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Fig. 3 in Prairie dog responses to vector control and vaccination during an initial Yersinia pestis invasion
Fig. 3. Predicted re-encounter rates (95% confidence intervals [CIs]) over a single trapping interval (2007–2008) for adult female and male black-tailed prairie dogs inoculated at Conata Basin, South Dakota in 2007 with F1–V fusion protein vaccine or placebo on the no dust and dusted plots (the latter with flea control). Sample sizes are depicted above the 95% CIs.
Fig. 1 in Prairie dog responses to vector control and vaccination during an initial Yersinia pestis invasion
Fig. 1. Categories of flea vector control (deltamethrin dust) and F1–V fusion protein plague vaccination (V = vaccine, P = placebo, N = no inoculation) used for analyses of black-tailed prairie dog annual re-encounter rates (2007–2008 and 2008–2009) at Conata Basin, South Dakota. Annual re-encounter rates were compared for subsets of animals, here each enclosed by unique rectangles. Sample sizes are depicted in subsequent figures with results from multivariate analyses.
Fig. 5 in Prairie dog responses to vector control and vaccination during an initial Yersinia pestis invasion
Fig. 5. Predicted re-encounter rates (95% confidence intervals [CIs]) over a single trapping interval 2007–2008 for non-inoculated adult and juvenile blacktailed prairie dogs on the no dust and dusted plots (the latter with flea control) at Conata Basin, South Dakota. Sample sizes are depicted above the 95% CIs.
Fig. 2 in Prairie dog responses to vector control and vaccination during an initial Yersinia pestis invasion
Fig. 2. Predicted flea parasitism (95% confidence intervals [CIs]) on blacktailed prairie dogs at the no dust and dusted plots, 2007–2008 at Conata Basin, South Dakota (prevalence on the left, intensity on the right). Prairie dog burrows on the dusted plots were treated annually with deltamethrin dust at ~4–6 g per burrow. Model predictions adjust (i.e., control) for year and Julian day (adjusted here as year 2008, and Julian day 212 for prevalence and 200 for intensity). Flea intensity data were log-transformed (log10) for analysis; hence, predicted flea intensity and 95% CIs could extend below 0. Sample sizes are depicted above the 95% CIs.
Fig. 4 in Prairie dog responses to vector control and vaccination during an initial Yersinia pestis invasion
Fig. 4. Predicted re-encounter rates (95% confidence intervals [CIs]) over two trapping intervals (2007–2008 and 2008–2009) for adult female and male black-tailed prairie dogs in Conata Basin, South Dakota inoculated in 2007 or 2008 with F1–V fusion protein vaccine or placebo on the dusted plots (with flea control). Sample sizes are depicted above or below the 95% CIs.
Figure 6 in Indiscriminate ingestion of entomopathogenic nematodes and their symbiotic bacteria by Aedes aegypti larvae: a novel strategy to control the vector of Chikungunya, dengue and yellow fever
Figure 6. Aedes aegypti larval mortality when exposed to 1000 infective juveniles (IJs) of Heterorhabditis bacteriophora at different depths of water.
Figure 2 in Indiscriminate ingestion of entomopathogenic nematodes and their symbiotic bacteria by Aedes aegypti larvae: a novel strategy to control the vector of Chikungunya, dengue and yellow fever
Figure 2. Susceptibility of Aedes aegypti larvae to different species of EPN. Five 3rd instar larvae exposed to 1000 infective juveniles (IJs) and mortality assessed daily over 3-day period (DPI).
Figure 4 in Indiscriminate ingestion of entomopathogenic nematodes and their symbiotic bacteria by Aedes aegypti larvae: a novel strategy to control the vector of Chikungunya, dengue and yellow fever
Figure 4. Melanization of Heterorhabditis bacteriophora within Aedes aegypti larvae (3rd instar). A melanized H. bacteriophora within dead Ae. aegypti larvae (a), close up picture of melanized nematode upon larval dissection (b), nematodes representing different stages of melanization recovered from one dead Ae. aegypti larvae (c). Arrows indicate melanized nematode within Ae. aegypti larvae.
