RESUMO
We report investigation of 22 TB cases with positive Xpert MTB/RIF result for resistance to Rifampin and "Very Low" MTB detection level. Twelve cases were false positive without rpoB mutations, 2 were false-positives with a silent mutation in rpoB codon T508, and only 10 were true positives.
Assuntos
Carga Bacteriana , Testes de Sensibilidade Microbiana , Mycobacterium tuberculosis/efeitos dos fármacos , Mycobacterium tuberculosis/genética , Reação em Cadeia da Polimerase em Tempo Real , Rifampina/farmacologia , Tuberculose Resistente a Múltiplos Medicamentos/diagnóstico , Tuberculose Resistente a Múltiplos Medicamentos/microbiologia , Humanos , Mutação , Reprodutibilidade dos Testes , Escarro/microbiologia , Tuberculose Pulmonar/diagnóstico , Tuberculose Pulmonar/microbiologiaRESUMO
More than 1 million HIV-exposed, uninfected infants are born annually to HIV-positive mothers worldwide. This growing population of infants experiences twice the mortality of HIV-unexposed infants. We found that although there were very few differences seen in the microbiomes of mothers with and without HIV infection, maternal HIV infection was associated with changes in the microbiome of HIV-exposed, uninfected infants. Furthermore, we observed that human breast milk oligosaccharides were associated with bacterial species in the infant microbiome. The disruption of the infant's microbiome associated with maternal HIV infection may contribute to the increased morbidity and mortality of HIV-exposed, uninfected infants.
Assuntos
Infecções por HIV/transmissão , Microbiota/fisiologia , Aleitamento Materno , Estudos Transversais , Feminino , Infecções por HIV/microbiologia , Humanos , Recém-Nascido , Transmissão Vertical de Doenças Infecciosas , Leite Humano/química , Mães , Oligossacarídeos/metabolismo , Gravidez , Complicações Infecciosas na Gravidez/microbiologia , Estudos Prospectivos , Fatores de RiscoRESUMO
Human immunodeficiency virus (HIV-1) infection causes chronic inflammation. COX-2-derived prostaglandin E(2) (PGE(2)) has been linked to both inflammation and carcinogenesis. We hypothesized that HIV-1 could induce COX-2 in cervical tissue and increase systemic PGE(2) levels and that these alterations could play a role in AIDS-related cervical cancer. Levels of cervical COX-2 mRNA and urinary PGE-M, a biomarker of systemic PGE(2) levels, were determined in 17 HIV-negative women with a negative cervical human papilloma virus (HPV) test, 18 HIV-infected women with a negative HPV test, and 13 HIV-infected women with cervical HPV and high-grade squamous intraepithelial lesions on cytology. Cervical COX-2 levels were significantly associated with HIV and HPV status (P = 0.006 and 0.002, respectively). Median levels of urinary PGE-M were increased in HIV-infected compared with uninfected women (11.2 vs. 6.8 ng/mg creatinine, P = 0.02). Among HIV-infected women, urinary PGE-M levels were positively correlated with plasma HIV-1 RNA levels (P = 0.003). Finally, levels of cervical COX-2 correlated with urinary PGE-M levels (P = 0.005). This study shows that HIV-1 infection is associated with increased cervical COX-2 and elevated systemic PGE(2) levels. Drugs that inhibit the synthesis of PGE(2) may prove useful in reducing the risk of cervical cancer or systemic inflammation in HIV-infected women.