Influence of Distinct Maternal Cytomegalovirus-Specific Neutralizing and Fc Receptor-Binding Responses on Congenital Cytomegalovirus Transmission in HIV-Exposed Neonates.

Congenital cytomegalovirus (cCMV) is the most common infectious cause of birth defects worldwide, affecting approximately 1 in every 200 live-born infants globally. Recent work has identified potential immune correlates of protection against cCMV transmission including maternal and placentally transferred antibody levels and their function, which may inform the development of maternal active (vaccine) and passive (mono/polyclonal antibody) immunizations. However, these correlates need to also be assessed in diverse cohorts, including women living with HIV who have increased risk of cCMV transmission.

Self-assembling peptide nanofiber HIV vaccine elicits robust vaccine-induced antibody functions and modulates Fc glycosylation.

To develop vaccines for certain key global pathogens such as HIV, it is crucial to elicit both neutralizing and non-neutralizing Fc-mediated effector antibody functions. Clinical evidence indicates that non-neutralizing antibody functions including antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP) contribute to protection against several pathogens. In this study, we demonstrated that conjugation of HIV Envelope (Env) antigen gp120 to a self-assembling nanofiber material named Q11 induced antibodies with higher breadth and functionality when compared to soluble gp120.

Pseudomonas aeruginosa high-level resistance to polymyxins and other antimicrobial peptides requires cprA, a gene that is disrupted in the PAO1 strain.

The arn locus, found in many Gram-negative bacterial pathogens, mediates resistance to polymyxins and other cationic antimicrobial peptides through 4-amino-l-arabinose modification of the lipid A moiety of lipopolysaccharide. In Pseudomonas aeruginosa, several two-component regulatory systems (TCSs) control the arn locus, which is necessary but not sufficient for these resistance phenotypes. A previous transposon mutagenesis screen to identify additional polymyxin resistance genes that these systems regulate implicated an open reading frame designated PA1559 in the genome of the P.