A large population sample of African HIV genomes from the 1980s reveals a reduction in subtype D over time associated with propensity for CXCR4 tropism

We present 109 near full-length HIV genomes amplified from blood serum samples obtained during early 1986 from across Uganda, which to our knowledge is the earliest and largest population sample from the initial phase of the HIV epidemic in Africa. Consensus sequences were made from paired-end Illumina reads with a target-capture approach to amplify HIV material following poor success with standard approaches. In comparisons with a smaller 'intermediate' genome dataset from 1998 to 1999 and a 'modern' genome dataset from 2007 to 2016, the proportion of subtype D was significantly higher initially, dropping from 67% (73/109), to 57% (26/46) to 17% (82/465) respectively (p < 0.0001). Subtype D has previously been shown to have a faster rate of disease progression than other subtypes in East African population studies, and to have a higher propensity to use the CXCR4 co-receptor ("X4 tropism"); associated with a decrease in time to AIDS. Here we find significant differences in predicted tropism between A1 and D subtypes in all three sample periods considered, which is particularly striking the 1986 sample: 66% (53/80) of subtype D env sequences were predicted to be X4 tropic compared with none of the 24 subtype A1. We also analysed the frequency of subtype in the envelope region of inter-subtype recombinants, and found that subtype A1 is over-represented in env, suggesting recombination and selection have acted to remove subtype D env from circulation. The reduction of subtype D frequency over three decades therefore appears to be a result of selective pressure against X4 tropism and its higher virulence. Lastly, we find a subtype D specific codon deletion at position 24 of the V3 loop, which may explain the higher propensity for subtype D to utilise X4 tropism

Migration experiences, employment status and psychological distress among Somali immigrants: a mixed-method international study

Background: The discourse about mental health problems among migrants and refugees tends to focus on adverse pre-migration experiences; there is less investigation of the environmental conditions in which refugee migrants live, and the contrasts between these situations in different countries. This cross-national study of two samples of Somali refugees living in London (UK) and Minneapolis, Minnesota, (USA) helps to fill a gap in the literature, and is unusual in being able to compare information collected in the same way in two cities in different countries. Methods: There were two parts to the study, focus groups to gather in-depth qualitative data and a survey of health status and quantifiable demographic and material factors. Three of the focus groups involved nineteen Somali professionals and five groups included twenty-eight lay Somalis who were living in London and Minneapolis. The quantitative survey was done with 189 Somali respondents, also living in London and Minneapolis. We used the MINI International Neuropsychiatric Interview (MINI) to assess ICD-10 and Results: The overall qualitative and quantitative results suggested that challenges to masculinity, thwarted aspirations, devalued refugee identity, unemployment, legal uncertainties and longer duration of stay in the host country account for poor psychological well-being and psychiatric disorders among this group. Conclusion: The use of a mixed-methods approach in this international study was essential since the quantitative and qualitative data provide different layers and depth of meaning and complement each other to provide a fuller picture of complex and multi-faceted life situations of refugees and asylum seekers. The comparison between the UK and US suggests that greater flexibility of access to labour markets for this refugee group might help to promote opportunities for better integration and mental well-being

Land use change alters malaria transmission parameters by modifying temperature in a highland area of Uganda

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/73403/1/j.1365-3156.2000.00551.x.pd

Individual, family and offence characteristics of high risk childhood offenders: comparing non-offending, one-time offending and re-offending Dutch-Moroccan migrant children in the Netherlands

<p>Abstract</p> <p>Background</p> <p>Childhood offenders are at an increased risk for developing mental health, social and educational problems later in life. An early onset of offending is a strong predictor for future persistent offending. Childhood offenders from ethnic minority groups are a vulnerable at-risk group. However, up until now, no studies have focused on them.</p> <p>Aims</p> <p>To investigate which risk factors are associated with (re-)offending of childhood offenders from an ethnic minority.</p> <p>Method</p> <p>Dutch-Moroccan boys, who were registered by the police in the year 2006-2007, and their parents as well as a control group (n = 40) were interviewed regarding their individual and family characteristics. Two years later a follow-up analysis of police data was conducted to identify one-time offenders (n = 65) and re-offenders (n = 35).</p> <p>Results</p> <p>All groups, including the controls, showed substantial problems. Single parenthood (OR 6.0) and financial problems (OR 3.9) distinguished one-time offenders from controls. Reading problems (OR 3.8), having an older brother (OR 5.5) and a parent having Dutch friends (OR 4.3) distinguished re-offenders from one-time offenders. First offence characteristics were not predictive for re-offending. The control group reported high levels of emotional problems (33.3%). Parents reported not needing help for their children but half of the re-offender's families were known to the Child Welfare Agency, mostly in a juridical framework.</p> <p>Conclusion</p> <p>The Moroccan subgroup of childhood offenders has substantial problems that might hamper healthy development. Interventions should focus on reaching these families tailored to their needs and expectations using a multi-system approach.</p