Figure 7 in Indiscriminate ingestion of entomopathogenic nematodes and their symbiotic bacteria by Aedes aegypti larvae: a novel strategy to control the vector of Chikungunya, dengue and yellow fever
Figure 7. Aedes aegypti larval mortality when exposed to supernatants and cell suspensions of Xenorhabdus nematophila (X. n.) and Photorhabdus laumondii (P. l.) in 24 well plates. Different uppercase or lower letters above error bars indicate statistical significance (Tukey's test p ≤ 0.05).
Figure 3 in Indiscriminate ingestion of entomopathogenic nematodes and their symbiotic bacteria by Aedes aegypti larvae: a novel strategy to control the vector of Chikungunya, dengue and yellow fever
Figure 3. Different stages of Heterorhabditis bacteriophora colonization of Aedes aegypti larvae (3rd instar). H. bacteriophora within larvae at 2-day post inoculation (a), H. bacteriophora emerging out of larvae upon larval dissection at 7-day post inoculation) (b), adult H. bacteriophora within larvae along with large number of infective juveniles (IJs) released from another adult H. bacteriophora (c). Black arrows indicate adult H. bacteriophora, whereas green arrows indicate newly emerged IJs.
Simulation Results Data for 'Modelling new insecticide-treated bed nets for malaria-vector control: How to strategically manage resistance?'
<p>GENERAL INFORMATION</p> <p>1. Title of Dataset: Simulation Results Data for 'Modelling new insecticide-treated bed-nets for malaria-vector control: How to strategically manage resistance?'</p> <p>2. Author Information<br> A. Investigator Contact Information<br> Name: Philip G. Madgwick<br> Institution: Syngenta <br> Address: Jealott’s Hill International Research Centre, Bracknell, RG42 6EY, UK<br> Email: philip.madgwick@syngenta.com</p> <p> B. Investigator Contact Information<br> Name: Ricardo Kanitz<br> Institution: Syngenta <br> Address: Syngenta Crop Protection, Rosentalstrasse 67, CH-4058 Basel, Switzerland<br> Email: ricardo.kanitz@syngenta.com</p> <p><br> 3. Date of data collection (single date, range, approximate date): 2021-01-13 to 2021-02-01 </p> <p>4. Geographic location of data collection: UK </p> <p>5. Information about funding sources that supported the collection of the data: </p> <p>This work was conducted during a postdoctoral research position for PGM funded by the Innovative Vector Control Consortium (IVCC).</p> <p><br> SHARING/ACCESS INFORMATION</p> <p>1. Licenses/restrictions placed on the data: NA</p> <p>2. Links to publications that cite or use the data: [UPDATE]</p> <p>3. Links to other publicly accessible locations of the data: NA</p> <p>4. Links/relationships to ancillary data sets: NA</p> <p>5. Was data derived from another source? No</p> <p>6. Recommended citation for this dataset: [UPDATE]</p> <p><br> DATA & FILE OVERVIEW</p> <p>1. File List: <br> PSData_random6.csv - 10^6 random samples of each of the 17 parameters in the model, where rows are samples and columns are parameters (with column names corresponding to the parameters identified in the rows of Table 1 of the manuscript; see also DATA-SPECIFIC INFORMATION)<br> Data_random6_maxpsMixture_Fixed_mm.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used in a mixture (at rate k=1; see manuscript) as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_maxpsMixture_Fixed_mn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used in a mixture (at rate k=1; see manuscript) as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_maxpsMixture_Fixed_nn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used in a mixture (at rate k=1; see manuscript) as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_Mixture_Fixed_mm.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used in a mixture (at rate k; see manuscript) as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_Mixture_Fixed_mn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used in a mixture (at rate k; see manuscript) as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_Mixture_Fixed_nn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used in a mixture (at rate k; see manuscript) as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_Mosaic_Fixed_mm.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used at 50% frequency each as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_Mosaic_Fixed_mn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used at 50% frequency each as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_Mosaic_Fixed_nn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A and B are used at 50% frequency each as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_Rotation_Fixed_mm.