Hepatitis B Awareness and Vaccination Patterns among Healthcare Workers in Africa.

Hepatitis B virus (HBV) vaccination patterns and the understanding of its risks among healthcare workers (HCWs) is a critical step to decrease transmission. However, the depth of this understanding is understudied. We distributed surveys to HCWs in 12 countries in Africa. Surveys had nine multiple-choice questions that assessed HCWs' awareness and understanding of HBV. Participants included consultants, medical trainees, nurses, students, laboratory personnel, and other hospital workers. Surveys were completed anonymously. Fisher's exact test was used for analysis, with a P-value of < 0.05 considered significant; 1,044 surveys were collected from Kenya, Egypt, Sudan, Tanzania, Ethiopia, Uganda, Malawi, Madagascar, Nigeria, Cameroon, Ghana, and Sierra Leone. Hepatitis B virus serostatus awareness, vaccination rate, and vaccination of HCWs' children were 65%, 61%, and 48%, respectively. Medical trainees had higher serostatus awareness, vaccination rate, and vaccination of their children than HCWs in other occupations (79% versus 62%, P < 0.001; 74% versus 58%, P < 0.001; and 62% versus 45%, P = 0.006, respectively). Cost was cited as the most frequent reason for non-vaccination. West African countries were more aware of their serostatus but less often vaccinated than East African countries (79% versus 59%, P < 0.0001 and 52% versus 60%, P = 0.03, respectively). West African countries cited cost as the reason for non-vaccination more than East African countries (59% versus 40%, P = 0.0003). Our study shows low HBV serostatus awareness and vaccination rate among HCWs in Africa, and reveals gaps in the perception and understanding of HBV prevention that should be addressed to protect HCWs and improve their capacity to control HBV infection.

Temporal/compartmental changes in viral RNA and neuronal injury in a primate model of NeuroAIDS.

Despite the advent of highly active anti-retroviral therapy HIV-associated neurocognitive disorders (HAND) continue to be a significant problem. Furthermore, the precise pathogenesis of this neurodegeneration is still unclear. The objective of this study was to examine the relationship between infection by the simian immunodeficiency virus (SIV) and neuronal injury in the rhesus macaque using in vivo and postmortem sampling techniques. The effect of SIV infection in 23 adult rhesus macaques was investigated using an accelerated NeuroAIDS model. Disease progression was modulated either with combination anti-retroviral therapy (cART, 4 animals) or minocycline (7 animals). Twelve animals remained untreated. Viral loads were monitored in the blood and cerebral spinal fluid, as were levels of activated monocytes in the blood. Neuronal injury was monitored in vivo using magnetic resonance spectroscopy. Viral RNA was quantified in brain tissue of each animal postmortem using reverse transcription polymerase chain reaction (RT-PCR), and neuronal injury was assessed by immunohistochemistry. Without treatment, viral RNA in plasma, cerebral spinal fluid, and brain tissue appears to reach a plateau. Neuronal injury was highly correlated both to plasma viral levels and a subset of infected/activated monocytes (CD14+CD16+), which are known to traffic the virus into the brain. Treatment with either cART or minocycline decreased brain viral levels and partially reversed alterations in in vivo and immunohistochemical markers for neuronal injury. These findings suggest there is significant turnover of replicating virus within the brain and the severity of neuronal injury is directly related to the brain viral load.

The correlation of serum and gingival crevicular fluid cytokines in obese subjects.

OBJECTIVE: To investigate the correlation between the gingival crevicular fluid (GCF) levels of IL-6 and TNF-alpha with the levels in serum in obese patients. DESIGN: Twenty-six obese adults (BMI > or = 30, age 33-74) provided serum and GCF samples. Smokers and uncontrolled diabetics (HbA1c > 8%) were excluded. Serum and GCF samples were analysed for IL-6 and TNF-alpha using commercially available ELISA kits. Within each subject GCF was collected from two healthy sites (n = 26 subjects) and two gingivitis sites, defined by bleeding on probing (n = 22 subjects). The levels of IL-6 and TNF-alpha in the GCF were compared and correlated with the levels found in serum using Spearman's correlation analysis. A Bland-Altman analysis was used to determine the level of agreement between serum and GCF samples. RESULTS: IL-6 was more frequently detected than TNF-alpha. This was consistent in serum (100% vs 64%) and GCF samples from healthy (73% vs 52%) and gingivitis (95% vs 36%) sites. There were no significant correlations between the TNF-alpha in serum and GCF samples from healthy (r = 0.27, p = 0.22) and gingivitis (r = -0.19, p = 0.40) sites. In contrast, positive correlations were found for IL-6 between serum and GCF samples from healthy (r = 0.48, p = 0.03) and gingivitis (r = 0.79, p = 0.0001) sites. The correlation and agreement was strongest for IL-6 between serum and gingivitis GCF samples. CONCLUSION: The results of this pilot study suggest a lack of correlation and poor agreement between serum and GCF samples in obese subjects. Studies examining the link between periodontitis and obesity should consider collecting both serum and GCF.

