Background: Naturally acquired immune responses to Plasmodium falciparum merozoite surface protein 3 (MSP3) and UB05 are implicated in semi immunity in populations living in malaria endemic areas. Thus designing chimeric malaria vaccine candidates involving MSP-3 and UB05 displayed upon the surface of a phage in its native form could potentiate their immunogenicity and antigenicity. In this study, we have engineered both MSP3 and UB05 upon the Qβ and assessed their antigenicity with plasma from children living in a high malaria transmission region of Cameroon. Methods: The surface of the RNA coliphage Qβ was genetically modified to display three Plasmodium falciparum derived immunogens including MSP3, UB05 and a chimera of the two UB05-MSP3. The resultant recombinant phages including QβMSP3, QβUB05 and QβUB05-MSP3 with surface displayed malaria immunogens were produced after transformation of the E. coli strain HB101. Plasma levels of antigen specific IgG antibody were then determined in samples from malaria positive and negative children living in a high malaria transmission region of Cameroon. Results: To improve yield each recombinant phage was scaled up to 10 14 pfu/ml using production strategies previously optimized in our group. This was significantly higher (P<0.001) relative to the 10 8 pfu/ml of the wild type C li nical M ic r o b io logy : O p e n Acces s

Thus targeting protein antigens to DCs using scDEC can be used either alone or in combination with other strategies for effective immunization.

Regulatory T (Treg) cells play a key role in dampening excessive immune activation. However, antiretroviral therapy (ART) -naive HIV-1 infection maintains the immune system in a sustained state of activation that could alter both Treg cell surface markers and functions. As Treg cell surface markers are directly linked to their functions the overall objective of this study was to determine how ART-naive HIV infection affects the phenotypic properties of Treg cells. Our data showed that in ART-naive HIV-1 infection, Treg cells are dominated by effector (CD45RA CD27 CCR7 CD62L ) and effector memory (CD45RA CD27 CCR7 CD62L ) cells. In contrast Treg cells from HIV-negative individuals were mainly naive (CD45RA CD27 CCR7 CD62L ) and central memory (CD45RA CD27 CCR7 CD62L ) cells. Whereas effector and effector memory Treg cells showed enhanced expression of CD39 (P < 0·05), CD73 (P < 0·001), HLA-DR and CD38 (P < 0·001); naive and central memory Treg cells showed a significant reduction in the expression of these markers. Overall Treg cell frequencies within total CD4 T cells correlated positively with plasmatic HIV-1 viral load. As increased viral load is associated with augmented CD4 T-cell destruction; this could suggest a resistance of peripheral Treg cells to HIV-1 destruction. Hence the modulation of Treg cell phenotype and frequencies could be considered in designing immunotherapeutic strategies targeting immune system restoration during HIV-1 infection.