyzed. The immune cells and chemokines involved in TLS formation were also evaluated and compared between smokers and non-smokers. Results Smoker patients with TB had significantly higher TLS than non-smokers (P < 0.001). The TLS quantity in both the lung parenchyma and peribronchial regions correlated with TB lesion severity on chest CT (parenchyma: r = 0.5767; peribronchial: r = 0.7373; both P < 0.001). Immunohistochemical analysis showed increased B cells, T cells, and C-X-C motif chemokine ligand 13 (CXCL13) expression in smoker patients with TB (P < 0.001). Conclusion Smoker TB patients exhibited increased pulmonary TLS, which was associated with exacerbated lung lesions on chest CT, suggesting that cigarette smoking may exacerbate lung damage by promoting TLS formation.
Objective To investigate the spatiotemporal patterns and socioeconomic factors influencing the incidence of tuberculosis (TB) in the Guangdong Province between 2010 and 2019. Method Spatial and temporal variations in TB incidence were mapped using heat maps and hierarchical clustering. Socioenvironmental influencing factors were evaluated using a Bayesian spatiotemporal conditional autoregressive (ST-CAR) model. Results Annual incidence of TB in Guangdong decreased from 91.85/100,000 in 2010 to 53.06/100,000 in 2019. Spatial hotspots were found in northeastern Guangdong, particularly in Heyuan, Shanwei, and Shantou, while Shenzhen, Dongguan, and Foshan had the lowest rates in the Pearl River Delta. The ST-CAR model showed that the TB risk was lower with higher per capita Gross Domestic Product (GDP) [Relative Risk (RR), 0.91; 95% Confidence Interval (CI): 0.86–0.98], more the ratio of licensed physicians and physician (RR, 0.94; 95% CI: 0.90-0.98), and higher per capita public expenditure (RR, 0.94; 95% CI: 0.90–0.97), with a marginal effect of population density (RR, 0.86; 95% CI: 0.86–1.00). Conclusion The incidence of TB in Guangdong varies spatially and temporally. Areas with poor economic conditions and insufficient healthcare resources are at an increased risk of TB infection. Strategies focusing on equitable health resource distribution and economic development are the key to TB control.
Objective To investigate chronic hepatitis C virus (HCV) infection’s effect on gestational liver function, pregnancy and delivery complications, and neonatal development. Methods A total of 157 HCV antibody-positive (anti-HCV[+]) and HCV RNA(+) patients (Group C) and 121 anti-HCV(+) and HCV RNA(-) patients (Group B) were included as study participants, while 142 anti-HCV(-) and HCV RNA(-) patients (Group A) were the control group. Data on biochemical indices during pregnancy, pregnancy complications, delivery-related information, and neonatal complications were also collected. Results Elevated alanine aminotransferase (ALT) rates in Group C during early, middle, and late pregnancy were 59.87%, 43.95%, and 42.04%, respectively—significantly higher than Groups B (26.45%, 15.70%, 10.74%) and A (23.94%, 19.01%, 6.34%) (P < 0.05). Median ALT levels in Group C were significantly higher than in Groups A and B at all pregnancy stages (P < 0.05). No significant differences were found in neonatal malformation rates across groups (P > 0.05). However, neonatal jaundice incidence was significantly greater in Group C (75.16%) compared to Groups A (42.25%) and B (57.02%) (χ2 = 33.552, P < 0.001). HCV RNA positivity during pregnancy was an independent risk factor for neonatal jaundice (OR = 2.111, 95% CI 1.242–3.588, P = 0.006). Conclusions Chronic HCV infection can affect the liver function of pregnant women, but does not increase the pregnancy or delivery complication risks. HCV RNA(+) is an independent risk factor for neonatal jaundice.
Objective This study aimed to investigate the prevalence of HIV pretreatment drug resistance (PDR) and the transmission clusters associated with PDR-related mutations in newly diagnosed, treatment-naive patients between 2020 and 2023 in Dehong prefecture, Yunnan province, China. Methods Demographic information and plasma samples were collected from study participants. PDR was assessed using the Stanford HIV Drug Resistance Database. The Tamura-Nei 93 model within HIV-TRACE was employed to compute pairwise matches with a genetic distance of 0.015 substitutions per site. Results Among 948 treatment-naive individuals with eligible sequences, 36 HIV subtypes were identified, with unique recombinant forms (URFs) being the most prevalent (18.8%, 178/948). The overall prevalence of PDR was 12.4% (118/948), and resistance to non-nucleotide reverse transcriptase inhibitors (NNRTIs), nucleotide reverse transcriptase inhibitors (NRTIs), and protease inhibitors (PIs) was 10.7%, 1.3%, and 1.6%, respectively. A total of 91 clusters were identified, among which eight showed evidence of PDR strain transmission. The largest PDR-associated cluster consisted of six CRF01_AE drug-resistant strains carrying K103N and V179T mutations; five of these individuals had initial CD4+ cell counts < 200 cells/μL. Conclusion The distribution of HIV subtypes in Dehong is diverse and complex. PDR was moderately prevalent (12.4%) between 2020 and 2023. Evidence of transmission of CRF01_AE strains carrying K103N and V179T mutations was found. Routine surveillance of PDR and the strengthening of control measures are essential to limit the spread of drug-resistance HIV strains.
