HTLV-1 and HTLV-2 prevalence in the United States.

During the 1980s and early 1990s, there was considerable interest in the seroepidemiology of human T-lymphotropic virus (HTLV) types 1 and 2. The limitations of these studies included a focus on areas of described high prevalence, distinct ancient populations, or high-risk groups through social behavior and the use of diagnostic assays that lacked specificity. However, based on these data, de Thé and Bomford could make a crude estimate of 10–20 million HTLV-1 infections in their review of the need for an HTLV-1 vaccine [1]. This was followed by a period of relative epidemiological inactivity, during which the global population increased by approximately 1 billion. The burden of this population growth has been in many of the regions that are endemic for HTLV1 infection. Gessain et al [2] recently published a revised estimate of 5–10 million infections but took care to note that this was based on only 1.5 billion of the world’s 7 billion inhabitants. Furthermore, Hlela et al [3] found only 17 published studies on the prevalence of HTLV infections in general populations, and none from Europe or North America. Although it does not completely fill this gap, the article by Chang et al [4] in this issue of The Journal is an extremely welcome addition to the literature. It is the first detailed study of HTLV-1 and HTLV-2 prevalence in new blood donors within the United States for more than a decade. It not only provides contemporary data from 2000–2009, which are sufficient to look in detail at trends over time, but also provides the opportunity for comparison with data from the same risk population during the early to mid-1990s [5]. Chang et al [4] show that HTLVs remain prevalent in the United States, withHTLV-2more common thanHTLV-1, and an overall prevalence of 22/ 100 000 population. As the authors clearly highlight, these data will underestimate the prevalence of infections in the general population because the aim of screening questionnaires is to identify and exclude high risk populations from blood donation. The authors suggest that this may underestimate the true prevalence of these bloodborne viruses in the general population by 3–5-fold. In data from Europe based on unselected antenatal clinic attendees, an imperfect surrogate, as the comparator, a 6-fold difference was observed in a multinational study despite widely differing prevalence rates [6]. Comparisons with the general population are further complicated because the prevalence of HTLV infection rises with age, most dramatically among women. However, applying this assumption to the data from Chang et al [4] suggests an overall general population prevalence in the United States of 0.1%–0.2%. Importantly, the authors have identified significant variation in HTLV prevalence by region and have reported that the pockets of high prevalence differ for HTLV-1 and HTLV-2. These are mapped only in the counties in which >5000 first -donors had been tested; thus, the extent of such pockets remains to be fully elucidated. Notable absenteesare counties inNewYork andFlorida, where patients commonly present with HTLV-related diseases are. Conversely, the data identify some counties that have a high prevalence among blood donors, but are less well recognized for a high incidence of HTLV-1–associated diseases. Further work is needed to complete this important mapping exercise. As reported in endemic regions, HTLV prevalence among the blood donors is highly age dependent, increasing from 1.3 to 9.3 per 100 000 for HTLV-1 and from 3.6 to 27 per 100 000 for HTLV-2 either side of age 30 years. The peak in HTLV-2 infection among women in the 40–49-year age cohort observed in the 1990–1996 data was attributed to a period during the 1960s and 1970s when injecting drug use was more widespread; this use later tailed off, presumably owing to health concerns related to human immunodeficiency virus. An alternative explanation may have been that HTLV-2 causes premature death. This seemed unlikely in the absence, apart from rare cases of HTLV-2–associated myelopathy, of clear disease associations with Received 11 October 2013; accepted 16 October 2013; electronically published 23 October 2013. Correspondence: Graham P. Taylor MD, Section of Infectious Diseases, Faculty of Medicine, Imperial College, Norfolk Place, London, W2 1PG, UK (g.p.taylor@imperial.ac.uk). The Journal of Infectious Diseases 2014;209:486–7 © The Author 2013. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail: journals. permissions@oup.com. DOI: 10.1093/infdis/jit558