Tuberculosis (TB) is one of the leading infectious causes of mortality worldwide. Although a significant proportion of the population (up to 36%, depending on the region) is infected with the latent form of TB, only about one in ten of these people will develop an active form of the disease in their lifetime. This is due to a complex interaction between the host’s genetic predisposition and environment. However, the genetic determinants of TB are not well established and have been insufficiently explored in previous genome-wide association studies (GWAS) with sparse and incongruent results. We reviewed recent evidence on host genetic susceptibility to TB, highlighting population-specific characteristics, host–pathogen coevolution, and the limitations of conventional GWAS approaches in terms of clinical and genetic heterogeneity. While rare variants with high penetrance, such as TYK2 P1104A, lead to monogenic susceptibility, most heritable risk results from the cumulative effect of numerous common variants. This cumulative effect may be summarized using polygenic risk scores (PRSs). Although their use has been proven for non-communicable diseases, PRSs are not applied to infectious disease susceptibility. To date, no PRS model for susceptibility to tuberculosis has been consistently validated. The development of PRSs for TB susceptibility is limited by phenotypic heterogeneity, population structure, and co-adaptation between host and pathogen. Another major challenge is to take into account the considerable influence of environmental factors. This difficulty in modeling environmental influences probably explains the current lack of a clinically applicable PRS for TB susceptibility. However, taking these caveats into account, polygenic models could improve risk stratification at the individual level compared to single-variant association and allow for earlier targeted treatment and prophylaxis.

Rabies is a globally prevalent viral zoonosis that causes 59,000 deaths per year and has important economic consequences. Most virus spread is associated with the migration of its primary hosts. Anthropogenic dissemination, mainly via the transportation of rabid dogs, shaped virus ecology a few hundred years ago and is responsible for several current outbreaks. A systematic analysis of aberrant long-distance events in the steppe and Arctic-like groups of rabies virus was performed using statistical (Bayesian) phylogeography and plots of genetic vs. geographic distances. The two approaches produced similar results but had some significant differences and complemented each other. No phylogeographic analysis could be performed for the Arctic group because polar foxes transfer the virus across the whole circumpolar region at high velocity, and there was no correlation between genetic and geographic distances in this virus group. In the Arctic-like group and the steppe subgroup of the cosmopolitan group, a significant number of known sequences (15–20%) was associated with rapid long-distance transfers, which mainly occurred within Eurasia. Some of these events have been described previously, while others have not been documented. Most of the recent long-distance transfers apparently did not result in establishing the introduced virus, but a few had important implications for the phylogeographic history of rabies. Thus, human-mediated long-distance transmission of the rabies virus remains a significant threat that needs to be addressed.

The taxonomic status of the H17N10 and H18N11 influenza A viruses isolated from bats remains unclear due to the absence of quantitative classification criteria at this taxonomic level. A total of 3328 representative IAV genomes, encompassing all eight protein-coding segments, were analysed. Various genetic distance-based metrics were assessed at the pairwise level, including intra- and intergroup nucleotide distances, dN/dS ratios, and transition/transversion ratios, to facilitate the differentiation of the Alphainfluenzavirus genus into distinct taxa. Pairwise distances for seven of the eight segments (PB2, PB1, PA, NP, M, NA, NS) consistently differentiated the H17–H18 group from H1–H16. Across segments, intergroup nucleotide divergence was consistently above a lower bound of ~25%, with segment-specific values extending to higher levels (up to ~40% in PB2 and PA), while intragroup divergence remained substantially lower. The HA segment did not conform to this pattern, which is consistent with the hypothesis of ancient reassortment. The distribution of pairwise dN/dS values for the PB2, PB1, PA, and NP segments is evidently bimodal. Intergroup comparisons were consistently higher across all segments, whereas intragroup values remained lower. A similar lower boundary of approximately 0.12 was observed across segments, while the upper range of intergroup values varied by gene. Overall, the results support a consistent gene-specific separation pattern. Previously demonstrated absence of reassortment compatibility between bat viruses (H17–H18) and canonical influenza A (H1–H16) viruses indicates that these lineages have evolved independently over an extended period. These consistent genomic patterns provide support for the hypothesis that H17N10 and H18N11 viruses may represent a separate species within the genus Alphainfluenzavirus.