Many studies focused on the exchange of genetic material between viruses and cellular hosts. The diversity of viruses argues that, along the evolutionary history, viruses have shaped the host genomes. While most viruses have many opportunities to exchange genetic material with their hosts, tracing such events is challenging as the origin of the sequences is masked by the high mutation rate of many viruses. On the other end, for completing a successful infection cycle the viruses must cope with the cell machinery for entry, replication and translation while hiding from the host immune system. We collected evidence for instances of viral protein sequences that were most probably ''stolen'' from the hosts. Additionally, a shared ancestry with metazoa is associated with 670 Pfam domain families. For half of these families, the origin of the viral proteins from its host is supported. For about 75% of the cross virus-metazoa families, the viral proteins are significantly shorter than their counterpart host proteins. Most of these cross-taxa viral proteins are single domain proteins and proteins with a simple domain composition relative to the proteins of their hosts. These viral proteins provide insights on the overlooked intimacy of viruses and their multicellular hosts. suggests that the phenomenon of shared sequences is quite broad, and many eukaryotes have been subjected to a genetic material exchange. Among the UniRef90 clusters that contain viruses and eukaryotes ( Figure 1B) , ,70% are from tetrapoda, 13% plants, 13% arthropoda, 4% fungi and only a smaller percentage of other taxa. We focused on the cross-taxa clusters of viruses and mammals (118 clusters include ,2,200 proteins, Figure 1D ). Viruses from Class I (dsDNA viruses with no RNA stage) and class VI (Retro-transcribing ssRNA, Plus strand) are prevalent among those that infect mammals [17] . The dominating Class VI viruses are characterized by their ability to integrate sequences into the host ( Figure 1A , left). Table 1 lists the Class I viral proteins that share sequences with mammals (23 clusters, Figure 1D ). In Class I viruses, the virus enters the nucleus before its replication (with the exception of Poxvirus family) and its infectivity is strongly dependent on the host cell division.