Purpose of review: The causes of ethnic or benign neutropenia have long been unclear. Here, we discuss the emerging data on the causes and consequences of neutropenia and discuss the relevance of these data for African populations, in which the prevalence of neutropenia is high.
Recent findings: Genetic deletion of the Duffy antigen receptor for chemokines (DARC-null genotype) has been identified as a major determinant for neutropenia. DARC acts as a receptor for Plasmodium vivax malaria and the DARC-null genotype has thus been positively selected among Africans; however, recent studies suggest that Duffy-null-linked neutropenia could increase the risk of HIV infection. Data are emerging that neutrophils are versatile cells that play a critical role not only in direct antimicrobial activity but also in priming and regulating the activity of other innate and adaptive immune cells. Therefore, we discuss here the imperative to better understand the causes, consequences, and the underlying mechanisms of neutropenia among Africans as a prerequisite for rational and optimal biomedical interventions to improve health outcomes.
Summary: Neutropenia among Africans, linked to the Duffy-null trait or otherwise, may have significant health consequences that remain largely undetermined and could have a significant impact on the pathogenesis of diseases.
aHIV Pathogenesis Programme, Doris Duke Medical Research Institute
bKwaZulu-Natal Research Institute for Tuberculosis and HIV, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, Durban, South Africa
cRagon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard University, Boston, Massachusetts, USA
dMax Planck Institute for Infection Biology, Berlin, Germany
Correspondence to Thumbi Ndung’u, PhD, HIV Pathogenesis Programme, Doris Duke Medical Research Institute, Nelson R. Mandela School of Medicine, University of KwaZulu-Natal, 719 Umbilo Road, Durban, 4013, South Africa. Tel: +27 31 260 4727; fax: +27 31 260 4623; e-mail: email@example.com