A 10-year longitudinal study reveals bat-driven SARSr-CoV evolution
Bats are recognized reservoirs for several zoonoses and have an exceptional tolerance to viruses, likely linked with strong evolutionary selection in immune genes. Notably, in light of the emergence history of severe acute respiratory syndrome coronavirus (SARS-CoV), SARS-CoV-2 is hypothesized to have originated from Rhinolophus bats as well. In-depth studies are still needed, however, to unravel…
A groundbreaking 10-year study of SARSr-CoV evolution in Rhinolophus bats has unveiled the intricate dynamics between viruses, hosts, and their interactions. The research underscores the remarkable resilience of bats to viral infections, which may stem from their robust immune gene selection. Despite SARS-CoV-2 being theorized to have emerged from these same bat populations, further research is required to fully comprehend the virus-host relationships and cross-species transmission patterns.
This pioneering study focused on BBCoV-EPI1, a SARSr-CoV found in Rhinolophus bats, shedding light on the viral ecosystem, emergence of new lineages, and the effects of host life cycles on viral prevalence. The study discovered that events such as hibernation, female gatherings, juvenile weaning, and mating periods contributed to significant seasonal fluctuations in viral presence, leading to increased viral diversification through bottlenecks, founder effects, and natural selection.
High mutation rates, rapid gradualism, and recombination were also found to play crucial roles in viral evolution, balanced by the relatively weaker antiviral effect of APOBEC3 in bats compared to humans.
Interestingly, the study identified ADAR enzyme as a surprisingly influential factor in viral evolution within bat hosts, despite RNA viruses' typically low replication fidelity attributed to their polymerases. Additionally, the research revealed that critical innovations in BBCoV-EPI1 were predominantly located in proteins involved in cell-cycle hijacking and suppressing bat cells' antiviral response, rather than in the Spike (S) protein.
The BBCoV-EPI1 S protein demonstrated successful entry into Rhinolophus bat cells via the angiotensin-converting enzyme 2 (ACE2) receptor; however, it showed limited ability to infect human or sympatric species cells due to specific amino-acid differences at the S-ACE2 interface.
Lastly, the findings provide a comprehensive list of 101 critical amino-acid changes frequently linked to changes in viral fitness and set the stage for future experimental studies aimed at understanding the SARSr-CoVs' adaptability to different hosts and their potential to cross species barriers.
Written by urgent.news from bioRxiv's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.
