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The impact of antiretroviral naïve HIV-1 infection on the modulation of Natural Killer (NK) cells phenotype has not been fully assessed. This study aimed to define the phenotype of NK cell in the context of antiretroviral naïve HIV-1 infection. A total of 85 ARV naïve HIV-1 infected and 55 healthy individuals were included in the study. Purified NK cells alongside bulk Peripheral Blood Mononuclear Cells (PBMC) were surface stained with fluorochrome conjugated antibodies and samples were acquired using a BD FACS canto II flow cytometer. A down-regulation of CD56 + /CD16 - and CD56 + /CD16 + NK cells (p= 0.003), and a significant expansion (p= 0.03) of CD56 - /CD16 + NK cells subset was observed in ARV naïve HIV-1 infection. The high expression of both CD38 (p= 0.02) and HLA-DR (p=0.001) in the CD56-/CD16+ NK cells subset, shows the activation status of NK cells from HIV-1 infected people. A reduced expression of activating markers NKp44 and NKp30 and the down regulation of NKG2A was observed  in CD56+/CD16- and CD56+/CD16+ NK cells from HIV-1 infected people (p= 0.006, p= 0.009, respectively).  Antiretroviral naive HIV-1 infected people living in Cameroon show a differential modulation of NK cell phenotype relative to HIV negative controls.

The impact of antiretroviral naïve HIV-1 infection on the modulation of Natural Killer (NK) cells phenotype has not been fully assessed. This study aimed to define the phenotype of NK cell in the context of antiretroviral naïve HIV-1 infection. A total of 85 ARV naïve HIV-1 infected and 55 healthy individuals were included in the study. Purified NK cells alongside bulk Peripheral Blood Mononuclear Cells (PBMC) were surface stained with fluorochrome conjugated antibodies and samples were acquired using a BD FACS canto II flow cytometer. A down-regulation of CD56 + /CD16 - and CD56 + /CD16 + NK cells (p= 0.003), and a significant expansion (p= 0.03) of CD56 - /CD16 + NK cells subset was observed in ARV naïve HIV-1 infection. The high expression of both CD38 (p= 0.02) and HLA-DR (p=0.001) in the CD56-/CD16+ NK cells subset, shows the activation status of NK cells from HIV-1 infected people. A reduced expression of activating markers NKp44 and NKp30 and the down regulation of NKG2A was observed  in CD56+/CD16- and CD56+/CD16+ NK cells from HIV-1 infected people (p= 0.006, p= 0.009, respectively).  Antiretroviral naive HIV-1 infected people living in Cameroon show a differential modulation of NK cell phenotype relative to HIV negative controls.

The impact of antiretroviral naïve HIV-1 infection on the modulation of Natural Killer (NK) cells phenotype has not been fully assessed. This study aimed to define the phenotype of NK cell in the context of antiretroviral naïve HIV-1 infection. A total of 85 ARV naïve HIV-1 infected and 55 healthy individuals were included in the study. Purified NK cells alongside bulk Peripheral Blood Mononuclear Cells (PBMC) were surface stained with fluorochrome conjugated antibodies and samples were acquired using a BD FACS canto II flow cytometer. A down-regulation of CD56 + /CD16 - and CD56 + /CD16 + NK cells (p= 0.003), and a significant expansion (p= 0.03) of CD56 - /CD16 + NK cells subset was observed in ARV naïve HIV-1 infection. The high expression of both CD38 (p= 0.02) and HLA-DR (p=0.001) in the CD56-/CD16+ NK cells subset, shows the activation status of NK cells from HIV-1 infected people. A reduced expression of activating markers NKp44 and NKp30 and the down regulation of NKG2A was observed  in CD56+/CD16- and CD56+/CD16+ NK cells from HIV-1 infected people (p= 0.006, p= 0.009, respectively).  Antiretroviral naive HIV-1 infected people living in Cameroon show a differential modulation of NK cell phenotype relative to HIV negative controls.

