The beta-chemokine receptor CCR5 is required as a coreceptor by non-syncytium-inducing (NSI) strains of human immunodeficiency virus type 1 (HIV-1). NSI viruses predominate early during an infection and are thought to be important for the transmission of HIV-1. The importance of CCR5 during parenteral transmission of HIV-1 was investigated. The distribution of the homozygous deleted CCR5 genotype among 566 exposed persons with hemophilia and 97 exposed transfusion recipients indicated that the lack of CCR5 expression protected persons from infection. This suggests that the initial predominance of NSI viruses during an infection does not result from limited availability of CXCR4-expressing cells within the mucosa but rather implies a more fundamental requisite for CCR5-expressing cells early during an infection regardless of the route of transmission. In addition, no difference in the rate of progression to AIDS (CDC 1987 definition) of infected heterozygous compared with homozygous wild type subjects was observed.
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http://dx.doi.org/10.1086/515675 | DOI Listing |
AIDS Patient Care STDS
January 2025
Department of Obstetrics, Gynecology & Reproductive Sciences, University of California San Francisco, Oakland, California, USA.
Community health workers (CHWs) play a significant role in supporting health services delivery in communities with few trained health care providers. There has been limited research on ways to optimize the role of CHWs in HIV prevention service delivery. This study explored CHWs' experiences with offering HIV prevention services [HIV testing and HIV pre- and post-exposure prophylaxis (PrEP and PEP)] during three pilot studies in rural communities in Kenya and Uganda, which aimed to increase biomedical HIV prevention coverage via a structured patient-centered HIV prevention delivery model.
View Article and Find Full Text PDFElife
January 2025
The University of Cambridge Metabolic Research Laboratories, Wellcome Trust-MRC Institute of Metabolic Science, Cambridge, United Kingdom.
encodes three regulatory subunits of class IA phosphoinositide 3-kinase (PI3K), each associating with any of three catalytic subunits, namely p110α, p110β, or p110δ. Constitutional mutations cause diseases with a genotype-phenotype relationship not yet fully explained: heterozygous loss-of-function mutations cause SHORT syndrome, featuring insulin resistance and short stature attributed to reduced p110α function, while heterozygous activating mutations cause immunodeficiency, attributed to p110δ activation and known as APDS2. Surprisingly, APDS2 patients do not show features of p110α hyperactivation, but do commonly have SHORT syndrome-like features, suggesting p110α hypofunction.
View Article and Find Full Text PDFInfect Drug Resist
January 2025
Department of Public Health, School of Allied Health Sciences, Kampala International University, Western Campus, Uganda.
Introduction: Coronavirus Disease 19 (COVID-19), caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), and Human Immunodeficiency Virus (HIV) are significant 21st-century pandemics with distinct virological and clinical characteristics. COVID-19 primarily presents as an acute respiratory illness, while HIV leads to chronic immune suppression. Understanding their differences can enhance public health strategies and treatment approaches.
View Article and Find Full Text PDFInfect Drug Resist
January 2025
Department of Clinical Medicine, School of Medicine, Qinghai University, Xining, People's Republic of China.
Pneumocystis jirovecii pneumonia (PJP) is an opportunistic fungal infection that often occurs secondary to human immunodeficiency virus (HIV) infection. However, for non-HIV immunocompromised patients, such as those undergoing novel immunosuppressive treatments to manage malignancies, organ transplants, or connective tissue diseases, PJP is emerging as an increasing threat. The clinical manifestations of PJP in HIV-infected and non-HIV-infected patients differ significantly.
View Article and Find Full Text PDFFront Immunol
January 2025
Institute for Immunodeficiency, Center for Chronic Immunodeficiency (CCI), Medical Center, Faculty of Medicine, University of Freiburg, Freiburg, Germany.
Introduction: Human Cytotoxic-T-lymphocyte-antigen-4 (CTLA-4) insufficiency caused by heterozygous germline mutations in is a complex immune dysregulation and immunodeficiency syndrome presenting with reduced penetrance and variable disease expressivity, suggesting the presence of disease modifiers that trigger the disease onset and severity. Various genetic and non-genetic potential triggers have been analyzed in CTLA-4 insufficiency cohorts, however, none of them have revealed a clear association to the disease. Multiple HLA haplotypes have been positively or negatively associated with various autoimmune diseases and inborn errors of immunity (IEI) due to the relevance of MHC in the strength of the T cell responses.
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