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In 2012, we witnessed a resurgence of West Nile virus (WNV) in the United States, with the largest outbreak of human cases reported since 2003. WNV is now endemic and will continue to produce epidemics over time, therefore defining the long-term consequences of WNV infection is critical. Over a period of eight years, we prospectively followed a cohort of 157 WNV-infected subjects in the Houston metropolitan area to observe recovery over time and define the long-term clinical outcomes. We used survival analysis techniques to determine percentage of recovery over time and the effects of demographic and co-morbid conditions on recovery. We found that 40% of study participants continued to experience symptoms related to their WNV infection up to 8 years later. Having a clinical presentation of encephalitis and being over age 50 were significantly associated with prolonged or poor recovery over time. Since the health and economic impact as a result of prolonged recovery, continued morbidity, and related disability is likely substantial in those infected with WNV, future research should be aimed at developing effective vaccines to prevent illness and novel therapeutics to minimize morbidity, mortality, and long-term complications from infection.

West Nile virus (WNV) has emerged as an important vector-borne pathogen in North America, with more than 3 million estimated to have been infected. Retinopathy from WNV infection has been previously reported in acute cases, though those prior reports did not evaluate the risk of retinopathy based on clinical severity of neurologic disease. The purpose of this cross-sectional study was to perform comprehensive ophthalmological and neurological examinations on 111 patients with a history of West Nile virus infection and describe the ocular manifestations. Out of 111 patients, 27 (24%) had evidence for West Nile virus associated retinopathy (WNVR); this observation was higher (49%) in those patients who initially presented with encephalitis. Individuals with WNVR had more frequent involvement of the macula and peripheral involvement compared to those patients without WNVR (p<0.05). WNVR was also associated with a greater likelihood of abnormal reflexes on neurological exam, poorer learning, greater dependence in activities of daily living, and lower quality of life (p<0.05). WNVR was seen more frequently in elderly patients (age > 60 years), and was associated with higher rates of diabetes mellitus and a history of encephalitis (p<0.05). A multivariable logistic regression revealed that only a history of encephalitis was independently associated with WNVR [Adjusted Odds Ratio = 4.9 (1.8-13.2); p = 0.001]. Our study found that WNVR occurs in one fourth of patients with a history of WNV infection and is more frequently observed in those with apparent severe neurological sequelae (e.g., encephalitis). The clinical relevance of WNVR was supported by its associations with dependence in activities of daily living and lower quality of life. This unique evaluation of WNV patients included fundoscopic examinations and their associations with neurologic impairment. Our findings can be used during ophthalmological consultation for the evaluation, treatment and rehabilitation phases of care for WNV patients.

Relapsing fever spirochetes are tick- and louse-borne pathogens that primarily afflict those in impoverished countries. Historically the pathogens have had a significant impact on public health, yet currently they are often overlooked because of the nonspecific display of disease. In this review, we discuss aspects of relapsing fever (RF) spirochete pathogenesis including the: (1) clinical manifestation of disease; (2) ability to diagnose pathogen exposure; (3) the pathogen’s life cycle in the tick and mammal; and (4) ecological factors contributing to the maintenance of RF spirochetes in nature.

Global food security demands the development and delivery of new technologies to increase and secure cereal production on finite arable land without increasing water and fertilizer use. There are several options for boosting wheat yields, but most offer only small yield increases. Wheat is an inbred plant, and hybrids hold the potential to deliver a major lift in yield and will open a wide range of new breeding opportunities. A series of technological advances are needed as a base for hybrid wheat programmes. These start with major changes in floral development and architecture to separate the sexes and force outcrossing. Male sterility provides the best method to block self-fertilization, and modifying the flower structure will enhance pollen access. The recent explosion in genomic resources and technologies provides new opportunities to overcome these limitations. This review outlines the problems with existing hybrid wheat breeding systems and explores molecular-based technologies that could improve the hybrid production system to reduce hybrid seed production costs, a prerequisite for a commercial hybrid wheat system.

