4 research outputs found
Low HIV incidence in pregnant and postpartum women receiving a community-based combination HIV prevention intervention in a high HIV incidence setting in South Africa
BACKGROUND:
Young Southern African women have the highest HIV incidence globally. Pregnancy doubles
the risk of HIV acquisition further, and maternal HIV acquisition contributes significantly
to the paediatric HIV burden. Little data on combination HIV prevention interventions during
pregnancy and lactation are available. We measured HIV incidence amongst pregnant and
postpartum women receiving a community-based combination HIV prevention intervention
in a high HIV incidence setting in South Africa.
METHODS:
A cohort study that included HIV-uninfected pregnant women was performed. Lay community-
based workers provided individualized HIV prevention counselling and performed
three-monthly home and clinic-based individual and couples HIV testing. Male partners
were referred for circumcision, sexually transmitted infections or HIV treatment as appropriate.
Kaplan-Meier analyses and Cox's regression were used to estimate HIV incidence and
factors associated with HIV acquisition. RESULTS
The 1356 women included (median age 22.5 years) received 5289 HIV tests. Eleven new
HIV infections were detected over 828.3 person-years (PY) of follow-up, with an HIV incidence
rate of 1.33 infections/100 PY (95% CI: 0.74±2.40). Antenatally, the HIV incidence
rate was 1.49 infections/100 PY (95% CI: 0.64±2.93) and postnatally the HIV incidence rate
was 1.03 infections/100 PY (95% CI: 0.33±3.19). 53% of male partners received HIV testing
and 66% of eligible partners received referral for circumcision. Women within known serodiscordant
couples, and women with newly diagnosed HIV-infected partners, adjusted hazard
ratio (aHR) = 32.7 (95% CI: 3.8±282.2) and aHR = 126.4 (95% CI: 33.8±472.2) had
substantially increased HIV acquisition, respectively. Women with circumcised partners had
a reduced risk of incident HIV infection, aHR = 0.22 (95% CI: 0.03±1.86).
CONCLUSIONS:
Maternal HIV incidence was substantially lower than previous regional studies. Community-based
combination HIV prevention interventions may reduce high maternal HIV incidence in
resource-poor settings. Expanded roll-out of home-based couples HIV testing and initiating
pre-exposure prophylaxis for pregnant women within serodiscordant couples is needed in
Southern Africa
The relationship between Helicobacter pylori motility, morphology and phase of growth: implications for gastric colonization and pathology
Expression of Surfactant Protein D in the Human Gastric Mucosa and during Helicobacter pylori Infection
Helicobacter pylori establishes persistent infection of gastric mucosa with diverse clinical outcomes. The innate immune molecule surfactant protein D (SP-D) binds selectively to microorganisms, inducing aggregation and phagocytosis. In this study, we demonstrated the expression of SP-D in gastric mucosa by reverse transcription-PCR and immuohistochemical analysis. SP-D is present at the luminal surface and within the gastric pits, with maximal expression at the surface. Levels of expression are significantly increased in H. pylori-associated gastritis compared to those in the normal mucosa. Immunofluorescence microscopy was used to demonstrate binding and agglutination of H. pylori by SP-D in a lectin-specific manner. These activities resulted in a 50% reduction in the motility of H. pylori, as judged on the basis of curvilinear velocity measured by using a Hobson BacTracker. Lipopolysaccharides extracted from three H. pylori strains were shown to bind SP-D in a concentration-dependent manner, and there was marked variation in the avidity of binding among the strains. SP-D may therefore play a significant role in the innate immune response to H. pylori infection
Variations in Helicobacter pylori Lipopolysaccharide To Evade the Innate Immune Component Surfactant Protein D
Helicobacter pylori is a common and persistent human pathogen of the gastric mucosa. Surfactant protein D (SP-D), a component of innate immunity, is expressed in the human gastric mucosa and is capable of aggregating H. pylori. Wide variation in the SP-D binding affinity to H. pylori has been observed in clinical isolates and laboratory-adapted strains. The aim of this study was to reveal potential mechanisms responsible for evading SP-D binding and establishing persistent infection. An escape variant, J178V, was generated in vitro, and the lipopolysaccharide (LPS) structure of the variant was compared to that of the parental strain, J178. The genetic basis for structural variation was explored by sequencing LPS biosynthesis genes. SP-D binding to clinical isolates was demonstrated by fluorescence-activated cell sorter analyses. Here, we show that H. pylori evades SP-D binding through phase variation in lipopolysaccharide. This phenomenon is linked to changes in the fucosylation of the O chain, which was concomitant with slipped-strand mispairing in a poly(C) tract of the fucosyltransferase A (fucT1) gene. SP-D binding organisms are predominant in mucus in vivo (P = 0.02), suggesting that SP-D facilitates physical elimination. Phase variation to evade SP-D contributes to the persistence of this common gastric pathogen