Zika virus (ZIKV) is causing an unprecedented epidemic linked to severe congenital syndromes1,2. In July 2016, mosquito-borne ZIKV transmission was reported in the continental United States and since then, hundreds of locally-acquired infections have been reported in Florida3,4. To gain insights into the timing, source, and likely route(s) of ZIKV introduction, we tracked the virus from its first detection in Florida by sequencing ZIKV genomes from infected patients and Aedes aegypti mosquitoes. We show that at least four introductions, but potentially as many as 40, contributed to the outbreak in Florida and that local transmission likely started in the spring of 2016 - several months before initial detection. By analyzing surveillance and genetic data, we discovered that ZIKV moved among transmission zones in Miami. Our analyses show that most introductions are linked to the Caribbean, a finding corroborated by the high incidence rates and traffic volumes from the region into the Miami area. Our study provides an understanding of how ZIKV initiates transmission in new regions.

A multicenter, retrospective study of patients infected with carbapenem-resistant Pseudomonas aeruginosa who were treated with ceftolozane/tazobactam was performed. Among 35 patients, pneumonia was the most common indication and treatment was successful in 26 (74%). Treatment failure was observed in all cases where isolates demonstrated ceftolozane-tazobactam minimum inhibitory concentrations ≥8 μg/mL.

Zika virus (ZIKV) is causing an unprecedented epidemic linked to severe congenital syndromes 1,2 . In July 2016, mosquito-borne ZIKV transmission was first reported in the continental United States and since then, hundreds of locally-acquired infections have been reported in Florida 3 . To gain insights into the timing, source, and likely route(s) of introduction of ZIKV into the continental United States, we tracked the virus from its first detection in Miami, Florida by direct sequencing of ZIKV genomes from infected patients and Aedes aegypti mosquitoes. We show that at least four distinct ZIKV introductions contributed to the outbreak in Florida and that local transmission likely started in the spring of 2016 -several months before its initial detection. By analyzing surveillance and genetic data, we discovered that ZIKV moved among transmission zones in Miami. Our analyses show that most introductions are phylogenetically linked to the Caribbean, a finding corroborated by the high incidence rates and traffic volumes from the region into the Miami area. By comparing mosquito abundance and travel flows, we describe the areas of southern Florida that are especially vulnerable to ZIKV introductions. Our study provides a deeper understanding of how ZIKV initiates and sustains transmission in new regions.

No abstract

Interruption of all antiretroviral therapy for HIV-1 infection when therapy is failing and antiretroviral resistance has emerged is frequently associated with the disappearance of detectable resistance-associated protease and reverse transcriptase substitutions. However, the effect that discontinuation of treatment with a particular antiretroviral class has on resistance to that class when other antiretroviral therapy is continued is unknown. We investigated differences in detectable genotypic resistance to protease inhibitors (PI) and non-nucleoside reverse transcriptase inhibitors (NNRTI) among two populations: patients undergoing testing at the moment class-specific treatment failed (Group 1) and patients undergoing testing for varying periods after class-specific treatment failed and was discontinued but therapy with other antiretroviral classes continued with incomplete viral suppression (Group 2). We found that the prevalence of detectable resistance to the PI and NNRTI classes was similar in both groups despite the absence of class-specific selective pressure for lengthy periods of time in Group 2. We hypothesize that this finding may be due to nonspecific selective pressure (i.e., to nucleoside reverse transcriptase inhibitors) selecting out PI- and, to a lesser extent, NNRTI-resistant viral variants.