In DT-8. It could be vital for SsHADV-1 to survive in strain DT-8. Viral DNA genomes possess a restricted coding capacity and thus harness cellular factors from the host to generate progeny virions [78]. By hijacking and manipulating host DNA replication and DNA Aryl Hydrocarbon Receptor Storage & Stability damage response processes, DNA viruses can selectively make use of or abrogate elements with the cellular machinery to complete their life cycles [79]. The smaller the viral genome, the more minimal the coding capacity, as well as the greater the need to harness cellular processes in the host [80]. As a circular ssDNA mycovirus, the HCV Protease Species genome of SsHADV-1 is only 2166 nt, coding for a single replication initiation protein (Rep) and one particular coat protein (CP) [36]. In our research, for the up-regulated genes, there have been a lot of enriched GO terms or KEGG pathways which were connected to DNA replication and DNA harm response processes. This may be the embodiment in which SsHADV-1 utilized cellular processes of strain DT-8 to finish the replication. Moreover, we located that the essential NHEJ genes (ssKu70, ssKu80, SS1G_02074, and SS1G_03342) had been up-regulated in strain DT-8. These genes have already been proven to be associated towards the replication of DNA virus. Choi et al. presented proof both in vivo and in vitro that Ku70/80 stimulates the replication with the linear single-stranded DNA virus, adeno-associated virus, within the presence of both adenovirus and herpes simplex virus coinfection [81]. Muylaert and Elias identified that the RNAi-mediated knockdown of DNA ligase IV and its co-factor XRCC4 caused aJ. Fungi 2021, 7,12 ofhundred-fold yield reduction of linear double-stranded DNA virus, Herpes simplex virus kind I, in human 1BR.three.N fibroblasts [82]. For SsHADV-1, these crucial NHEJ genes could also be key factors for replication in strain DT-8. five. Conclusions Previously, we investigated the early transcriptional response when S. sclerotiorum hyphae had been inoculated with purified SsHADV-1 virions. The results showed that SsHADV1 infection could influence the host Ras-small G protein signal transduction pathway, which may possibly modulate alterations in host metabolism to supply the power for SsHADV-1 invasion and proliferation [29]. In this study, to further study the influence of SsHADV-1 infection on its fungal host, we performed digital RNA-seq and studied the diverse gene expression profiles among the hypovirulent strain DT-8 and virulent virus-free strain DT-8VF in the vegetative stage. We found the SsHADV-1 infection could influence carbohydrate metabolism, suppress the expression of some virulence factors and antiviral RNA silencing genes, and activate the DNA replication and DNA damage response processes. These benefits provide a view of expression difference of S. sclerotiorum genes among manage as well as the infection of SsHADV-1, and also the mechanisms underlying requires further study.Supplementary Materials: The following are readily available on the internet at 10.3390/jof7070493/s1: Figure S1: The cumulative production price of OA of strains DT-8 and DT-8VF; Figure S2: The expression of S. sclerotiorum genes detected by qRT-PCR and RNA-seq; Table S1: Summary of sequencing data. Table S2: The GO enrichment analysis with the up-regulated genes; Table S3: The GO enrichment evaluation from the down-regulated genes; Table S4: The KEGG enrichment evaluation of the up-regulated genes; Table S5: The KEGG enrichment analysis on the down-regulated genes; Table S6: The InterPro domains of SS1G_03342 and SS1G_02074; Table S7: The q.