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Introduction: The World Health Organization (WHO) recommends tenofovir disoproxil fumarate (TDF) for pregnant women with hepatitis B virus (HBV) presenting with HBV DNA levels of 106 copies/mL or more to hinder mother-to-child transmission (MTCT). Moreover, it is suggested that neonates of HBV-infected mothers receive an HBV vaccine birth dose within 24 hours of birth to mitigate transmission risk., Methodology: The study included 661 HBV-infected pregnant women and 316 infants from 3 hospitals in Southern Vietnam between October 2019 and November 2020. Infants were classified on the basis of their mothers' TDF prophylaxis into I-TDF (+) group (107 infants) whose mothers received TDF; I-TDF (-) group (56 infants) whose mothers missed TDF; and I-NTDF group (153 infants) whose mothers did not necessitate TDF. Almost all infants received an HBV vaccine birth dose with HBIG administered on the basis of parents' financial standing., Results: MTCT was found in 2.2% of the cases. The respective MTCT rates for I-TDF (+), I-TDF (-), and I-NTDF groups were 2.8%, 5.4%, and 0.7%. Immune response rates to the HBV vaccination in the total cohort, I-TDF (+), I-TDF (-), and I-NTDF groups, were 88.6%, 87.9%, 85.7%, and 90.2%, respectively. Vaccinated infants exhibited a statistically lower risk of HBV infection postbirth (aRR = 0.1; 95% confidence interval, 0.0-0.6; P = .01)., Conclusion: TDF can equate the MTCT risk in pregnant women with HBV DNA levels of 106 copies/mL or more to those with lower levels. Early administration of the HBV vaccine postbirth also effectively curtails MTCT. Thus, expanding TDF prophylaxis and vaccine coverage is pivotal to impede MTCT., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Bacteria can acquire mobile genetic elements (MGEs) to combat infection by viruses (phages). Satellite viruses, including the PLEs (phage-inducible chromosomal island-like elements) in epidemic Vibrio cholerae, are MGEs that restrict phage replication to the benefit of their host bacterium. PLEs parasitize the lytic phage ICP1, unleashing multiple mechanisms to restrict phage replication and promote their own spread. In the arms race against PLE, ICP1 uses nucleases, including CRISPR-Cas, to destroy PLE's genome during infection. However, through an unknown CRISPR-independent mechanism, specific ICP1 isolates subvert restriction by PLE. Here, we discover ICP1-encoded Adi that counteracts PLE by exploiting the PLE's large serine recombinase (LSR), which normally mobilizes PLE in response to ICP1 infection. Unlike previously characterized ICP1-encoded anti-PLE mechanisms, Adi is not a nuclease itself but instead appears to modulate the activity of the LSR to promote destructive nuclease activity at the LSR's specific attachment site, attP. The PLE LSR, its catalytic activity, and attP are additionally sufficient to sensitize a PLE encoding a resistant variant of the recombination module to Adi activity. This work highlights a unique type of adaptation arising from inter-genome conflicts, in which the intended activity of a protein can be weaponized to overcome the antagonizing genome., (© The Author(s) 2022. Published by Oxford University Press on behalf of Nucleic Acids Research.)

This analysis highlights the evolution of the theory of maternal role attainment. Reva Rubin established the foundation for theory of maternal role attainment in her 1967 article. In 2004, Ramona Mercer made the argument to change the name from maternal role attainment to becoming a mother. In this analysis, recommendations are made to further develop this theory including updated theoretical models. This theory remains relevant to nursing, especially to nurses working with families during this transitionary time., (Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.)

Thalassemias are inherited blood disorders that are found in high prevalences in the Mediterranean, Southeast Asia and the Pacific. These diseases provide varying levels of resistance to malaria and are proposed to have emerged as an adaptive response to malaria in these regions. The transition to agriculture in the Holocene has been suggested to have influenced the selection for thalassemia in the Mediterranean as land clearance for farming encouraged interaction between Anopheles mosquitos, the vectors for malaria, and human groups. Here we document macroscopic and microscopic skeletal evidence for the presence of thalassemia in both hunter-gatherer (Con Co Ngua) and early agricultural (Man Bac) populations in northern Vietnam. Firstly, our findings demonstrate that thalassemia emerged prior to the transition to agriculture in Mainland Southeast Asia, from at least the early seventh millennium BP, contradicting a long-held assumption that agriculture was the main driver for an increase in malaria in Southeast Asia. Secondly, we describe evidence for significant malarial burden in the region during early agriculture. We argue that the introduction of farming into the region was not the initial driver of the selection for thalassemia, as it may have been in other regions of the world.

Vibrio cholerae is a significant threat to global public health in part due to its propensity for large-scale evolutionary sweeps where lineages emerge and are replaced. These sweeps may originate from the Bay of Bengal, where bacteriophage predation and the evolution of antiphage counterdefenses is a recurring theme. The bacteriophage ICP1 is a key predator of epidemic V. cholerae and is notable for acquiring a CRISPR-Cas system to combat PLE, a defensive subviral parasite encoded by its V. cholerae host. Here, we describe the discovery of four previously unknown PLE variants through a retrospective analysis of >3,000 publicly available sequences as well as one additional variant (PLE10) from recent surveillance of cholera patients in Bangladesh. In recent sampling we also observed a lineage sweep of PLE-negative V. cholerae occurring within the patient population in under a year. This shift coincided with a loss of ICP1's CRISPR-Cas system in favor of a previously prevalent PLE-targeting endonuclease called Odn. Interestingly, PLE10 was resistant to ICP1-encoded Odn, yet it was not found in any recent V. cholerae strains. We also identified isolates from within individual patient samples that revealed both mixed PLE(+)/PLE(-) V. cholerae populations and ICP1 strains possessing CRISPR-Cas or Odn with evidence of in situ recombination. These findings reinforce our understanding of the successive nature of V. cholerae evolution and suggest that ongoing surveillance of V. cholerae, ICP1, and PLE in Bangladesh is important for tracking genetic developments relevant to pandemic cholera that can occur over relatively short timescales. IMPORTANCE With 1 to 4 million estimated cases annually, cholera is a disease of serious global concern in regions where access to safe drinking water is limited by inadequate infrastructure, inequity, or natural disaster. The Global Task Force on Cholera Control (GTFCC.org) considers outbreak surveillance to be a primary pillar in the strategy to reduce mortality from cholera worldwide. Therefore, developing a better understanding of temporal evolutionary changes in the causative agent of cholera, Vibrio cholerae, could help in those efforts. The significance of our research is in tracking the genomic shifts that distinguish V. cholerae outbreaks, with specific attention paid to current and historical trends in the arms race between V. cholerae and a cooccurring viral (bacteriophage) predator. Here, we discover additional diversity of a specific phage defense system in epidemic V. cholerae and document the loss of a phage-encoded CRISPR-Cas system, underscoring the dynamic nature of microbial populations across cholera outbreaks.