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A is used first in a rotation that switch between insecticides every 36 generations as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_Rotation_Fixed_mn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A is used first in a rotation that switch between insecticides every 36 generations as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_Rotation_Fixed_nn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A is used first in a rotation that switch between insecticides every 36 generations as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_Rotation_Fixed_revmm.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide B is used first in a rotation that switch between insecticides every 36 generations as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_Rotation_Fixed_revmn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide B is used first in a rotation that switch between insecticides every 36 generations as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_Rotation_Fixed_revnn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide B is used first in a rotation that switch between insecticides every 36 generations as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_SoloA_Fixed_mm.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A is used solo as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_SoloA_Fixed_mn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A is used solo as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_SoloA_Fixed_nn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide A is used solo as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has nuclear inheritance <br> Data_random6_SoloB_Fixed_mm.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide B is used solo as a fixed strategy for the entire run; the resistance allele at locus 1 has mitochondrial inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_SoloB_Fixed_mn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide B is used solo as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has mitochondrial inheritance <br> Data_random6_SoloB_Fixed_nn.csv - simulation dataset of 10^6 runs for each set of randomly sampled parameters; insecticide B is used solo as a fixed strategy for the entire run; the resistance allele at locus 1 has nuclear inheritance and the resistance allele at locus 2 has nuclear inheritance </p> <p>2. Relationship between files, if important: </p> <p>Files are named in accordance with the variables that describe each simulation setup, as described above. Each simulation dataset has 10^6 runs that correspond to the 10^6 random samples of each of the 17 parameters in the model in 'PSData_random6.csv'.</p> <p>3. Additional related data collected that was not included in the current data package: NA</p> <p>4. Are there multiple versions of the dataset? No</p> <p><br> METHODOLOGICAL INFORMATION</p> <p>1. Description of methods used for collection/generation of data: Data were collected using Simulator.R, which is in the vignettes of the 'detsims' R package that accompanies the manuscript. </p> <p>2. Methods for processing the data: Data were processed using Figures.R, which is in the vignettes of the 'detsims' R package that accompanies the manuscript. </p> <p>3. Instrument- or software-specific information needed to interpret the data: Analysis was conducted in R version 4.0.3 (2020-10-10), using R packages identified in Figures.R, which is in the vignettes of the 'detsims' R package that accompanies the manuscript. </p> <p>4. Standards and calibration information, if appropriate: NA</p> <p>5. Environmental/experimental conditions: NA</p> <p>6. Describe any quality-assurance procedures performed on the data: NA</p> <p>7. People involved with sample collection, processing, analysis and/or submission: NA </p> <p><br> DATA-SPECIFIC INFORMATION FOR: PSData_random6.csv</p> <p>1. Number of variables: </p> <p>17 variables with column names that have the following parameter meanings (see Table 1 in the manuscript): <br> Population Size = N = starting population size (and carrying capacity in logistic model); random sample range on log-scale: 10^2 - 10^9<br> Intrinsic Birth Rate = b = % population growth rate (in logistic model); random sample following a standard log-normal distribution with mean=0 and sd=1<br> Intrinsic Death Rate = d = % breeding mosquitoes that die into next generation; random sample range: 0 - 1<br> Female Exposure = x_[female-symbol] = % female mosquitoes that receive a dose; random sample range: 0 - 1<br> Male Exposure x_[male-symbol] = % male mosquitoes that receive a dose; random sample range: 0 - 1<br> Initial Frequency A = f_0,A = starting frequency of allele A; random sample range on log-scale: 10^-9 - 10^-2, limited to be within the range 1/N - N/100 where N is Population Size<br> Effectiveness 1 = m_1 = % dosed mosquitoes that die from insecticide 1; random