First evidence of host range expansion in virophages and its potential impact on giant viruses and host cells

Said Mougari; Nisrine Chelkha; Dehia Sahmi-Bounsiar; Fabrizio Di Pinto; Philippe Colson; Jonatas Abrahao; Bernard La Scola

We first quantified the impact of virophage on genome replication of Tupanvirus at 48 h p.i. Figure 5a shows that mutant Guarani decreases the replication of Tupanvirus DNA by approximately 3-fold. This low inhibition rate appears relatively similar to what has been found between the wild-type strain and APMV 24 . Experimental studies supported by bioinformatic analyses have shown that in contrast to their virus hosts, virophages become active during a late phase of giant virus infection 17, 24, 35 . Since genome replication is an early step in the cycle of giant viruses, this property may allow them to anticipate virophage parasitism and produce some genomic copies. We then tested the effect on the production of viable particles by quantifying the titer of Tupanvirus from 0 h to 72 h p.i. Our results reveal that mutant Guarani induces a severe decrease in the production of Tupanvirus virions during the virus cycle (Fig. 5b) . We found that in the absence of virophage, the virus was able to increase its titer by up to 500-fold during a one-step growth curve in amoebae. In contrast, infection with the mutant genotype prevented any increase in the virus titer. This inhibition is significantly far higher than that of the wild-type toward APMV 24 , but at 48 h p.i., we still were able to detect the production of infectious virions by end point dilution.