George Uchenna Eleje,1,2 Henrietta Aritetsoma Ogbunugafor,1,3 Chiemelu Dickson Emegoakor,1,4 Ebere Innocent Okoye,1,5 Ogochukwu Ifeanyi Ezejiofor,6 Shirley Nneka Chukwurah,7 Joseph Ifeanyichukwu Ikechebelu,1,2 Godwin W Nchinda,8 Chidozie Godwin Ugochukwu,3 Lucy Ijeoma Nnaji-Ihedinmah,9 Festus Basden C Okoye,1,10 Frank Uchenna Eneh,3 Michael Emeka Onwukamuche,11 Charles Okechukwu Esimone1,12 1Biomedicine Research Group, Nnamdi Azikiwe University, Awka, Nigeria; 2Effective Care Research Unit, Faculty of Medicine, College of Health Sciences, Nnamdi Azikiwe University, Awka, Nigeria; 3Department of Applied Biochemistry, Nnamdi Azikiwe University, Awka, Nigeria; 4Department of General Surgery, Nnamdi Azikiwe University, Awka, Nigeria; 5Department of Pharmaceutics and Pharmaceutical Technology, Nnamdi Azikiwe University, Awka, Nigeria; 6Department of Medicine, Nnamdi Azikiwe University, Awka, Nigeria; 7Gastroenterology Unit, Department of Medicine, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Nigeria; 8Laboratory of Vaccinology/Biobanking, CIRCB BP 3077, Messa Yaounde, Cameroon; 9Department of Chemical Pathology, Nnamdi Azikiwe University Teaching Hospital, Nnewi, Nigeria; 10Department of Pharmaceutical and Medicinal Chemistry, Nnamdi Azikiwe University, Awka, Nigeria; 11Department of Histopathology, Faculty of Medicine, Nnamdi Azikiwe University, Awka, Nigeria; 12Department of Pharmaceutical Microbiology and Biotechnology, Nnamdi Azikiwe University, Awka, Nigeria Background: To our knowledge, there is no prior randomized study on the utility of Syferol-IHP (blend of virgin coconut oil and Ocimum sanctum oil) when coadministered with a triple therapy schedule.Aim: This study determined the efficacy and safety of Syferol-IHP as adjunct to conventional triple therapy for the treatment of peptic ulcer disease (PUD).Methods: A pilot double-blind randomized trial was conducted in patients with confirmed diagnosis (endoscopy-guided biopsy) of PUD. Eligible patients were

Recent outbreaks of Ebola virus disease and Zika virus disease highlight the need for disseminating accurate predictions of emerging zoonotic viruses to national governments for disease surveillance and response. Although there are published maps for many emerging zoonotic viruses, it is unknown if there is agreement among different models or if they are concordant with national expert opinion. Therefore, we reviewed existing predictions for five high priority emerging zoonotic viruses with national experts in Cameroon to investigate these issues and determine how to make predictions more useful for national policymakers. Predictive maps relied primarily on environmental parameters and species distribution models. Rift Valley fever virus and Crimean-Congo hemorrhagic fever virus predictions differed from national expert opinion, potentially because of local livestock movements. Our findings reveal that involving national experts could elicit additional data to improve predictions of emerging pathogens as well as help repackage predictions for policymakers.

Recent outbreaks of Ebola virus disease and Zika virus disease highlight the need for disseminating accurate predictions of emerging zoonotic viruses to national governments for disease surveillance and response. Although there are published maps for many emerging zoonotic viruses, it is unknown if there is agreement among different models or if they are concordant with national expert opinion. Therefore, we reviewed existing predictions for five high priority emerging zoonotic viruses with national experts in Cameroon to investigate these issues and determine how to make predictions more useful for national policymakers. Predictive maps relied primarily on environmental parameters and species distribution models. Rift Valley fever virus and Crimean-Congo hemorrhagic fever virus predictions differed from national expert opinion, potentially because of local livestock movements. Our findings reveal that involving national experts could elicit additional data to improve predictions of emerging pathogens as well as help repackage predictions for policymakers.

