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Our knowledge of the diversity and frequency of genomic structural variation segregating in populations of large double-stranded (ds) DNA viruses is limited. Here, we sequenced the genome of a baculovirus (Autographa californica multiple nucleopolyhedrovirus [AcMNPV]) purified from beet armyworm (Spodoptera exigua) larvae at depths >195,000× using both short- (Illumina) and long-read (PacBio) technologies. Using a pipeline relying on hierarchical clustering of structural variants (SVs) detected in individual short- and long-reads by six variant callers, we identified a total of 1,141 SVs in AcMNPV, including 464 deletions, 443 inversions, 160 duplications, and 74 insertions. These variants are considered robust and unlikely to result from technical artifacts because they were independently detected in at least three long reads as well as at least three short reads. SVs are distributed along the entire AcMNPV genome and may involve large genomic regions (30,496 bp on average). We show that no less than 39.9 per cent of genomes carry at least one SV in AcMNPV populations, that the vast majority of SVs (75%) segregate at very low frequency (

Pathogens should evolve to avirulence. However, while baculoviruses can be transmitted through direct contact, their main route of infection goes through the death and liquefaction of their caterpillar hosts and highly virulent strains still seem to be advantaged through infection cycles. Furthermore, one of them,Autographa californicamultiple nucleopolyhedrovirus, is so generalist that it can infect more than 100 different hosts.To understand and characterize the evolutionary potential of this virus and how it is maintained while killing some of its hosts in less than a week, we performed an experimental evolution starting from an almost natural isolate of AcMNPV, known for its generalist infection capacity. We made it evolve on 4 hosts of different susceptibilities for 10 cycles and followed hosts survival each day. We finally evaluated whether the generalist capacity was maintained after evolving on one specific host species and tested an epidemiological model through simulations to understand how.Finally, on very highly susceptible hosts, transmission-virulence trade-offs seem to disappear and the virus can maximize transmission and virulence. When less adapted to its host, the pathogen’s virulence has not been modified along cycles but the yield was increased, apparently through an increased transmission probability and an increased latent period between exposition and infection.