sample range: 0 - 1<br> Resistance Restoration A = r_A = % return to baseline fitness with resistance allele A; random sample range: 0 - 1<br> Dominance of Resistance Restoration A = h^r_A = % resistance restoration in heterozygote with allele A; random sample range: 0 - 1<br> Resistance Cost A = c_A = % non-dosed mosquitoes that die from carrying allele A; random sample range on log-scale: 10^-3 - 10^-0.5<br> Dominance of Resistance Cost A = h^c_A = % resistance cost in heterozygote with allele A; random sample range: 0 - 1<br> Initial Frequency B = f_0,B = starting frequency of allele B; random sample range on log-scale: 10^-9 - 10^-2, limited to be within the range 1/N - N/100 where N is Population Size<br> Effectiveness 2 = m_2 = % dosed mosquitoes that die from insecticide 2; random sample range: 0 - 1<br> Resistance Restoration B = r_B = % return to baseline fitness with resistance allele B; random sample range: 0 - 1<br> Dominance of Resistance Restoration B = h^r_B = % resistance restoration in heterozygote with allele B; random sample range: 0 - 1<br> Resistance Cost B = c_B = % non-dosed mosquitoes that die from carrying allele B; random sample range on log-scale: 10^-3 - 10^-0.5<br> Dominance of Resistance Cost B = h^c_B = % resistance cost in heterozygote with allele B; random sample range: 0 - 1</p> <p>2. Number of cases/rows: </p> <p>10^6, corresponding to the number of random samples </p> <p>3. Variable List: NA </p> <p>4. Missing data codes: NA</p> <p>5. Specialized formats or other abbreviations used: NA</p> <p><br> DATA-SPECIFIC INFORMATION FOR: all other dataset files (e.g. Data_random6_maxpsMixture_Fixed_mm.csv) </p> <p>1. Number of variables: </p> <p>10 variables with column names that have the following meanings:<br> A_t_50% = the recorded number of generations that it takes for resistance allele A to reach >50% frequency; 0 means that resistance allele A never reaches >50% frequency <br> A_f_250 = the frequency of resistance allele A at the 250th generation <br> A_f_bar = the mean frequency of resistance allele A over the first 250 generations <br> B_t_50% = the recorded number of generations that it takes for resistance allele B to reach >50% frequency; 0 means that resistance allele B never reaches >50% frequency <br> B_f_250 = the frequency of resistance allele B at the 250th generation <br> B_f_bar = the mean frequency of resistance allele B over the first 250 generations <br> nf_80% = the recorded number of generations that it takes for the female population size to recover to >80% of its original size in the 0th generation; 0 means that the female population size never reaches >80% recovery; 1 means that the female population size never drops below 80% of its original size in the 1st generation<br> nf_250 = the female population size at the 250th generation<br> nf_bar = the mean female population size over the first 250 generations <br> nf_ext = the recorded number of generations that it takes for the female population size to drop below 1 (i.e. population extinction); 0 means that female population size never reaches <1</p> <p>2. Number of cases/rows: </p> <p>10^6, corresponding to the number of random samples </p> <p>3. Variable List: NA</p> <p>4. Missing data codes: all missing data is recorded as 0 </p> <p>5. Specialized formats or other abbreviations used: NA</p>
All data for the preprint Population genetics of Glossina palpalis gambiensis in the sleeping sickness focus of Boffa (Guinea) before and after eight years of vector control: no effect of control despite a significant decrease of human exposure to the disease
<p>Data set for the paper titled "Population genetics of <em>Glossina palpalis gambiensis</em> in the sleeping sickness focus of Boffa (Guinea) before and after eight years of vector control: no effect of control despite a significant decrease of human exposure to the disease"</p>
Raw data to: "Vectored antibody gene delivery restores host B and T cell control of persistent viral infection"
<p>Raw data underlying the publication by Ertuna et al. entitled "Vectored antibody gene delivery restores host B and T cell control of persistent viral infection"</p>
THREE-DIMENSIONAL VOLUMETRIC EVALUATION OF ROOT RESORPTION IN MAXILLARY ANTERIORS FOLLOWING EN-MASSE RETRACTION WITH VARYING FORCE VECTORS - A RANDOMIZED CONTROL TRIAL
<p>To assess the severity of root resorption (RR) during retraction of maxillary anteriors with and without skeletal anchorage (three different force systems); and analyze it comprehensively using cone-beam computed tomography (CBCT) superimpositions.</p>
A machine learning approach to integrating genetic and ecological data in tsetse flies (Glossina pallidipes) for spatially explicit vector control planning
Open the record for dataset details and reuse information.
