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Leveraging weather radar technology for environmental monitoring, particularly the detection of biometeors like birds, bats, and insects, presents a significant challenge due to the dynamic nature of their behavior. Unlike hydrometeor targets, biometeor targets exhibit arbitrary changes in direction and position, which significantly alter radar wave polarization upon scattering. This study addresses this challenge by introducing a novel methodology utilizing Rwanda's C-Band Polarization Radar. Our approach exploits the capabilities of dual-polarization radar by analyzing parameters such as differential reflectivity (ZDR) and correlation coefficient (RHOHV) to derive the Depolarization Ratio (DR). While existing radar metrics offer valuable insights, they have limitations in fully capturing depolarization effects. To address this, we propose an advanced fuzzy logic algorithm (FL_DR) integrating the DR parameter. The FL_DR's performance was rigorously evaluated against a standard FL algorithm. Leveraging a substantial dataset comprising nocturnal clear air radar echoes collected during a Fall Armyworm (FAW) outbreak in maize fields from September 2020 to January 2021, the FL_DR demonstrated a notable improvement in accuracy compared to the existing FL algorithm. This improvement is evident in the Fraction of Echoes Correctly Identified (FEI), which increased from 98.42% to 98.93% for biological radar echoes and from 87.02% to 95.81% for meteorological radar echoes. This enhanced detection capability positions FL_DR as a valuable system for monitoring, identification, and warning of environmental phenomena in regions similar to tropical areas facing FAW outbreaks. Additionally, it could be tested and further refined for other migrating biological targets such as birds, insects, or bats. [ABSTRACT FROM AUTHOR]

Combined HIV antiretroviral therapy (cART) has been effective except if drug resistance emerges. As cART has been rolled out in low-income countries, drug resistance has emerged at higher rates than observed in high income countries due to factors including initial use of these less tolerated cART regimens, intermittent disruptions in drug supply, and insufficient treatment monitoring. These socioeconomic factors impacting drug resistance are compounded by viral mechanistic differences by divergent HIV-1 non-B subtypes compared to HIV-1 subtype B that largely infects the high-income countries (just 10% of 37 million infected). This review compares the inhibition and resistance of diverse HIV-1 subtypes and strains to the various approved drugs as well as novel inhibitors in clinical trials. Initial sequence variations and differences in replicative fitness between HIV-1 subtypes pushes strains through different fitness landscapes to escape from drug selective pressure. The discussions here provide insight to patient care givers and policy makers on how best to use currently approved ART options and reduce the emergence of drug resistance in ∼33 million individuals infected with HIV-1 subtype A, C, D, G, and recombinants forms. Unfortunately, over 98% of the literature on cART resistance relates to HIV-1 subtype B. [ABSTRACT FROM AUTHOR]

Background Although WHO recommends viral load (VL) monitoring for those on antiretroviral therapy (ART), availability in low-income countries remains limited. We investigated long-term VL and resistance in HIV-infected children managed without real-time VL monitoring. Methods and findings In the ARROW factorial trial, 1,206 children initiating ART in Uganda and Zimbabwe between 15 March 2007 and 18 November 2008, aged a median 6 years old, with median CD4% of 12%, were randomised to monitoring with or without 12-weekly CD4 counts and to receive 2 nucleoside reverse transcriptase inhibitors (2NRTI, mainly abacavir+lamivudine) with a non-nucleoside reverse transcriptase inhibitor (NNRTI) or 3 NRTIs as long-term ART. All children had VL assayed retrospectively after a median of 4 years on ART; those with >1,000 copies/ml were genotyped. Three hundred and sixteen children had VL and genotypes assayed longitudinally (at least every 24 weeks). Overall, 67 (6%) switched to second-line ART and 54 (4%) died. In children randomised to WHO-recommended 2NRTI+NNRTI long-term ART, 308/378 (81%) monitored with CD4 counts versus 297/375 (79%) without had VL Conclusions In this study, children receiving first-line ART in sub-Saharan Africa without real-time VL monitoring had good virological and resistance outcomes over 4 years, regardless of CD4 monitoring strategy. Many children with detectable low-level viraemia spontaneously resuppressed, highlighting the importance of confirming virological failure before switching to second-line therapy. Children experiencing rebound [greater than or equal to]5,000 copies/ml were much less likely to resuppress, but NRTI resistance increased only slowly. These results are relevant to the increasing numbers of HIV-infected children receiving first-line ART in sub-Saharan Africa with limited access to virological monitoring. Trial registration ISRCTN Registry, ISRCTN24791884, Author(s): Alexander J. Szubert 1,*, Andrew J. Prendergast 1,2, Moira J. Spyer 1, Victor Musiime 3,4, Philippa Musoke 5, Mutsa Bwakura-Dangarembizi 6, Patricia Nahirya-Ntege 7, Margaret J. Thomason 1, Emmanuel [...]

Background Limited viral load (VL) testing in human immunodeficiency virus (HIV) treatment programs in low-income countries often delays detection of treatment failure. The impact of remaining on failing protease inhibitor (PI)–containing regimens is unclear. Methods We retrospectively tested VL in 2164 stored plasma samples from 386 patients randomized to receive lopinavir monotherapy (after initial raltegravir induction) in the Europe–Africa Research Network for Evaluation of Second-line Therapy (EARNEST) trial. Protease genotypic resistance testing was performed when VL >1000 copies/mL. We assessed evolution of PI resistance mutations from virological failure (confirmed VL >1000 copies/mL) until PI monotherapy discontinuation and examined associations using mixed-effects models. Results Median post-failure follow-up (in 118 patients) was 68 (interquartile range, 48–88) weeks. At failure, 20% had intermediate/high-level resistance to lopinavir. At 40–48 weeks post-failure, 68% and 51% had intermediate/high-level resistance to lopinavir and atazanavir; 17% had intermediate-level resistance (none high) to darunavir. Common PI mutations were M46I, I54V, and V82A. On average, 1.7 (95% confidence interval 1.5–2.0) PI mutations developed per year; increasing after the first mutation; decreasing with subsequent mutations (P <.0001). VL changes were modest, mainly driven by nonadherence (P =.006) and PI mutation development (P =.0002); I47A was associated with a larger increase in VL than other mutations (P =.05). Conclusions Most patients develop intermediate/high-level lopinavir resistance within 1 year of ongoing viral replication on monotherapy but retain susceptibility to darunavir. Viral load increased slowly after failure, driven by non-adherence and PI mutation development. Clinical Trials Registration NCT00988039. [ABSTRACT FROM AUTHOR]