Last data update: May 28, 2024. (Total: 46864 publications since 2009)
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Query Trace: Descamps D [original query] |
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Recommendations on data sharing in HIV drug resistance research
Inzaule SC , Siedner MJ , Little SJ , Avila-Rios S , Ayitewala A , Bosch RJ , Calvez V , Ceccherini-Silberstein F , Charpentier C , Descamps D , Eshleman SH , Fokam J , Frenkel LM , Gupta RK , Ioannidis JPA , Kaleebu P , Kantor R , Kassaye SG , Kosakovsky Pond SL , Kouamou V , Kouyos RD , Kuritzkes DR , Lessells R , Marcelin AG , Mbuagbaw L , Minalga B , Ndembi N , Neher RA , Paredes R , Pillay D , Raizes EG , Rhee SY , Richman DD , Ruxrungtham K , Sabeti PC , Schapiro JM , Sirivichayakul S , Steegen K , Sugiura W , van Zyl GU , Vandamme AM , Wensing AMJ , Wertheim JO , Gunthard HF , Jordan MR , Shafer RW . PLoS Med 2023 20 (9) e1004293 Author summary • Human immunodeficiency virus (HIV) drug resistance has implications for antiretroviral treatment strategies and for containing the HIV pandemic because the development of HIV drug resistance leads to the requirement for antiretroviral drugs that may be less effective, less well-tolerated, and more expensive than those used in first-line regimens. • HIV drug resistance studies are designed to determine which HIV mutations are selected by antiretroviral drugs and, in turn, how these mutations affect antiretroviral drug susceptibility and response to future antiretroviral treatment regimens. • Such studies collectively form a vital knowledge base essential for monitoring global HIV drug resistance trends, interpreting HIV genotypic tests, and updating HIV treatment guidelines. • Although HIV drug resistance data are collected in many studies, such data are often not publicly shared, prompting the need to recommend best practices to encourage and standardize HIV drug resistance data sharing. • In contrast to other viruses, sharing HIV sequences from phylogenetic studies of transmission dynamics requires additional precautions as HIV transmission is criminalized in many countries and regions. • Our recommendations are designed to ensure that the data that contribute to HIV drug resistance knowledge will be available without undue hardship to those publishing HIV drug resistance studies and without risk to people living with HIV. |
Notes from the field: Exposures to mpox among cases in children aged 12 years - United States, September 25-December 31, 2022
Nemechek K , Stefanos R , Miller EL , Riser A , Kebede B , Galang RR , Hufstetler K , Descamps D , Balenger A , Hennessee I , Neelam V , Hutchins HJ , Labuda SM , Davis KM , McCormick DW , Marx GE , Kimball A , Ruberto I , Williamson T , Rzucidlo P , Willut C , Harold RE , Mangla AT , English A , Brikshavana D , Blanding J , Kim M , Finn LE , Marutani A , Lockwood M , Johnson S , Ditto N , Wilton S , Edmond T , Stokich D , Shinall A , Alravez B , Crawley A , Nambiar A , Gateley EL , Schuman J , White SL , Davis K , Milleron R , Mendez M , Kawakami V , Segaloff HE , Bower WA , Ellington SR , McCollum AM , Pao LZ . MMWR Morb Mortal Wkly Rep 2023 72 (23) 633-635 During May 17–December 31, 2022, 125 probable or confirmed U.S. monkeypox (mpox)† cases were reported among patients aged <18 years, including 45 (36%) in children aged ≤12 years. Eighty-three cases in persons aged <18 years diagnosed during May 17–September 24, 2022 were previously described (1); 28 (34%) of these were in children aged ≤12 years, 29% of whom did not have reported information on exposure. Among 20 (71%) of 28 patients with documented information on exposure, most were exposed by a household contact. This report updates the previous report using data collected during September 25–December 31, 2022, proposes possible mpox exposure routes in children aged ≤12 years, and describes three U.S. mpox cases in neonates. Household members or caregivers with mpox, including pregnant women and their health care providers, should be informed of the risk of transmission to persons aged <18 years, and strategies to protect persons aged <18 years at risk for exposure, including isolating household contacts with mpox, should be implemented immediately. | | During September 25–December 31, 2022, 17 children aged ≤12 years with probable or confirmed mpox were identified through national surveillance. CDC provided a questionnaire to state and local health departments for collection of the child’s history of exposure to any person with mpox§ during the previous 3 weeks, exposure settings, types of contact (e.g., skin-to-skin, being held or cuddled, diaper change, or toilet use), and precautions taken by the person with mpox (e.g., practiced isolation or covered lesions). This activity was reviewed by CDC and was conducted consistent with applicable federal law and CDC policy.¶ |
Geographic and temporal trends in the molecular epidemiology and genetic mechanisms of transmitted HIV-1 drug resistance: an individual-patient- and sequence-level meta-analysis.