Data from: Human movement, cooperation, and the effectiveness of coordinated vector control strategies
Vector-borne disease transmission is often typified by highly focal transmission and influenced by movement of hosts and vectors across different scales. The ecological and environmental conditions (including those created by humans through vector control programmes) that result in metapopulation dynamics remain poorly understood. The development of control strategies that would most effectively limit outbreaks given such dynamics is particularly urgent given the recent epidemics of dengue, chikungunya and Zika viruses. We developed a stochastic, spatial model of vector-borne disease transmission, allowing for movement of hosts between patches. Our model is applicable to arbovirus transmission by Aedes aegypti in urban settings and was parametrized to capture Zika virus transmission in particular. Using simulations, we investigated the extent to which two aspects of vector control strategies are affected by human commuting patterns: the extent of coordination and cooperation between neighbouring communities. We find that transmission intensity is highest at intermediate levels of host movement. The extent to which coordination of control activities among neighbouring patches decreases the prevalence of infection is affected by both how frequently humans commute and the proportion of neighbouring patches that commits to vector surveillance and control activities. At high levels of host movement, patches that do not contribute to vector control may act as sources of infection in the landscape, yet have comparable levels of prevalence as patches that do cooperate. This result suggests that real cooperation among neighbours will be critical to the development of effective pro-active strategies for vector-borne disease control in today's commuter-linked communities.
Data from: Effective population size of malaria mosquitoes: large impact of vector control
Malaria vectors in sub-Saharan Africa have proven themselves very difficult adversaries in the global struggle against malaria. Decades of anti-vector interventions have yielded mixed results – with successful reductions in transmission in some areas, and limited impacts in others. These varying successes can be ascribed to a lack of universally effective vector control tools, as well as the development of insecticide resistance in mosquito populations. Understanding the impact of vector control on mosquito populations is crucial for planning new interventions and evaluating existing ones. However, estimates of population size changes in response to control efforts are often inaccurate because of limitations and biases in collection methods. Attempts to evaluate the impact of vector control on mosquito effective population size (Ne) have produced inconclusive results thus far. Therefore, we obtained data for 13-15 microsatellite markers for over 1,500 mosquitoes representing multiple time points for seven populations of three important vector species – Anopheles gambiae, An. melas and An. moucheti in Equatorial Guinea. These populations were subjected to indoor residual spraying or long-lasting insecticidal nets in recent years. For comparison, we also analyzed data from two populations that have no history of organized vector control. We used Approximate Bayesian Computation to reconstruct their demographic history, allowing us to evaluate the impact of these interventions on the effective population size. In six of the seven study populations, vector control had a dramatic impact on the effective population size, reducing Ne between 55-87%, the exception being a single An. melas population. In contrast, the two negative control populations did not experience a reduction in effective population size. This study is the first to conclusively link anti-vector intervention programs in Africa to sharply reduced effective population sizes of malaria vectors.
