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1.
Clin Infect Dis ; 77(10): 1416-1422, 2023 11 17.
Article in English | MEDLINE | ID: mdl-37078712

ABSTRACT

BACKGROUND: In North American countries, national guidelines have strongly recommended formula over breastmilk for people with human immunodeficiency virus (HIV) because of concern for HIV transmission. However, data from resource-limited settings suggest the risk is <1% among virally suppressed people. Information regarding breastfeeding experience in high-resource settings is lacking. METHODS: A retrospective multisite study was performed for individuals with HIV who breastfed during 2014-2022 in the United States (8 sites) and Canada (3 sites). Descriptive statistics were used for data analysis. RESULTS: Among the 72 cases reported, most had been diagnosed with HIV and were on antiretroviral therapy prior to the index pregnancy and had undetectable viral loads at delivery. Most commonly reported reasons for choosing to breastfeed were health benefits, community expectations, and parent-child bonding. Median duration of breastfeeding was 24 weeks (range, 1 day to 72 weeks). Regimens for infant prophylaxis and protocols for testing of infants and birthing parents varied widely among institutions. No neonatal transmissions occurred among the 94% of infants for whom results were available ≥6 weeks after weaning. CONCLUSIONS: This study describes the largest cohort to date of people with HIV who breastfed in North America. Findings demonstrate high variability among institutions in policies, infant prophylaxis, and infant and parental testing practices. The study describes challenges in weighing the potential risks of transmission with personal and community factors. Finally, this study highlights the relatively small numbers of patients with HIV who chose to breastfeed at any 1 location, and the need for further multisite studies to identify best care practices.


Subject(s)
Breast Feeding , HIV Infections , Female , Humans , Infant , HIV Infections/epidemiology , HIV Infections/prevention & control , HIV Infections/drug therapy , Infectious Disease Transmission, Vertical/prevention & control , Milk, Human , North America/epidemiology , Retrospective Studies , Infant, Newborn
2.
J Immunol ; 196(5): 2239-48, 2016 Mar 01.
Article in English | MEDLINE | ID: mdl-26829988

ABSTRACT

We used two different infection models to investigate the kinetics of the PcpA-dependent pneumococcal disease in mice. In a bacteremic pneumonia model, we observed a PcpA-dependent increase in bacterial burden in the lungs, blood, liver, bronchoalveolar lavage, and spleens of mice at 24 h postinfection. This PcpA-dependent effect on bacterial burden appeared earlier (within 12 h) in the focal pneumonia model, which lacks bacteremia or sepsis. Histological changes show that the ability of pneumococci to make PcpA was associated with unresolved inflammation in both models of infection. Using our bacteremic pneumonia model we further investigated the effects of PcpA on recruitment of innate immune regulatory cells. The presence of PcpA was associated with increased IL-6 levels, suppressed production of TRAIL, and reduced infiltration of polymorphonuclear cells. The ability of pneumococci to make PcpA negatively modulated both the infiltration and apoptosis of macrophages and the recruitment of myeloid-derived suppressor-like cells. The latter have been shown to facilitate the clearance and control of bacterial pneumonia. Taken together, the ability to make PcpA was strongly associated with increased bacterial burden, inflammation, and negative regulation of innate immune cell recruitment to the lung tissue during bacteremic pneumonia.


Subject(s)
Bacterial Proteins/immunology , Carrier Proteins/immunology , Immunomodulation , Myeloid Cells/immunology , Pneumonia, Pneumococcal/immunology , Pneumonia, Pneumococcal/microbiology , Streptococcus pneumoniae/immunology , Animals , Bacteremia , Bacterial Load , Bacterial Proteins/genetics , Bacterial Proteins/metabolism , Carrier Proteins/genetics , Carrier Proteins/metabolism , Cytokines/biosynthesis , Disease Models, Animal , Female , Gene Expression Regulation, Bacterial , Inflammation Mediators/metabolism , Intracellular Signaling Peptides and Proteins , Macrophages/immunology , Macrophages/metabolism , Macrophages/pathology , Mice , Mice, Transgenic , Mutation , Myeloid Cells/metabolism , Pneumonia, Pneumococcal/mortality , Pneumonia, Pneumococcal/pathology , Streptococcus pneumoniae/genetics , Streptococcus pneumoniae/metabolism , TNF-Related Apoptosis-Inducing Ligand/metabolism , Time Factors
4.
J Immunol ; 189(11): 5327-35, 2012 Dec 01.
Article in English | MEDLINE | ID: mdl-23105137

ABSTRACT

In the presence of normal serum, complement component C3 is deposited on pneumococci primarily via the classical pathway. Pneumococcal surface protein A (PspA), a major virulence factor of pneumococci, effectively inhibits C3 deposition. PspA's C terminus has a choline-binding domain that anchors PspA to the phosphocholine (PC) moieties on the pneumococcal surface. C-reactive protein (CRP), another important host defense molecule, also binds to PC, and CRP binding to pneumococci enhances complement C3 deposition through the classical pathway. Using flow cytometry of PspA(+) and PspA(-) strains, we observed that the absence of PspA led to exposure of PC, enhanced the surface binding of CRP, and increased the deposition of C3. Moreover, when the PspA(-) mutant was incubated with a pneumococcal eluate containing native PspA, there was decreased deposition of CRP and C3 on the pneumococcal surface compared with incubation with an eluate from a PspA(-) strain. This inhibition was not observed when a recombinant PspA fragment, which lacks the choline-binding region of PspA, was added to the PspA(-) mutant. Also, there was much greater C3 deposition onto the PspA(-) pneumococcus when exposed to normal mouse serum from wild-type mice as compared with that from CRP knockout mice. Furthermore, when CRP knockout mouse serum was replenished with CRP, there was a dose-dependent increase in C3 deposition. The combined data reveal a novel mechanism of complement inhibition by a bacterial protein: inhibition of CRP surface binding and, thus, diminution of CRP-mediated complement deposition.


Subject(s)
Bacterial Proteins/metabolism , C-Reactive Protein/metabolism , Complement C3/metabolism , Phosphorylcholine/metabolism , Streptococcus pneumoniae/metabolism , Animals , Bacterial Proteins/chemistry , Bacterial Proteins/pharmacology , Binding, Competitive , C-Reactive Protein/antagonists & inhibitors , C-Reactive Protein/immunology , Complement C3/antagonists & inhibitors , Complement C3/immunology , Culture Media , Humans , Mice , Phosphorylcholine/chemistry , Phosphorylcholine/immunology , Protein Binding , Protein Structure, Tertiary , Recombinant Proteins/chemistry , Recombinant Proteins/metabolism , Recombinant Proteins/pharmacology , Streptococcus pneumoniae/drug effects , Streptococcus pneumoniae/immunology
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