Rhee SY , Blanco JL , Jordan MR , Taylor J , Lemey P , Varghese V , Hamers RL , Bertagnolio S , de Wit TF , Aghokeng AF , Albert J , Avi R , Avila-Rios S , Bessong PO , Brooks JI , Boucher CA , Brumme ZL , Busch MP , Bussmann H , Chaix ML , Chin BS , D'Aquin TT , De Gascun CF , Derache A , Descamps D , Deshpande AK , Djoko CF , Eshleman SH , Fleury H , Frange P , Fujisaki S , Harrigan PR , Hattori J , Holguin A , Hunt GM , Ichimura H , Kaleebu P , Katzenstein D , Kiertiburanakul S , Kim JH , Kim SS , Li Y , Lutsar I , Morris L , Ndembi N , Ng KP , Paranjape RS , Peeters M , Poljak M , Price MA , Ragonnet-Cronin ML , Reyes-Teran G , Rolland M , Sirivichayakul S , Smith DM , Soares MA , Soriano VV , Ssemwanga D , Stanojevic M , Stefani MA , Sugiura W , Sungkanuparph S , Tanuri A , Tee KK , Truong HH , van de Vijver DA , Vidal N , Yang C , Yang R , Yebra G , Ioannidis JP , Vandamme AM , Shafer RW . PLoS Med 2015 12 (4) e1001810 BACKGROUND: Regional and subtype-specific mutational patterns of HIV-1 transmitted drug resistance (TDR) are essential for informing first-line antiretroviral (ARV) therapy guidelines and designing diagnostic assays for use in regions where standard genotypic resistance testing is not affordable. We sought to understand the molecular epidemiology of TDR and to identify the HIV-1 drug-resistance mutations responsible for TDR in different regions and virus subtypes. METHODS AND FINDINGS: We reviewed all GenBank submissions of HIV-1 reverse transcriptase sequences with or without protease and identified 287 studies published between March 1, 2000, and December 31, 2013, with more than 25 recently or chronically infected ARV-naive individuals. These studies comprised 50,870 individuals from 111 countries. Each set of study sequences was analyzed for phylogenetic clustering and the presence of 93 surveillance drug-resistance mutations (SDRMs). The median overall TDR prevalence in sub-Saharan Africa (SSA), south/southeast Asia (SSEA), upper-income Asian countries, Latin America/Caribbean, Europe, and North America was 2.8%, 2.9%, 5.6%, 7.6%, 9.4%, and 11.5%, respectively. In SSA, there was a yearly 1.09-fold (95% CI: 1.05-1.14) increase in odds of TDR since national ARV scale-up attributable to an increase in non-nucleoside reverse transcriptase inhibitor (NNRTI) resistance. The odds of NNRTI-associated TDR also increased in Latin America/Caribbean (odds ratio [OR] = 1.16; 95% CI: 1.06-1.25), North America (OR = 1.19; 95% CI: 1.12-1.26), Europe (OR = 1.07; 95% CI: 1.01-1.13), and upper-income Asian countries (OR = 1.33; 95% CI: 1.12-1.55). In SSEA, there was no significant change in the odds of TDR since national ARV scale-up (OR = 0.97; 95% CI: 0.92-1.02). An analysis limited to sequences with mixtures at less than 0.5% of their nucleotide positions-a proxy for recent infection-yielded trends comparable to those obtained using the complete dataset. Four NNRTI SDRMs-K101E, K103N, Y181C, and G190A-accounted for >80% of NNRTI-associated TDR in all regions and subtypes. Sixteen nucleoside reverse transcriptase inhibitor (NRTI) SDRMs accounted for >69% of NRTI-associated TDR in all regions and subtypes. In SSA and SSEA, 89% of NNRTI SDRMs were associated with high-level resistance to nevirapine or efavirenz, whereas only 27% of NRTI SDRMs were associated with high-level resistance to zidovudine, lamivudine, tenofovir, or abacavir. Of 763 viruses with TDR in SSA and SSEA, 725 (95%) were genetically dissimilar; 38 (5%) formed 19 sequence pairs. Inherent limitations of this study are that some cohorts may not represent the broader regional population and that studies were heterogeneous with respect to duration of infection prior to sampling. CONCLUSIONS: Most TDR strains in SSA and SSEA arose independently, suggesting that ARV regimens with a high genetic barrier to resistance combined with improved patient adherence may mitigate TDR increases by reducing the generation of new ARV-resistant strains. A small number of NNRTI-resistance mutations were responsible for most cases of high-level resistance, suggesting that inexpensive point-mutation assays to detect these mutations may be useful for pre-therapy screening in regions with high levels of TDR. In the context of a public health approach to ARV therapy, a reliable point-of-care genotypic resistance test could identify which patients should receive standard first-line therapy and which should receive a protease-inhibitor-containing regimen. |
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