We took advantage of the 2015-2016 Brazilian arbovirus outbreak (ZIKV/DENV/CHIKV), associated with neurological complications, to type HLA-DRB1/DQA1/DQB1 variants in patients exhibiting neurological complications and in bone marrow donors from the same endemic geographical region.
 
  . DRB1/DQA1/DQB1 loci were typed using sequence-specific oligonucleotides. In silico studies were performed using X-ray resolved dimer constructions.
 
  The DQA1*01, DQA1*05, DQB1*02 or DQB1*06 genotypes/haplotypes and DQA1/DQB1 haplotypes that encode the putative DQA1/DQB1 dimers were overrepresented in the whole group of patients and in patients exhibiting peripheral neurological spectrum disorders (PSD) or encephalitis spectrum disorders (ESD). The DRB1*04, DRB1*13 and DQA1*03 allele groups protected against arbovirus neurological manifestation, being underrepresented in whole group of patients and/or ESD, PSD groups. Genetic and in silico studies revealed that DQA1/DQB1 dimers i) were primarily associated with susceptibility to arbovirus infections, ii) can bind to a broad range of ZIKV peptides (235 out of a library of 1,878 peptides, stressing prM and NS2A), and iii) exhibited hydrophilic and highly positively charged grooves when compared to the DRA1/DRB1 cleft. The protective dimer (DRA1/DRB1*04) bound a limited number of ZIKV peptides (40 out of 1,878 peptides, primarily prM).
 
  Protective haplotypes may recognize arbovirus peptides more specifically than susceptible haplotypes.
 Protective haplotypes may recognize arbovirus peptides more specifically than susceptible haplotypes.
  This commentary addresses the state of the evidence on tobacco products, nicotine, and COVID-19. The evidence of the effects of smoking on respiratory infections and the immune system in general are examined and the current understanding of tobacco products and risk for SARS-CoV-2 infection and the course of COVID-19 is addressed.
 This commentary addresses the state of the evidence on tobacco products, nicotine, and COVID-19. The evidence of the effects of smoking on respiratory infections and the immune system in general are examined and the current understanding of tobacco products and risk for SARS-CoV-2 infection and the course of COVID-19 is addressed.Implications In this commentary, we describe the evidence-based approach used to identify the primary cause of EVALI and to curb the 2019 outbreak. We also discuss future research opportunities and public health practice considerations to prevent a resurgence of EVALI.
  This study assessed the association of exclusive and concurrent use of cigarettes, electronic nicotine delivery systems (ENDS), and cigars with ever and past 12-month wheezing symptoms among a nationally representative sample of US adult current tobacco users.
 
  Cross-sectional data from the Population Assessment of Tobacco and Health (PATH) Study Wave 3 (W3) were used.  https://www.selleckchem.com/products/yd23.html  The weighted prevalence of self-reported ever and past 12-month wheezing symptoms for noncurrent users compared with users of cigarettes, ENDS, cigars, and any combination of these products (polytobacco use of these tobacco products) were presented for 28 082 adults. The cross-sectional association of tobacco use with self-reported wheezing symptoms was assessed using weighted multivariable and ordinal logistic regression with consideration of complex sampling design.
 
  Significantly higher odds of ever had wheezing or whistling in the chest at any time in the past were observed among current cigarette (adjusted odds ratio 2.62, 95% confidenymptoms were found to be the strongest among cigarette users, exclusively or in combination. Future longitudinal research is needed to better understand how cigarette use interacts with other tobacco and nicotine products and contributes to respiratory symptoms.
  Flavor aldehydes in e-cigarettes, including vanillin, ethyl vanillin (vanilla), and benzaldehyde (berry/fruit), rapidly undergo chemical reactions with the e-liquid solvents, propylene glycol, and vegetable glycerol (PG/VG), to form chemical adducts named flavor aldehyde PG/VG acetals that can efficiently transfer to e-cigarette aerosol. The objective of this study was to compare the cytotoxic and metabolic toxic effects of acetals and their parent aldehydes in respiratory epithelial cells.
 
  Cell metabolic assays were carried out in bronchial (BEAS-2B) and alveolar (A549) epithelial cells assessing the effects of benzaldehyde, vanillin, ethyl vanillin, and their corresponding PG acetals on key bioenergetic parameters of mitochondrial function. The potential cytotoxic effects of benzaldehyde and vanillin and their corresponding PG acetals were analyzed using the LIVE/DEAD cell assay in BEAS-2B cells and primary human nasal epithelial cells (HNEpC). Cytostatic effects of vanillin and vanillin PG acetal were ggests that manufacturers' disclosure of e-liquid ingredients at time of production may be insufficient to inform a comprehensive risk assessment of e-liquids and electronic nicotine delivery systems use, due to the chemical instability of e-liquids over time and the formation of new compounds.
 With no inhalation toxicity studies available for acetals, data from this study will provide a basis for further toxicological studies using in vitro and in vivo models. This study suggests that manufacturers' disclosure of e-liquid ingredients at time of production may be insufficient to inform a comprehensive risk assessment of e-liquids and electronic nicotine delivery systems use, due to the chemical instability of e-liquids over time and the formation of new compounds.
  The link between e-cigarette use and subsequent development of respiratory diseases remains an open question.
 
  A subset of a probability sample of U.S. adults from the Population Assessment of Tobacco and Health Study Waves 1 and 2 were selected for biospecimen analysis (n = 4614). Subjects were divided into three mutually exclusive groups at baseline nonusers (n = 2849), exclusive e-cigarette users (n = 222), and poly e-cigarette/tobacco users (n = 1,543). Geometric mean concentrations of baseline biomarkers from five classes of harmful and potentially harmful constituents were reported. Multivariable linear regressions were conducted to examine the relationship between baseline biomarkers and subsequent respiratory symptoms among user groups.
 
  Baseline exclusive e-cigarette users (33.6%[confidence interval, CI 26.7% to 41.4%]) and poly e-cigarette/tobacco users (50.8%[CI 47.4% to 54.2%]) had higher prevalence of subsequent respiratory symptoms than nonusers (21.7%[19.2% to 24.4%]). As compared with nonusers, poly e-cigarette/tobacco users had higher concentrations in clinically relevant biomarkers at baseline than exclusive e-cigarette users.