Brain creatine elevation and N-Acetylaspartate reduction indicates neuronal dysfunction in the setting of enhanced glial energy metabolism in a macaque model of neuroAIDS.

Proton magnetic resonance spectroscopy has emerged as one of the most informative neuroimaging modalities for studying the effect of HIV infection in the brain, providing surrogate markers by which to assess disease progression and monitor treatment. Reductions in the level of N-Acetylaspartate and N-Acetylaspartate/creatine are established markers of neuronal injury or loss. However, the biochemical basis of altered creatine levels in neuroAIDS is not well understood. This study used a rapid progression macaque model of neuroAIDS to elucidate the changes in creatine. As the disease progressed, proton magnetic resonance spectroscopy revealed a decrease in N-Acetylaspartate, indicative of neuronal injury, and an increase in creatine yet to be elucidated. Subsequently, immunohistochemistry and stereology measures of decreased synaptophysin, microtubule-associated protein 2, and neuronal density confirmed neuronal injury. Furthermore, increases in ionized calcium binding adaptor molecule 1 and glial fibrillary acidic protein indicated microglial and astroglial activation, respectively. Given these data, elevated creatine may reflect enhanced high-energy phosphate turnover in highly metabolizing activated astrocytes and microglia.

Proton magnetic resonance spectroscopy reveals neuroprotection by oral minocycline in a nonhuman primate model of accelerated NeuroAIDS.

BACKGROUND: Despite the advent of highly active anti-retroviral therapy (HAART), HIV-associated neurocognitive disorders continue to be a significant problem. In efforts to understand and alleviate neurocognitive deficits associated with HIV, we used an accelerated simian immunodeficiency virus (SIV) macaque model of NeuroAIDS to test whether minocycline is neuroprotective against lentiviral-induced neuronal injury. METHODOLOGY/PRINCIPAL FINDINGS: Eleven rhesus macaques were infected with SIV, depleted of CD8+ lymphocytes, and studied until eight weeks post inoculation (wpi). Seven animals received daily minocycline orally beginning at 4 wpi. Neuronal integrity was monitored in vivo by proton magnetic resonance spectroscopy and post-mortem by immunohistochemistry for synaptophysin (SYN), microtubule-associated protein 2 (MAP2), and neuronal counts. Astrogliosis and microglial activation were quantified by measuring glial fibrillary acidic protein (GFAP) and ionized calcium binding adaptor molecule 1 (IBA-1), respectively. SIV infection followed by CD8+ cell depletion induced a progressive decline in neuronal integrity evidenced by declining N-acetylaspartate/creatine (NAA/Cr), which was arrested with minocycline treatment. The recovery of this ratio was due to increases in NAA, indicating neuronal recovery, and decreases in Cr, likely reflecting downregulation of glial cell activation. SYN, MAP2, and neuronal counts were found to be higher in minocycline-treated animals compared to untreated animals while GFAP and IBA-1 expression were decreased compared to controls. CSF and plasma viral loads were lower in MN-treated animals. CONCLUSIONS/SIGNIFICANCE: In conclusion, oral minocycline alleviates neuronal damage induced by the AIDS virus.

Secondary flow mixing due to biofilm growth in capillaries of varying dimensions.

Using a magnetic resonance microscopy (MRM) technique, velocity perturbations due to biofouling in capillaries were detected in 3D velocity maps. The velocity images in each of the three square capillary sizes (2, 0.9, and 0.5 mm i.d.) tested indicate secondary flow in both the x- and y-directions for the biofouled capillaries. Similar flow maps generated in a clean square capillary show only an axial component. Investigation of these secondary flows and their geometric and dynamic similarity is the focus of this study. The results showed significant secondary flows present in the 0.9 mm i.d. capillary, on the scale of 20% of the bulk fluid flow. Since this is the "standard 1 mm" size capillary used in confocal microscopy laboratory bioreactors to investigate biofilm properties, it is important to understand how these enhanced flows impact bioreactor transport.