Background Targeting of protein antigens to dendritic cells (DC) via the DEC205 receptor enhances presentation of antigen-derived peptides on MHC-I and MHC-II molecules and, in the presence of costimulatory signals, antigen-specific immune responses. The immunogenicity and efficacy of DNA vaccination can also be enhanced by fusing the encoded antigen to single chain antibodies directed against DEC205. To further improve this strategy, we evaluated different toll-like receptor ligands (TLR) and CD40 ligands (CD40L) as adjuvants for DNA vaccines encoding a DEC205-single-chain antibody fused to the ovalbumin model antigen or HIV-1 Gag and assessed the priming efficacy of DNA in a DNA prime adenoviral vector boost immunization regimen. Results Mice were primed with the adjuvanted DEC-205 targeted DNA vaccines and boosted with adenoviral vectors encoding the same antigens. CD8+ T cell responses were determined after the adenoviral booster immunization, to determine how well the different DNA immunization regimens prime for the adenoviral boost. In the absence of adjuvants, targeting of DNA-encoded ovalbumin to DCs suppressed CD8+ T-cell responses after the adenoviral booster immunization. CD8+ T-cell responses to the DEC205 targeted DNA vaccines increased only slightly by adding either the TLR-9 ligand CpG, the TLR-3 ligand Poly I:C, or CD40 ligand expression plasmids. However, the combination of both TLR-ligands led to a strong enhancement of CD8+ T-cell responses compared to a non-targeted DNA vaccine. This finding was confirmed using HIV Gag as antigen. Conclusion Although DNA prime adenoviral vector boost immunizations belong to the strongest inducers of cytotoxic T cell responses in different animal models and humans, the CD8+ T cell responses can be further improved by targeting the DNA encoded antigen to DEC205 in the presence of synergistic TLR ligands CpG and Poly I:C.

Background Targeting of protein antigens to dendritic cells (DC) via the DEC205 receptor enhances presentation of antigen-derived peptides on MHC-I and MHC-II molecules and, in the presence of costimulatory signals, antigen-specific immune responses. The immunogenicity and efficacy of DNA vaccination can also be enhanced by fusing the encoded antigen to single chain antibodies directed against DEC205. To further improve this strategy, we evaluated different toll-like receptor ligands (TLR) and CD40 ligands (CD40L) as adjuvants for DNA vaccines encoding a DEC205-single-chain antibody fused to the ovalbumin model antigen or HIV-1 Gag and assessed the priming efficacy of DNA in a DNA prime adenoviral vector boost immunization regimen. Results Mice were primed with the adjuvanted DEC-205 targeted DNA vaccines and boosted with adenoviral vectors encoding the same antigens. CD8+ T cell responses were determined after the adenoviral booster immunization, to determine how well the different DNA immunization regimens prime for the adenoviral boost. In the absence of adjuvants, targeting of DNA-encoded ovalbumin to DCs suppressed CD8+ T-cell responses after the adenoviral booster immunization. CD8+ T-cell responses to the DEC205 targeted DNA vaccines increased only slightly by adding either the TLR-9 ligand CpG, the TLR-3 ligand Poly I:C, or CD40 ligand expression plasmids. However, the combination of both TLR-ligands led to a strong enhancement of CD8+ T-cell responses compared to a non-targeted DNA vaccine. This finding was confirmed using HIV Gag as antigen. Conclusion Although DNA prime adenoviral vector boost immunizations belong to the strongest inducers of cytotoxic T cell responses in different animal models and humans, the CD8+ T cell responses can be further improved by targeting the DNA encoded antigen to DEC205 in the presence of synergistic TLR ligands CpG and Poly I:C.