”The targets to end AIDS stipulates that 90 per cent of persons living with HIV would know their status by 2020 and 90 per cent of those diagnosed with HIV would receive antiretroviral therapy and 90 per cent of those receiving treatment would be virally suppressed.
Moma-Efretuei said that this imitative would form the bedrock on which future interventions would lie.
The FCT Regional Manager, Institute of Human Virology, Nigeria, Dr Olayemi Olupitan, urged the Nigerian government to intensify efforts and awareness on HIV testing and treatment.
Olupitan added that UNAIDS had reached advanced stage in its trategy to end AIDS epidemic by 2030 in Nigeria
She added that the Institute of Human Virology, Nigeria, was collaborating with the National Assembly and Methodist Church to provide free medical services to the residents of Karimajiji IDPs.
The Chairman, Karimajiji IDP camp, Mohammed Abubarka, called on the Federal Government to support the IDPs to return to their homes.
Abubarka said that the suffering was too much and it would be appreciated if they could go back home.
”We want to go back home, we want to go back to farming and working, there is no place like home, we are not happy here.
”We have no food, hospital or school, we are suffering and we need help, we have been here for over three years,” he said..
Because PARP1 is a DNA repair enzyme and mtDNA encodes essential components of the respiratory chain, we determined if mitochondrial translocation of PARP1/PAR preserved the mtDNA in chagasic myocardium. Long qPCR amplification of 10 kb mtDNA fragment showed the basal level of mtDNA content was not changed in WT, PARP1+/-, and PARP1-/- mice. The long mtDNA (vs. short mtDNA fragment) in chagasic WT, PARP1+/-, and PARP1-/- mice (vs. matched controls) was decreased by 70%, 46%, and 32%, respectively (Fig 2A, Fig 2B.a, and S2 Fig panels A & B.a, p<0.001). When compared to nuDNA fragment, the long mtDNA content was decreased by 85% and 30%, respectively, in the myocardium of chagasic WT and PARP1+/- mice (p<0.001) and no change was noted in PARP1-/- mice (Fig 2B.b, S2 Fig panel B.b). The protection of mtDNA content was associated with preservation of mtDNA-encoded genes’ expression at mRNA (ND4, CYTB, COI, ATP6, and ATP8, Fig 2C–2G) and protein (COI, Fig 2H & 2I) levels in chronically infected PARP1-/- (vs. control) mice. In comparison, WT.Tc (vs. WT) mice exhibited 21–51% decline in mtDNA-encoded gene expression and >80% decline in COI protein level (Fig 2C–2I, p<0.05). Mitochondrial (and total) levels of AMPK-like protein were equally increased in chagasic WT and PARP1-/- mice, and no changes in COIV (nuDNA encoded complex IV subunit) were noted in WT and PARP1-/- mice (Fig 2H, 2J & 2K). Our results suggest that a) Tc-induced PARP1/PAR were detrimental to mtDNA integrity and mtDNA-encoded gene expression, and b) depletion of PARP1/PAR prevented the loss in mtDNA content in chronic Chagas disease. Though a potential contamination with cytoplasmic material may explain the finding of AMPK-like protein in mitochondrial fractions, we believe that this observation indicates a novel role for AMPK in mitochondrial biogenesis..