Understanding how cell adhesion proteins form adhesion domains is a key challenge in cell biology. Here, we use single-molecule atomic force microscopy (AFM) to demonstrate the force-induced formation and propagation of adhesion nanodomains in living fungal cells, focusing on the covalently anchored cell-wall protein Als5p from Candida albicans. We show that pulling on single adhesins with AFM tips terminated with specific antibodies triggers the formation of adhesion domains of 100–500 nm and that the force-induced nanodomains propagate over the entire cell surface. Control experiments (with cells lacking Als5p, single-site mutation in the protein, bare tips, and tips modified with irrelevant antibodies) demonstrate that Als5p nanodomains result from protein redistribution triggered by force-induced conformational changes in the initially probed proteins, rather than from nonspecific cell-wall perturbations. Als5p remodeling is independent of cellular metabolic activity because heat-killed cells show the same behavior as live cells. Using AFM and fluorescence microscopy, we also find that nanodomains are formed within ∼30 min and migrate at a speed of ∼20 nm·min⁻¹, indicating that domain formation and propagation are slow, time-dependent processes. These results demonstrate that mechanical stimuli can trigger adhesion nanodomains in fungal cells and suggest that the force-induced clustering of adhesins may be a mechanism for activating cell adhesion.

Cell adhesion molecules in Saccharomyces cerevisiae and Candida albicans contain amyloid-forming sequences that are highly conserved. We have now used site-specific mutagenesis and specific peptide perturbants to explore amyloid-dependent activity in the Candida albicans adhesin Als5p. A V326N substitution in the amyloid-forming region conserved secondary structure and ligand binding, but abrogated formation of amyloid fibrils in soluble Als5p and reduced cell surface thioflavin T fluorescence. When displayed on the cell surface, Als5p with this substitution prevented formation of adhesion nanodomains and formation of large cellular aggregates and model biofilms. In addition, amyloid nanodomains were regulated by exogenous peptides. An amyloid-forming homologous peptide rescued aggregation and biofilm activity of Als5p(V326N) cells, and V326N substitution peptide inhibited aggregation and biofilm activity in Als5p(WT) cells. Therefore, specific site mutation, inhibition by anti-amyloid peturbants, and sequence-specificity of pro-amyloid and anti-amyloid peptides showed that amyloid formation is essential for nanodomain formation and activation.

The study examines the association of gender, parenthood, and marriage with reports of perceived pandemic precarity among Mexican and Central American immigrants during the COVID-19 pandemic (Fall 2020) to understand predictors of vulnerability in periods of crisis. Latinos/as, immigrants, parents, and women have faced significant challenges during the COVID-19 pandemic. Family structure, along with social expectations for gender (i.e., self-sacrificing femininity for women and hegemonic masculinity for men), parenthood, and marriage may explain perceptions of pandemic precarity - defined as the material deprivation and economic anxiety resulting from the COVID-19 pandemic. This study used data from the Hispanic COVID-19 Rapid Response Study (n=400), a follow-up of the VidaSana Study of Mexican and Central American immigrants, to examine how family structure is associated with pandemic precarity (i.e., food, housing, and economic insecurity). Using linear regression models, average marginal effects (AMEs), and tests for group differences we investigate the independent and interactive effects of gender, parenthood, and marriage on pandemic precarity. Men and parents reported the highest pandemic precarity. Fathers reported higher pandemic precarity than mothers. For men, marriage is associated with greater precarity, and for women, marriage is associated with less precarity, yet marriage increased precarity for those without children. We discuss the importance and implications of examining gender along with family structure to understand how immigrant families were faring in response to the pandemic.

