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Olivia Sánchez-Cabral,1 Dina Martínez-Mendoza,1,2 Ángel Paul Flores-Bello,3 José Arturo Martínez-Orozco,4 Rosa María Rivera-Rosales,5 César Luna-Rivero,5 Patricio Santillán-Doherty,6 Gustavo Reyes-Terán7 1Interventional Pulmonology Unit, 2Hospital Epidemiology Surveillance Unit, 3Clinic of Tuberculosis and Pleural Diseases, 4Department of Infectious Diseases and Clinical Microbiology, 5Anatomic Pathology Service, 6Medical Direction, 7Department of Research in Infectious Diseases, National Institute of Respiratory Diseases Ismael Cosío Villegas, Mexico City, Mexico Background: The key diagnostic method for the evaluation of lung diseases associated with HIV infection is bronchoscopy, with bronchoalveolar lavage (BAL) being the most commonly used sampling technique. Transbronchial biopsy (TBB) is often complementary. Setting: This is a retrospective cross-sectional study to determine the diagnostic usefulness of bronchoscopy with simultaneous samples obtained through BAL and TBB in HIV-infected patients with pneumonia at the National Institute of Respiratory Diseases Ismael Cosío Villegas. Methods: In this cross-sectional study (January 2014–December 2015), the diagnostic yield of bronchoscopic samples from all HIV-positive patients with pneumonia aged >18years, from procedures performed in the Interventional Pulmonology Unit, was analyzed and recorded in its database. The diagnostic yield concordance between BAL and TBB samples was evaluated by kappa index calculation. Results: A total of 198 procedures on 189 HIV-infected patients with pneumonia were performed. A total of 167/189 (88.4%) patients were male, and the mean age was 34.7years (SD ±9.0). Overall, the diagnostic yield for either technique was 87.9% (174/198), but it was higher for TBB, its yield being 78.8% (156/198). In contrast, that of BAL was 62.1% (123/198) (P=0.001). The overall diagnostic yield concordance between TBB and BAL was insignificant (κ=0.213, P

Background Antiretroviral therapy (ART) is crucial for controlling HIV-1 infection through wide-scale treatment as prevention and pre-exposure prophylaxis (PrEP). Potent tenofovir disoproxil fumarate-containing regimens are increasingly used to treat and prevent HIV, although few data exist for frequency and risk factors of acquired drug resistance in regions hardest hit by the HIV pandemic. We aimed to do a global assessment of drug resistance after virological failure with first-line tenofovir-containing ART. Methods The TenoRes collaboration comprises adult HIV treatment cohorts and clinical trials of HIV drug resistance testing in Europe, Latin and North America, sub-Saharan Africa, and Asia. We extracted and harmonised data for patients undergoing genotypic resistance testing after virological failure with a first-line regimen containing tenofovir plus a cytosine analogue (lamivudine or emtricitabine) plus a non-nucleotide reverse-transcriptase inhibitor (NNRTI; efavirenz or nevirapine). We used an individual participant-level meta-analysis and multiple logistic regression to identify covariates associated with drug resistance. Our primary outcome was tenofovir resistance, defined as presence of K65R/N or K70E/G/Q mutations in the reverse transcriptase (RT) gene. Findings We included 1926 patients from 36 countries with treatment failure between 1998 and 2015. Prevalence of tenofovir resistance was highest in sub-Saharan Africa (370/654 [57%]). Pre-ART CD4 cell count was the covariate most strongly associated with the development of tenofovir resistance (odds ratio [OR] 1·50, 95% CI 1·27–1·77 for CD4 cell count

Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associa

Background Some individuals repeatedly exposed to Human Immunodeficiency Virus do not seroconvert and are resistant to HIV infection. Here, in a pediatric cohort of HIV seronegative infants born of HIV-infected mothers, we have studied eight non-breastfed children in whom viral DNA was detected in their PBMC. Our objective was to assess whether silent infection in these children can be explained by the presence of integrated viral DNA. Methods The presence of viral DNA was corroborated by nested PCR with primers for gag and the nef/LTR regions of HIV-1. Integration of HIV DNA into the host genome was assessed by an Alu-LTR PCR. Amplicons were sequenced and phylogenetic analyzes were done. Results HIV-1 DNA was detected in the earliest available PBMC sample from all eight infants, and two of them tested positive for HIV DNA at 2 years of age. Nested PCR resulted in the amplification of gag, nef/LTR and Alu-LTR fragments, which demostrated that HIV-1 DNA was integrated in the host cell genome. Each individual has a characteristic sequence pattern and is different from the LTR sequence of HXB2 prototype virus and other Mexican isolates. Conclusion HIV-1 DNA was observed in PBMC from HIV exposed seronegative children in this pediatric cohort.

Infection with the human immunodeficiency virus (HIV) leads to a decrease in CD4(+) T cells and disease progression within a decade of seroconversion. However, a small group of infected people, despite being infected by HIV for 10 or more years, remain clinically asymptomatic and have stable CD4(+) cell counts without taking antiretroviral medication. To determine why these individuals, known as long-term survivors (LTS), remain healthy, the hematological profiles, viral load and properties, HIV coreceptor genotype, and anti-HIV immune responses of these people were compared with those of individuals who have progressed to disease (Progressors) over the same time period. Unlike Progressors, LTS have a low circulating viral load and a low number of HIV-infected cells. These differences in the levels of the viral load were not associated with a dominant biologic viral phenotype, varying growth kinetics of the virus, mutation in the cellular CCR5 gene, or the presence of neutralizing antibodies. Importantly, the difference in viral load could be explained by the enhanced ability of CD8(+) cells from LTS to suppress HIV replication.