A human cytomegalovirus prefusion-like glycoprotein B subunit vaccine elicits humoral immunity similar to that of postfusion gB in mice.

Human cytomegalovirus (HCMV) is the leading infectious cause of birth defects. Despite the global disease burden, there is no Food and Drug Administration (FDA)-approved HCMV vaccine. The most efficacious HCMV vaccine candidates to date have used glycoprotein B (gB), a class III viral fusion protein, in its postfusion form.

SARS-CoV-2 Vaccine-Elicited Antibody Responses in Human Milk.

Background: SARS-CoV-2 mRNA-LNP immunizations significantly reduce severe coronavirus disease 2019 (COVID-19) disease and have been widely administered throughout the world including those who are pregnant and postpartum. However, our understanding of the immune response within the context of pregnancy and breastfeeding, especially the antibody kinetics and function within the breast milk compartment, is limited. To address this gap, we studied longitudinal blood and breast milk samples from lactating women throughout the primary immunization schedule and for several months after.

The human malaria parasite can sense environmental changes and respond by antigenic switching.

The primary antigenic and virulence determinant of the human malaria parasite is a variant surface protein called PfEMP1. Different forms of PfEMP1 are encoded by a multicopy gene family called , and switching between active genes enables the parasites to evade the antibody response of their human hosts. gene switching is key for the maintenance of chronic infections; however, what controls switching is unknown, although it has been suggested to occur at a constant frequency with little or no environmental influence.

A coordinated transcriptional switching network mediates antigenic variation of human malaria parasites.

Malaria parasites avoid immune clearance through their ability to systematically alter antigens exposed on the surface of infected red blood cells. This is accomplished by tightly regulated transcriptional control of individual members of a large, multicopy gene family called and is the key to both the virulence and chronic nature of malaria infections. Expression of genes is mutually exclusive and controlled epigenetically, however how large populations of parasites coordinate gene switching to avoid premature exposure of the antigenic repertoire is unknown.

Evolution of transcriptional control of antigenic variation and virulence in human and ape malaria parasites.

Background: The most severe form of human malaria is caused by the protozoan parasite Plasmodium falciparum. This unicellular organism is a member of a subgenus of Plasmodium called the Laverania that infects apes, with P. falciparum being the only member that infects humans.