Objective Human brucellosis is a serious public health concern in the Xilingol League, Inner Mongolia; however, the epidemic trends are unclear. Method In this study, Joinpoint regression analysis and spatiotemporal analysis were applied to investigate the epidemic evolution of human brucellosis. Result From 2004 to 2023, a total of 35,747 cases were reported, with an annual average of 1787.35 cases and an annual average incidence rate of 176.04/100,000. The incidence increased from 173.96/100,000 in 2004 to 500.71/100,000 in 2009 and fluctuated to 61.43/100,000 in 2023. Three epidemic join points were observed in which the disease experienced an alternative rise and fall, peaking in 2009 (APC = 21.73, P > 0.001) and 2020 (APC = 21.51, P > 0.001). The disease showed a persistent decline trend in lentitude (AAPC = –5.30, P > 0.001), suggesting challenges in disease control and a higher risk of rebound. The most cases were reported in Xilinhot City (n = 4,777), followed by 4,391 in Sonid Left Banner, and 4,324 in Abaga Banner. Spatiotemporal analysis revealed two high clusters (CI and CII) from 2005 to 2012, the high cluster encompassing eight counties and shifting from north to south. Conclusion The present analysis highlights that human brucellosis has decreased significantly in the Xilingol League, but the epidemic is still severe; further implementation of a strict control program is necessary.
Objective Pseudomonas aeruginosa (P. aeruginosa) is a prevalent pathogenic bacterium involved in meningitis; however, the virulence factors contributing to this disease remain poorly understood. Methods The virulence of the P. aeruginosa A584, isolated from meningitis samples, was evaluated by constructing in vitro blood-brain barrier and in vivo systemic infection models. qPCR, whole-genome sequencing, and drug efflux assays of A584 were performed to analyze the virulence factors. Results Genomic sequencing showed that A584 formed a phylogenetic cluster with the reference strains NY7610, DDRC3, Pa58, and Pa124. Its genome includes abundant virulence factors, such as hemolysin, the Type IV secretion system, and pyoverdine. A584 is a multidrug-resistant strain, and its wide-spectrum resistance is associated with enhanced drug efflux. Moreover, this strain caused significantly more severe damage to the blood-brain barrier than the standard strain, PAO1. qPCR assays further revealed the downregulation of the blood-brain barrier-associated proteins Claudin-5 and Occludin by A584. During systemic infection, A584 exhibited a higher capacity of brain colonization than PAO1 (37.1 × 106 CFU/g brain versus 2.5 × 106 CFU/g brain), leading to higher levels of the pro-inflammatory factors IL-1β and TNF-α. Conclusion This study sheds light on the virulence factors of P. aeruginosa involved in meningitis.
2015, 28(1): 57-71.
doi: 10.3967/bes2015.006
2022, 35(7): 573-603.
doi: 10.3967/bes2022.079
2018, 31(2): 87-96.
doi: 10.3967/bes2018.011
2023, 36(8): 669-701.
doi: 10.3967/bes2023.106
2012, 25(3): 317-324.
doi: 10.3967/0895-3988.2012.03.010
2019, 32(8): 559-570.
doi: 10.3967/bes2019.074
2014, 27(8): 606-613.
doi: 10.3967/bes2014.093
2018, 31(3): 208-214.
doi: 10.3967/bes2018.026
2003, 16(3): 246-255.
2019, 32(9): 659-672.
doi: 10.3967/bes2019.085
2022, 35(5): 381-392.
doi: 10.3967/bes2022.054
2016, 29(3): 212-218.
doi: 10.3967/bes2016.026
2022, 35(7): 648-651.
doi: 10.3967/bes2022.084
2018, 31(9): 637-644.
doi: 10.3967/bes2018.088
2019, 32(8): 578-591.
doi: 10.3967/bes2019.076
2019, 32(10): 769-778.
doi: 10.3967/bes2019.096
2017, 30(5): 384-389.
doi: 10.3967/bes2017.051
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