Objective: The HIV epidemic has carved contrasting trajectories around the world with sub-Saharan Africa (SSA) being most affected. We hypothesized that mean HIV-1 plasma RNA viral loads are higher in SSA than other areas, and that these elevated levels may contribute to the scale of epidemics in this region.
Design And Methods: To evaluate this hypothesis, we constructed a database of means of 71,668 viral load measurements from 44 cohorts in seven regions of the world. We used linear regression statistical models to estimate differences in viral load between regions. We also constructed and analyzed a mathematical model to describe the impact of the regional viral load differences on HIV epidemic trajectory.
Results: We found substantial regional viral load heterogeneity. The mean viral load in SSA was 0.58 log(10) copies/ml higher than in North America (95% confidence interval 0.45-0.71); this represents about a four-fold increase. The highest mean viral loads were found in Southern and East Africa, whereas in Asia, Europe, North America, and South America, mean viral loads were comparable. Mathematical modeling indicated that conservatively 14% of HIV infections in a representative population in Kenya could be attributed to the enhanced infectiousness of patients with heightened viral load.
Conclusion: We conclude that community viral load appears to be higher in SSA than in other regions and this may be a central driver of the massive HIV epidemics in this region. The elevated viral loads in SSA may reflect, among other factors, the high burden of co-infections or the preponderance of HIV-1 subtype C infection.
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http://dx.doi.org/10.1097/QAD.0b013e32835cb927 | DOI Listing |
Enferm Infecc Microbiol Clin (Engl Ed)
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Microbiology Service, Clinic University Hospital, INCLIVA Health Research Institute, Valencia, Spain; CIBER de Enfermedades Infecciosas, Instituto de Salud Carlos III, Madrid, Spain; Department of Microbiology, School of Medicine, University of Valencia, Valencia, Spain. Electronic address:
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Department of Histology and Embryology, Erciyes University, Faculty of Medicine, 38039 Kayseri, Turkey. Electronic address:
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National Key Laboratory of Veterinary Public Health Security, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China; Key Laboratory of Animal Epidemiology of the Ministry of Agriculture, College of Veterinary Medicine, China Agricultural University, Beijing 100193, China. Electronic address:
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Laboratory of Fish Molecular Immunology, College of Fisheries and Life Science, Shanghai Ocean University, Shanghai, 201306, China.
The accurate assembly of the ribonucleoprotein (RNP) complex is fundamental for the replication and transcription of rhabdoviruses, which are known for their broad pathogenic impact. A novel 119-amino-acid protein, NLRP12-119aa is identified, encoded by the circular RNA circNLRP12, that effectively disrupts the formation of rhabdovirus RNP complexes through two distinct mechanisms and significantly reduces their replication. NLRP12-119aa exhibits a strong affinity for the conserved 18-nucleotide sequence at the start of the leader RNA of rhabdoviruses VSV, SCRV, and RABV, outcompeting their native N protein interactions, thereby disrupting the assembly of RNP complexes and inhibiting viral replication.
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Department of Pediatrics, Children's Medical Center, The First Hospital of Jilin University, Lequn Branch, No. 3302 Jilin Road, Changchun, 130021, China.
The global spread of the novel coronavirus disease 2019, caused by SARS-CoV-2 virus, impacts individuals of all age groups, including lactating women and children. Concerns have been raised regarding the potential transmission of SARS-CoV-2 from mother to child, following the discovery of SARS-CoV-2 RNA in human milk. Therefore, this study aims to investigate whether the Omicron novel coronavirus variants are transmitted through human milk.
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