Finally we hypothesized that hepcidin concentrations might i

Finally we hypothesized that hepcidin concentrations might influence the subsequent risk of malaria. Intriguing data from mouse studies suggest that hepcidin might play a role in modulating clinical malaria (Wang et al., 2011; Portugal et al., 2011), but we are not aware of any previous studies that have investigated this possibility in humans. After adjustment for potential confounders, we found no significant association between hepcidin and the subsequent risk of either P. falciparum malaria or non-malarial fever. A number of possible explanations can be put forward for this negative finding. It is possible that, in CCT251545 analogue to mouse studies (Wang et al., 2011), hepcidin concentrations are not associated with severity of malaria or other infections in humans, perhaps due to hepcidin-independent iron restriction (Guida et al., 2015). However, if they are, we may have failed to detect an effect for a number of reasons. Firstly, baseline hepcidin may not influence hepcidin at the time of, or just prior to, acute malaria infection and a limitation of our study is that hepcidin was not measured routinely at the time of acute malaria. Second, given that hepcidin is controlled by multiple competing stimuli (Huang et al., 2009), hepcidin might only influence the subsequent risk of infection when very strong down-regulatory signals from ID and erythropoietic drive overwhelm weaker up-regulatory signals from malaria and other infections (Casals-Pascual et al., 2012; Jonker et al., 2013). However, the study cohort consisted of ‘healthy’ community-based children. Finally, there may also be counter-balancing effects, for example a reduced risk of malaria due to ID (Nyakeriga et al., 2004; Gwamaka et al., 2012) may counter a protective effect of higher hepcidin concentrations: all questions for future studies. In conclusion, we have shown that asymptomatic and recent febrile malaria both significantly increase hepcidin in a population of children where ID is an important cause of morbidity. Given that dietary iron absorption is impaired by elevated hepcidin (Cercamondi et al.; 2010; Prentice et al., 2012; Glinz et al., 2015), our data suggest that asymptomatic and febrile malaria contribute to the high prevalence of ID in African children. Unless malaria episodes are controlled, iron supplementation may be ineffective because of hepcidin-mediated poor iron absorption. Strategies to prevent and eliminate malaria may therefore have the added benefit of addressing an important cause of ID for children living in sub-Saharan Africa.
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Acknowledgements
Introduction Human papillomavirus (HPV) is one of the most diffuse sexually-transmitted diseases, with 60% of sexually active people being infected with at least one high-risk HPV type during their lifetime (Schiffman et al., 2007). 90% of these infections are generally cleared by the immune system within 2years from primary exposure (Woodman et al., 2007). However, in the remaining cases, infection persists for a long time causing lesions that can progress into cancer (Castle et al., 2011). In particular, a reduced number of HPV types infecting the ano-genital area are actually oncogenic viruses that lead to cervical carcinoma (Tornesello et al., 2014), the seventh most common cancer in the world (Forman et al., 2012) and the second most common cancer among women (Arbyn et al., 2011). High-risk HPVs are also responsible for other types of cancer common to both genders. In fact, around 80% of tumours of the anus, 60% of the vagina, and 40% of vulva and penis are induced by HPV, mainly the HPV 16 type (Parkin and Bray, 2006). Moreover, nearly 90% of oropharynx, 50% of nasopharynx, and 26% of oral cavity tumours show positive detection for high risk-HPV types, highlighting the causative role of this virus in head and neck cancers (Walline et al., 2013).