We discovered a highly virulent variant of subtype-B HIV-1 in the Netherlands. One hundred nine individuals with this variant had a 0.54 to 0.74 log 10 increase (i.e., a ~3.5-fold to 5.5-fold increase) in viral load compared with, and exhibited CD4 cell decline twice as fast as, 6604 individuals with other subtype-B strains. Without treatment, advanced HIV—CD4 cell counts below 350 cells per cubic millimeter, with long-term clinical consequences—is expected to be reached, on average, 9 months after diagnosis for individuals in their thirties with this variant. Age, sex, suspected mode of transmission, and place of birth for the aforementioned 109 individuals were typical for HIV-positive people in the Netherlands, which suggests that the increased virulence is attributable to the viral strain. Genetic sequence analysis suggests that this variant arose in the 1990s from de novo mutation, not recombination, with increased transmissibility and an unfamiliar molecular mechanism of virulence.
In this population of CL patients displaying variable degrees of complexity and severity, almost two-thirds of patients could be initially managed without systemic therapy. Of these, 60 were cured before day 60. The WHO-recommended stepwise approach favoring initial local therapy therefore resulted in at least 44% of all patients being cured without exposure to the risk of systemic adverse events. Efforts are needed to further simplify local therapy of CL and to improve the management of patients with complex lesions and/or preexisting comorbidities.
Treponema pallidum subsp. pallidum, the causative agent of sexually transmitted syphilis, detected in clinical samples from France, was subjected to molecular typing using the recently developed Multilocus Sequence Typing system. The samples (n = 133) used in this study were collected from 2010–2016 from patients with diagnosed primary or secondary syphilis attending outpatient centers or hospitals in several locations in France. Altogether, 18 different allelic profiles were found among the fully typed samples (n = 112). There were five allelic variants identified for TP0136, 12 for TP0548, and eight for TP0705. Out of the identified alleles, one, seven, and three novel alleles were identified in TP0136, TP0548, and TP0705, respectively. Partial allelic profiles were obtained from 6 samples. The majority of samples (n = 110) belonged to the SS14-like cluster of TPA isolates while 7 clustered with Nichols-like isolates. Patients infected with Nichols-like samples were more often older (p = 0.041) and more often diagnosed with secondary syphilis (p = 0.033) compared to patients infected with SS14-like samples. In addition, macrolide resistance caused by the A2058G mutation was found to be associated with allelic profile 1.3.1 or with strains belonging to the 1.3.1 lineage (p<0.001). The genetic diversity among TPA strains infecting the European population was surprisingly high, which suggests that additional studies are needed to reveal the full genetic diversity of TPA pathogens infecting humans.
ObjectivesTo determine the incidence rate and risk factors for loss to follow-up (LFU) in HIV-infected individuals. MethodsWe estimated the incidence rate of LFU in 1756 HIV-infected patients enrolled in the Tourcoing Clinical Cohort from January 1985 to January 1998. We then investigated potential LFU risk factors at inclusion through a case-control study. Cases were 209 patients who had attended neither our clinic nor another HIV clinic for at least 1 year. Controls were 209 patients randomly selected from the group of HIV-infected patients followed up regularly. ResultsThe incidence of LFU was estimated at 4.3 per 100 person-years [95% confidence interval (CI) 3.7-4.9]. Independent risk factors for LFU were (i) year of enrolment before 1993 [odds ratio (OR) 6.7; 95% CI 2.7-16.5 versus after 1997]; (ii) year of enrolment between 1993 and 1997 (OR 5.1; 95% CI 2.0-13.0 versus after 1997); (iii) ageo30 years (OR 1.8; 95% CI 1.0-3.5 versus 440 years); (iv) injecting drug use (OR 5.3; 95% CI 2.7-10.5 versus men who have sex with men); (v) homelessness and/or illegal immigrant status (OR 2.2; 95% CI 1.0-4.9); and (vi) lack of a primary care provider (OR 6.0; 95% CI 2.4-15.1). A history of an AIDS-defining illness (OR 0.3; 95% CI 0.2-0.6) and a history of psychiatric disease (OR 0.4; 95% CI 0.3-0.8) were both associated with a decreased risk of LFU. ConclusionsThis study assessed the sociodemographic, clinical and behavioural characteristics associated with LFU in HIV-infected patients. The findings of this study may allow clinicians to identify patients at risk of LFU, so that appropriate interventions may be initiated.
Diagnoses of bacterial sexually transmitted infections (STI) have been increasing in France since their resurgence in the late 1990s. This article presents recent epidemiological trends until 2016 and the patients’ characteristics. STI surveillance relies on sentinel networks: a clinician-based network RésIST (clinical, biological and behavioural data for early syphilis and gonorrhoea), the lymphogranuloma venereum (LGV) network (clinical, biological and behavioural data for rectal LGV, and the laboratory networks Rénachla and Rénago (demographic and biological data for chlamydial infections and gonorrhoea, respectively). Here we describe trends between 2014 and 2016, using data from diagnostic centres which participated regularly during the study period. The number of early syphilis, gonorrhoea and LGV diagnoses increased between 2014 and 2016, particularly in men who have sex with men. An increase in syphilis and gonorrhoea cases was also observed in heterosexuals. Nevertheless, we observed a drop in 2016 for syphilis and chlamydial infections after two decades of increases. Under-reporting and shortage of benzathine penicillin in 2016 may explain this latest evolution. Regular screening of patients and partners, followed by prompt treatment, remains essential to interrupt STI transmission in a context where human immunodeficiency virus (HIV) prevention has expanded towards biomedical prophylaxis.
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