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IntroductionHealth researchers from low-income and middle-income countries (LMICs) are under-represented in the academic literature. Scientific writing and publishing interventions may help researchers publish their findings; however, we lack evidence about the prevalence and effectiveness of such interventions. This review describes interventions for researchers in LMICs aimed at strengthening capacity for writing and publishing academic journal articles.MethodsWe followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines to report literature searches in PubMed, Embase, Global Health, Scopus and ERIC. Our keywords included LMICs, low-income and middle-income countries, health research and writing/publication support interventions, with no restrictions on publication date. Our screening process consisted of title screening, abstract review and full-text review. We collected information about the content, implementation and evaluation of each intervention, if included.ResultsWe identified 20 interventions designed to strengthen capacity for scientific writing and publishing. We summarised information from the 14 interventions that reported submitted or published papers as outcomes separately, reasoning that because they provide quantifiable metrics of success, they may offer particular insights into intervention components leading to publication. The writing and publishing components in this ‘Publications Reported’ group were an average length of 5.4 days compared with 2.5 days in the other group we refer to as ‘Other Interventions.’ Whereas all 14 Publications Reported interventions incorporated mentors, only two of five in the Other Interventions group incorporated mentors. Across interventions, leaders expressed the importance of a high ratio of mentors to participants, the need to accommodate time demands of busy researchers, and the necessity of a budget for open access fees and high-quality internet connectivity.ConclusionWriting and publishing interventions in LMICs are an underutilised opportunity for capacity strengthening. To facilitate the implementation of high-quality interventions, future writing and publishing interventions should share their experiences by publishing detailed information about the approach and effectiveness of the interventions.

HIV-exposed uninfected (HEU) infants have higher rates of severe and fatal infections compared with HIV-unexposed (HUU) infants, likely due to immune perturbations. We hypothesized that alterations in natural killer (NK) cell activity might occur in HEU infants and predispose them to severe infections. Case-control study using cryopreserved peripheral blood mononuclear cells (PBMCs) at birth and 6 months from HEU infants enrolled from 2002 to 2009 and HUU infants enrolled from 2011 to 2013. NK cell phenotype and function were assessed by flow cytometry after 20-h incubation with and without K562 cells. The proportion of NK cells among PBMCs was lower at birth in 12 HEU vs. 22 HUU (1.68 vs. 10.30%,  < 0.0001) and at 6 months in 52 HEU vs. 72 HUU (3.09 vs. 4.65%,  = 0.0005). At birth, HEU NK cells demonstrated increased killing of K562 target cells (  < 0.0001) and increased expression of CD107a (21.65 vs. 12.70%,  = 0.047), but these differences resolved by 6 months. Stimulated HEU NK cells produced less interferon (IFN)γ at birth (0.77 vs. 2.64%,  = 0.008) and at 6 months (4.12 vs. 8.39%,  = 0.001), and showed reduced perforin staining at 6 months (66.95 vs. 77.30%,  = 0.0008). Analysis of cell culture supernatants indicated that lower NK cell activity in HEU was associated with reduced interleukin (IL)-12, IL-15, and IL-18. Addition of recombinant human IL-12 to stimulated HEU PBMCs restored IFNγ production to that seen in stimulated HUU cultures. NK cell proportion, phenotype, and function are altered in HEU infants. NK cell cytotoxicity and degranulation are increased in HEU at birth, but HEU NK cells have reduced IFNγ and perforin production, suggesting an adequate initial response, but decreased functional reserve. NK cell function improved with addition of exogenous IL-12, implicating impaired production of IL-12 by accessory cells. Alterations in NK cell and accessory cell function may contribute to the increased susceptibility to infection in HEU infants.