Chagas disease (Trypanosoma cruzi infection) is the leading cause of non-ischemic dilated cardiomyopathy in Latin America. Texas, particularly the southern region, has compounding factors that could contribute to T. cruzi transmission; however, epidemiologic studies are lacking. The aim of this study was to ascertain the prevalence of T. cruzi in three different mammalian species (coyotes, stray domestic dogs, and humans) and vectors (Triatoma species) to understand the burden of Chagas disease among sylvatic, peridomestic, and domestic cycles. To determine prevalence of infection, we tested sera from coyotes, stray domestic dogs housed in public shelters, and residents participating in related research studies and found 8%, 3.8%, and 0.36% positive for T. cruzi, respectively. PCR was used to determine the prevalence of T. cruzi DNA in vectors collected in peridomestic locations in the region, with 56.5% testing positive for the parasite, further confirming risk of transmission in the region. Our findings contribute to the growing body of evidence for autochthonous Chagas disease transmission in south Texas. Considering this region has a population of 1.3 million, and up to 30% of T. cruzi infected individuals developing severe cardiac disease, it is imperative that we identify high risk groups for surveillance and treatment purposes.

Chagas disease (Trypanosoma cruzi infection) has recently been identified as an important neglected tropical disease in the United States. Anecdotally referred to as a \"silent killer,\" it leads to the development of potentially fatal cardiac disease in approximately 30% of those infected. In an attempt to better understand the potential of Chagas disease as a significant underlying cause of morbidity in Texas, we performed a historical literature review to assess disease burden. Human reports of triatomine bites and disease exposure were found to be prevalent in Texas. Despite current beliefs that Chagas disease is a recently emerging disease, we report historical references dating as far back as 1935. Both imported cases and autochthonous transmission contribute to the historical disease burden in Texas. We end by discussing the current knowledge gaps, and recommend priorities for advancing further epidemiologic studies and their policy implications.

Alzheimer's disease (AD) pathology can start accumulating 20-30 years before cognitive symptoms occur, with increases in inflammation, amyloid-β (Aβ), and hyperphosphorylated Tau during this time. Previous studies have shown that the post-translational modification of a single N-acetylglucosamine moiety to serine or threonine residues to cytosolic or nuclear proteins, known as O-GlcNAcylation, can modify a plethora of cellular processes, including the processing of the amyloid precursor protein, competing with phosphorylation on tau, as well as having anti-inflammatory effects. This study is designed to evaluate how increasing O-GlcNAcylation is impacting AD pathology in the most comprehensive AD rat model to date, the TgF344-AD rat model. For these experiments, we used 6-month-old TgF344-AD (Tg) rats and non-transgenic (nTg) littermates injected with 10mg/kg of thiamet-G (TMG), an inhibitor of O-GlcNAcase, (nTg-TMG or Tg-TMG) or saline (nTg-S or Tg-S) as a control, 3 times a week from 6-9 months. We then sacrificed the animals via cardiac perfusion with oxygenated artificial cerebrospinal fluid before splitting the brain in half; one hemisphere to be drop fixed in PFA for immunohistochemistry and half to be sub dissected and flash frozen for protein analysis. We have preliminary results that confirm significant increases in GFAP, Iba1 and Amyloid-β in Tg-S rats compared to nTg-S rats, however GFAP and Iba1 protein levels in Tg-TMG rats are no longer significantly different from nTg-S rats after 3 months of TMG injections to increase O-GlcNAcylation. We have also evaluated noradrenergic innervation into the dentate gyrus using anti-tyrosine hydroxylase (TH) immunohistochemistry and confocal imaging to evaluate if increasing O-GlcNAc protects against loss of TH innervation of the dentate gyrus, and have so far confirmed our previous results at this time point; TMG treated animals are not significantly different from their saline controls. We report that increasing O-GlcNAcylation from 6-9 months in the TgF344-AD rats is reducing reactive astrocytes. While this could be beneficial to preserving their function and neuronal health, this work is still ongoing. We are working to increase our sample size, and to examine the locus coeruleus for changes in hyperphosphorylated tau and other biomarkers.