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Endogenous retroviruses (ERVs), comprising a substantial portion of the vertebrate genome, are remnants of ancient genetic invaders. ERVs with near-intact coding potential reactivate in B cell–deficient mice. To study how B cells contribute to host anti-ERV immunity, we used an antigen-baiting strategy to enrich B cells reactive to ERV surface antigens. We identified ERV-reactive B-1 cells expressing germline-encoded natural IgM antibodies in naïve mice, the level of which further increases upon innate immune sensor stimulation. B cell receptor repertoire profiling of ERV-reactive B-1 cells revealed increased usage of the Igh VH gene that gives rise to glycan-specific antibodies targeting terminal N-acetylglucosamine moieties on ERV glycoproteins, which further engage the complement pathway to mediate anti-ERV responses. These same antibodies also recognize glycoproteins of other enveloped viruses but not self-proteins. These results reveal an innate antiviral mechanism of germline-encoded antibodies with broad reactivity to enveloped viruses, which constitutes a natural antibody repertoire capable of preventing the emergence of infectious ERVs. Editor's summary: Control of endogenous retrovirus (ERV) reactivation is mediated through a T cell–independent (TI) B cell response, but precisely how B cells mediate surveillance and prevention of ERV reactivation is unclear. Yang et al. developed an antigen-baiting assay to detect ERV-reactive B cells in mice, identifying that peritoneal B-1 cells expressing germline-encoded IgM were the major source of anti-ERV antibodies. A monoclonal antibody produced by ERV-reactive B-1 cells recognized not only terminal N-acetylglucosamine (GlcNAc) on the surface of ERV glycoproteins but also GlcNAc found on a broader range of viral glycoproteins and enveloped viruses. These results demonstrate that recognition of viral glycans by natural antibodies is a general innate antiviral mechanism. —Hannah Isles [ABSTRACT FROM AUTHOR]

Acinetobacter baumannii has emerged as an important nosocomial pathogen, particularly for patients in intensive care units and with invasive indwelling devices. The most recent clinical isolates are resistant to several classes of clinically important antibiotics, greatly restricting the ability to effectively treat critically ill patients. The bacterial envelope is an important driver of A. baumannii disease, both at the level of battling against antibiotic therapy and at the level of protecting from host innate immune function. This review provides a comprehensive overview of key features of the envelope that interface with both the host and antimicrobial therapies. Carbohydrate structures that contribute to protecting from the host are detailed, and mutations that alter these structures, resulting in increased antimicrobial resistance, are explored. In addition, protein complexes involved in both intermicrobial and host-microbe interactions are described. Finally we discuss regulatory mechanisms that control the nature of the cell envelope and its impact on host innate immune function. [ABSTRACT FROM AUTHOR]