Data from: First-in-human randomized controlled trial of an oral, replicating Adenovirus 26 vector vaccine for HIV-1
Background: Live, attenuated viral vectors that express HIV-1 antigens are being investigated as an approach to generating durable immune responses against HIV-1 in humans. We recently developed a replication-competent, highly attenuated Ad26 vector that expresses mosaic HIV-1 Env (rcAd26.MOS1.HIV-Env, "rcAd26"). Here we present the results of a first-in-human, placebo-controlled clinical trial to test the safety, immunogenicity and mucosal shedding of rcAd26 given orally. Methods: Healthy adults were randomly assigned to receive a single oral dose of vaccine or placebo at 5:1 ratio in a dosage escalation of 10^8 to 10^11 rcAd26 VP (nominal doses) at University of Rochester Medical Center, Rochester, NY, USA. Participants were isolated and monitored for reactogenicity for 10 days post-vaccination, and adverse events were recorded up to day 112. Rectal and oropharyngeal secretions were evaluated for shedding of the vaccine. Humoral and cellular immune responses were measured. Household contacts were monitored for secondary vaccine transmission. Results: We enrolled 22 participants and 11 household contacts between February 7 and June 24, 2015. 18 participants received one dose of HIV-1 vaccine and 4 participants received placebo. The vaccine caused only mild to moderate adverse events. No vaccine-related SAEs were observed. No infectious rcAd26 viral particles were detected in rectal or oropharyngeal secretions from any participant. Env-specific ELISA and ELISPOT responses were undetectable. No household contacts developed vaccine-induced HIV-1 seropositivity or vaccine-associated illness. Conclusions: The highly attenuated rcAd26.MOS1.HIV-Env vaccine was well tolerated up to 10^11 VP in healthy, HIV-1-uninfected adults, though the single dose was poorly immunogenic suggesting the replicative capacity of the vector was too attenuated. There was no evidence of shedding of infectious virus or secondary vaccine transmission following the isolation period. These data suggest the use of less attenuated viral vectors in future studies of live, oral HIV-1 vaccines. Clinical Trials Registration: NCT02366013
Data from: Genetic diversity and population structure of the tsetse fly Glossina fuscipes fuscipes (Diptera: Glossinidae) in Northern Uganda: implications for vector control
Uganda is the only country where the chronic and acute forms of human African Trypanosomiasis (HAT) or sleeping sickness both occur and are separated by < 100 km in areas north of Lake Kyoga. In Uganda, Glossina fuscipes fuscipes is the main vector of the Trypanosoma parasites responsible for these diseases as well for the animal African Trypanosomiasis (AAT), or Nagana. We used highly polymorphic microsatellite loci and a mitochondrial DNA (mtDNA) marker to provide fine scale spatial resolution of genetic structure of G. f. fuscipes from 42 sampling sites from the northern region of Uganda where a merger of the two disease belts is feared. Based on microsatellite analyses, we found that G. f. fuscipes in northern Uganda are structured into three distinct genetic clusters with varying degrees of interconnectivity among them. Based on genetic assignment and spatial location, we grouped the sampling sites into four genetic units corresponding to northwestern Uganda in the Albert Nile drainage, northeastern Uganda in the Lake Kyoga drainage, western Uganda in the Victoria Nile drainage, and a transition zone between the two northern genetic clusters characterized by high level of genetic admixture. An analysis using HYBRIDLAB supported a hybrid swarm model as most consistent with tsetse genotypes in these admixed samples. Results of mtDNA analyses revealed the presence of 30 haplotypes representing three main haplogroups, whose location broadly overlaps with the microsatellite defined clusters. Migration analyses based on microsatellites point to moderate migration among the northern units located in the Albert Nile, Achwa River, Okole River, and Lake Kyoga drainages, but not between the northern units and the Victoria Nile drainage in the west. Effective population size estimates were variable with low to moderate sizes in most populations and with evidence of recent population bottlenecks, especially in the northeast unit of the Lake Kyoga drainage. Our microsatellite and mtDNA based analyses indicate that G. f. fuscipes movement along the Achwa and Okole rivers may facilitate northwest expansion of the Rhodesiense disease belt in Uganda. We identified tsetse migration corridors and recommend a rolling carpet approach from south of Lake Kyoga northward to minimize disease dispersal and prevent vector re-colonization. Additionally, our findings highlight the need for continuing tsetse monitoring efforts during and after control.
Field Evaluations of Innovative Tools for Vector-borne Disease Control in Conflict-affected Communities
ClinicalTrials.gov study NCT06179732. IPD Sharing: NO. Countries: 1. Publications: 1.
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