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Introduction: Understanding the differences between respiratory syncytial virus (RSV) subgroups A and B provides insights for the development of prevention strategies and public health interventions. We aimed to describe the structural differences of RSV subgroups, their epidemiology, and genomic diversity. The associated immune response and differences in clinical severity were also investigated. Methods: A literature review from PubMed and Google Scholar (1985–2023) was performed and extended using snowballing from references in captured publications. Results: RSV has two major antigenic subgroups, A and B, defined by the G glycoprotein. The RSV F fusion glycoprotein in the prefusion conformation is a major target of virus neutralizing antibodies and differs in surface exposed regions between RSV A and RSV B. The subgroups co-circulate annually, but there is considerable debate as to whether clinical severity is impacted by the subgroup of the infecting RSV strain. Large variations between the studies reporting RSV subgroup impact on clinical severity were observed. A tendency for higher disease severity may be attributed to RSV A but no consensus could be reached as to whether infection by one of the subgroup caused more severe outcomes. RSV genotype diversity decreased over the last two decades, and ON and BA have become the sole lineages detected for RSV A and RSV B, since 2014. No studies with data obtained after 2014 reported a difference in disease severity between the two subgroups. RSV F is relatively well conserved and highly similar between RSV A and B, but changes in the amino acid sequence have been observed. Some of these changes led to differences in F antigenic sites compared to reference F sequences (e.g., RSV/A Long strain), which are more pronounced in antigenic sites of the prefusion conformation of RSV B. Initial results from the second season after vaccination suggest specific RSV B efficacy wanes more rapidly than RSV A for RSV PreF-based monovalent vaccines. Conclusions: RSV A and RSV B both contribute substantially to the global RSV burden. Both RSV subgroups cause severe disease and none of the available evidence to date suggests any differences in clinical severity between the subgroups. Therefore, it is important to implement measures effective at preventing disease due to both RSV A and RSV B to ensure impactful public health interventions. Monitoring overtime will be needed to assess the impact of waning antibody levels on subgroup-specific efficacy.

Healthcare‐associated antibiotic‐resistant (AR) infections increase patient morbidity and mortality and might be impossible to successfully treat with any antibiotic. CDCassessed healthcare‐associated infections (HAI), including Clostridium difficileinfections (CDI), and the role of six ARbacteria of highest concern nationwide in several types of healthcare facilities. During 2014, approximately 4000 short‐term acute care hospitals, 501 long‐term acute care hospitals, and 1135 inpatient rehabilitation facilities in all 50 states reported data on specific infections to the National Healthcare Safety Network. National standardized infection ratios and their percentage reduction from a baseline year for each HAItype, by facility type, were calculated. The proportions of ARpathogens and HAIs caused by any of six resistant bacteria highlighted by CDCin 2013 as urgent or serious threats were determined. In 2014, the reductions in incidence in short‐term acute care hospitals and long‐term acute care hospitals were 50% and 9%, respectively, for central line‐associated bloodstream infection; 0% (short‐term acute care hospitals), 11% (long‐term acute care hospitals), and 14% (inpatient rehabilitation facilities) for catheter‐associated urinary tract infection; 17% (short‐term acute care hospitals) for surgical site infection, and 8% (short‐term acute care hospitals) for CDI. Combining HAIs other than CDIacross all settings, 47.9% of Staphylococcus aureusisolates were methicillin resistant, 29.5% of enterococci were vancomycin resistant, 17.8% of Enterobacteriaceae were extended‐spectrum beta‐lactamase phenotype, 3.6% of Enterobacteriaceae were carbapenem resistant, 15.9% of Pseudomonas aeruginosaisolates were multidrug resistant, and 52.6% of Acinetobacterspecies were multidrug resistant. The likelihood of HAIs caused by any of the six resistant bacteria ranged from 12% in inpatient rehabilitation facilities to 29% in long‐term acute care hospitals. Although there has been considerable progress in preventing some HAIs, many remaining infections could be prevented with implementation of existing recommended practices. Depending upon the setting, more than one in four of HAIs excluding CDIare caused by ARbacteria. Physicians, nurses, and healthcare leaders need to consistently and comprehensively follow all recommendations to prevent catheter‐ and procedure‐related infections and reduce the impact of ARbacteria through antimicrobial stewardship and measures to prevent spread. This report details the rates of antibiotic resistance in hospital‐acquired bacterial infections, important information for transplant patients given their increased risk for these infections.

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