ACE I/D (Rs1799752), MTHFR C677T (Rs1801133), and CCR5 D32 (Rs333) Genes and their Association with Hypertension and Diabetic Nephropathy in Urban Areas of Costa Rica, Nicaragua, and Mexico

Aim: Type 2 diabetes mellitus (T2DM) is a procoagulant state because it is associated with increased risk of atherosclerosis. The purpose of this study was to investigate the prevalence in thrombotic markers that lead to hypercoagulability and its association with hypertension and diabetic nephropathy (DN)

Dengue immunopathogenesis : a cross talk between host and viral factors leading to disease : part I - Dengue virus tropism, host innate immune responses, and subversion of antiviral responses

Two part articleThis detailed paper addresses the general features of the dengue virus (DENV) infections complex, including the virus structure and genome, epidemiology, and clinical outcomes. This is followed by an updated review of the literature describing the host innate immune strategies as well as the viral mechanisms acting against and in favor of the DENV replication cycle and infection.Canadian Institutes of Health ResearchFondo Mixto CONACYT-Gobierno del Estado de Yucatá

Dengue Immunopathogenesis: A Crosstalk between Host and Viral Factors Leading to Disease: Part I - Dengue Virus Tropism, Host Innate Immune Responses, and Subversion of Antiviral Responses

Dengue is the most prevalent emerging mosquito-borne viral disease, affecting more than 40% of the human population worldwide. Many symptomatic dengue virus (DENV) infections result in a relatively benign disease course known as dengue fever (DF). However, a small proportion of patients develop severe clinical manifestations, englobed in two main categories known as dengue hemorrhagic fever (DHF) and dengue shock syndrome (DSS). Secondary infection with any of the four dengue virus serotypes (DENV1, -2, -3, and -4) is a risk factor to develop severe forms of dengue disease. DSS is primarily characterized by sudden and abrupt endothelial dysfunction, resulting in vascular leak and organ impairment, which may progress to hypovolemic shock and death. Severe DENV disease (DHF/DSS) is thought to follow a complex relationship between distinct immunopathogenic processes involving host and viral factors, such as the serotype cross-reactive antibody-dependent enhancement (ADE), the activation of T cells and complement pathways, the phenomenon of the cytokine storm, and the newly described viral toxin activity of the nonstructural protein 1 (NS1), which together play critical roles in inducing vascular leak and virus pathogenesis. In this chapter that is divided in two parts, we will outline the recent advances in our understanding of DENV pathogenesis, highlighting key viral-host interactions and discussing how these interactions may contribute to DENV immunopathology and the development of vascular leak, a hallmark of severe dengue. Part I will address the general features of the DENV complex, including the virus structure and genome, epidemiology, and clinical outcomes, followed by an updated review of the literature describing the host innate immune strategies as well as the viral mechanisms acting against and in favor of the DENV replication cycle and infection

Dengue Immunopathogenesis: A Crosstalk between Host and Viral Factors Leading to Disease: PART II - DENV Infection, Adaptive Immune Responses, and NS1 Pathogenesis

Severe disease is associated with serial infection with DENV of different serotypes. Thus, primary DENV infections normally cause asymptomatic infections, and secondary heterotypic infections with a new DENV serotype potentially increase the risks of developing severe disease. Despite many proposed hypotheses trying to explain it, the exact immunological mechanism leading to severe dengue disease is unknown. In turn, severe manifestations are believed to be a consequence of the combinations of many immunopathogenic mechanisms involving viral and host factors leading to increased pathogenesis and disease. Of these mechanisms, the adaptive immune response has been proposed to play a critical role in the development of severe dengue manifestations. This includes the effect of non-neutralizing but enhancing antibodies produced during primary infections, which results in enhanced-DENV infection of Fc-γ-receptor-expressing cells (e.g. monocytes and macrophages) during DENV heterotypic exposure in a phenomenon called antibody-dependent enhancement (ADE); the increased activation of memory T cells during secondary infections, which has low affinity for the current infecting serotype and high affinity for a past infection with a different serotype known as the original antigenic sin; the unbalanced production of pro-inflammatory cytokines that have a direct effect on vascular endothelial cells resulting in plasma leak in a phenomenon known as cytokine storm; and the excessive activation of the complement system that causes exacerbated inflammatory responses, increasing disease severity. In addition to the adaptive immune responses, a secreted viral factor known as the nonstructural protein 1 (NS1) has been recently proposed as the missing corner piece of the DENV pathogenesis influencing disease. This Part II of the chapter will discuss the interplay between the distinct host adaptive immune responses and viral factors that together contribute to the development of DENV pathogenesis and severe disease

Estimating absolute indoor density of Aedes aegypti using removal sampling

Exhaustive removal sampling represents a promising method for quantification of absolute indoor Aedes aegypti density, leading to improved entomological estimates of mosquito distribution. The study describes the use of sequential removal sampling to estimate absolute numbers of indoor resting Aedes in the city of Merida, Mexico. The study was performed in 200 houses based on recent occurrence of Aedes-borne viral illness in residents. The lack of a numerical association between relative and absolute density of adult Ae. aegypti represent a significant gap in vector surveillance. Merida is highly endemic for dengue and other Aedes-borne viruses.Bureau for Global HealthU.S Agency for International Development (USAID)US Centers for Disease Control and Prevention (CDC)Canadian Institutes of Health Research (CIHR

Photography-based taxonomy is inadequate, unnecessary, and potentially harmful for biological sciences

The question whether taxonomic descriptions naming new animal species without type specimen(s) deposited in collections should be accepted for publication by scientific journals and allowed by the Code has already been discussed in Zootaxa (Dubois & Nemésio 2007; Donegan 2008, 2009; Nemésio 2009a–b; Dubois 2009; Gentile & Snell 2009; Minelli 2009; Cianferoni & Bartolozzi 2016; Amorim et al. 2016). This question was again raised in a letter supported by 35 signatories published in the journal Nature (Pape et al. 2016) on 15 September 2016. On 25 September 2016, the following rebuttal (strictly limited to 300 words as per the editorial rules of Nature) was submitted to Nature, which on 18 October 2016 refused to publish it. As we think this problem is a very important one for zoological taxonomy, this text is published here exactly as submitted to Nature, followed by the list of the 493 taxonomists and collection-based researchers who signed it in the short time span from 20 September to 6 October 2016

Dengue immunopathogenesis : a crosstalk between host and viral factors leading to disease : part II—DENV infection, adaptive immune responses, and NS1 pathogenesis

Two part articleThis chapter details the interplay between distinct host adaptive immune responses and viral factors that together contribute to the development of the dengue virus (DENV) pathogenesis and severe disease. As Part II, it addresses: the multifactorial immunopathogenic process of DENV infection from the perspective of the pre-existing serotype cross-reactive antibodies; the hyperactivation of DENV infected immune cells (monocytes, mast cells) leading to increased cytokine production; the role of T cell responses; the activation of complement pathways; and the new pathogenic roles of the secreted NS1 of DENV that may act together to occasionally cause severe dengue manifestations.Canadian Institutes of Health ResearchFondo Mixto CONACYT-Gobierno del Estado de Yucata