An integrative conceptual and mathematical framework of immune variation that includes unique basal profiles associated with differential susceptibility to disease, distinct acute immune signatures associated with disease severity, and how different determinants can lead to individual pathways of illness outcome.

The mathematical modeling approach disentangles the impacts of the COVID-19 pandemic on antibiotic resistance in Streptococcus pneumoniae in the community setting and identifies the three most plausible driving mechanisms responsible for the observed trends in invasive isolates and pneumococcal carriage.

During adaptation in dogs, H3N2 canine influenza viruses (CIVs) became to recognize human-like SAα2,6-Gal receptor, increased replication ability in human cells, acquired a 100% transmission rate via respiratory droplet in ferret model, and human population lacked immunity to H3N2 CIVs.

The overall mortality consequences of the COVID-19 pandemic in the United States are predominantly attributable to the direct impact of SARS-CoV-2 infection but there are substantial indirect effects among children and young adults, and in mortality from accidents, homicides, and overdoses.

The thymic selection of the human T-cell receptor repertoire releases polyspecific receptors with the ability to recognize and respond to peptides from unrelated viruses.

The analysis of the genomes of two lineages of influenza B virus (Victoria and Yamagata) reveal that their phylodynamics are fundamentally different, and are determined by a complex relationship between virus transmission, age of infection and receptor binding preference.

CR9114, one of the most broadly neutralizing anti-influenza antibodies characterized to date, acquires affinity to divergent HA subtypes sequentially, due to higher order interactions between the nested sets of mutations required for binding each distinct subtype.

Deleterious mutations slow down flu's antigenic evolution, make it more punctuated in nature, and reduce the virus's genetic diversity.

Broader case variation in respiratory viral load, and in shedding virus via droplets and aerosols, for SARS-CoV-2 than influenza A(H1N1)pdm09 facilitates greater transmission heterogeneity in the COVID-19 pandemic than the 2009 flu pandemic.

A general method for inferring fitness from a sample of nucleotide sequences can predict the progenitor of next year's seasonal influenza.