Intronic ATTTC repeat expansions in STARD7 in familial adult myoclonic epilepsy linked to chromosome 2

Familial Adult Myoclonic Epilepsy (FAME) is characterised by cortical myoclonic tremor usually from the second decade of life and overt myoclonic or generalised tonic-clonic seizures. Four independent loci have been implicated in FAME on chromosomes (chr) 2, 3, 5 and 8. Using whole genome sequencing and repeat primed PCR, we provide evidence that chr2-linked FAME (FAME2) is caused by an expansion of an ATTTC pentamer within the first intron of STARD7. The ATTTC expansions segregate in 158/158 individuals typically affected by FAME from 22 pedigrees including 16 previously reported families recruited worldwide. RNA sequencing from patient derived fibroblasts shows no accumulation of the AUUUU or AUUUC repeat sequences and STARD7 gene expression is not affected. These data, in combination with other genes bearing similar mutations that have been implicated in FAME, suggest ATTTC expansions may cause this disorder, irrespective of the genomic locus involved

Intronic ATTTC repeat expansions in STARD7 in familial adult myoclonic epilepsy linked to chromosome 2

Familial Adult Myoclonic Epilepsy (FAME) is characterised by cortical myoclonic tremor usually from the second decade of life and overt myoclonic or generalised tonic-clonic seizures. Four independent loci have been implicated in FAME on chromosomes (chr) 2, 3, 5 and 8. Using whole genome sequencing and repeat primed PCR, we provide evidence that chr2-linked FAME (FAME2) is caused by an expansion of an ATTTC pentamer within the first intron of STARD7. The ATTTC expansions segregate in 158/158 individuals typically affected by FAME from 22 pedigrees including 16 previously reported families recruited worldwide. RNA sequencing from patient derived fibroblasts shows no accumulation of the AUUUU or AUUUC repeat sequences and STARD7 gene expression is not affected. These data, in combination with other genes bearing similar mutations that have been implicated in FAME, suggest ATTTC expansions may cause this disorder, irrespective of the genomic locus involved

Epidemiology and interactions of Human Immunodeficiency Virus - 1 and Schistosoma mansoni in sub-Saharan Africa.

Human Immunodeficiency Virus-1/AIDS and Schistosoma mansoni are widespread in sub-Saharan Africa and co-infection occurs commonly. Since the early 1990s, it has been suggested that the two infections may interact and potentiate the effects of each other within co-infected human hosts. Indeed, S. mansoni infection has been suggested to be a risk factor for HIV transmission and progression in Africa. If so, it would follow that mass deworming could have beneficial effects on HIV-1 transmission dynamics. The epidemiology of HIV in African countries is changing, shifting from urban to rural areas where the prevalence of Schistosoma mansoni is high and public health services are deficient. On the other side, the consequent pathogenesis of HIV-1/S. mansoni co-infection remains unknown. Here we give an account of the epidemiology of HIV-1 and S. mansoni, discuss co-infection and possible biological causal relationships between the two infections, and the potential impact of praziquantel treatment on HIV-1 viral loads, CD4+ counts and CD4+/CD8+ ratio. Our review of the available literature indicates that there is evidence to support the hypothesis that S. mansoni infections can influence the replication of the HIV-1, cell-to-cell transmission, as well as increase HIV progression as measured by reduced CD4+ T lymphocytes counts. If so, then deworming of HIV positive individuals living in endemic areas may impact on HIV-1 viral loads and CD4+ T lymphocyte counts.RIGHTS : This article is licensed under the BioMed Central licence at http://www.biomedcentral.com/about/license which is similar to the 'Creative Commons Attribution Licence'. In brief you may : copy, distribute, and display the work; make derivative works; or make commercial use of the work - under the following conditions: the original author must be given credit; for any reuse or distribution, it must be made clear to others what the license terms of this work are

Cellular therapies for treating pain associated with spinal cord injury

Spinal cord injury leads to immense disability and loss of quality of life in human with no satisfactory clinical cure. Cell-based or cell-related therapies have emerged as promising therapeutic potentials both in regeneration of spinal cord and mitigation of neuropathic pain due to spinal cord injury. This article reviews the various options and their latest developments with an update on their therapeutic potentials and clinical trialing