Identification of a Chlorovirus PBCV-1 Protein Involved in Degrading the Host Cell Wall during Virus Infection

Viruses

Ahmed Esmael¹  LeslieC. Lane²  Abraham Minsky³  Elad Milrot³  IrinaV. Agarkova⁴  JamesL. Van Etten⁴  DavidD. Dunigan⁴  CristianF. Quispe⁴  GarryA. Duncan⁴  JayadriS. Ghosh⁴ 

[1] Botany and Microbiology Department, Faculty of Science, Benha University, Qalubiya Governorate, Banha 13511, Egypt;Department of Plant Pathology, University of Nebraska-Lincoln, Lincoln, NE 68583-0722, USA;Department of Structural Biology, The Weizmann Institute of Science, Rehovot 76100, Israel;Nebraska Center for Virology, University of Nebraska-Lincoln, Lincoln, NE 68583-0900, USA;

关键词: Chlorella;    Phycodnaviridae;    chlorovirus;    PBCV-1;    algal lytic activity;    cell wall degrading activity;   

DOI  :  10.3390/v13050782

来源: DOAJ

【 摘 要 】

Chloroviruses are unusual among viruses infecting eukaryotic organisms in that they must, like bacteriophages, penetrate a rigid cell wall to initiate infection. Chlorovirus PBCV-1 infects its host, Chlorella variabilis NC64A by specifically binding to and degrading the cell wall of the host at the point of contact by a virus-packaged enzyme(s). However, PBCV-1 does not use any of the five previously characterized virus-encoded polysaccharide degrading enzymes to digest the Chlorella host cell wall during virus entry because none of the enzymes are packaged in the virion. A search for another PBCV-1-encoded and virion-associated protein identified protein A561L. The fourth domain of A561L is a 242 amino acid C-terminal domain, named A561L^D4, with cell wall degrading activity. An A561L^D4 homolog was present in all 52 genomically sequenced chloroviruses, infecting four different algal hosts. A561L^D4 degraded the cell walls of all four chlorovirus hosts, as well as several non-host Chlorella spp. Thus, A561L^D4 was not cell-type specific. Finally, we discovered that exposure of highly purified PBCV-1 virions to A561L^D4 increased the specific infectivity of PBCV-1 from about 25–30% of the particles forming plaques to almost 50%. We attribute this increase to removal of residual host receptor that attached to newly replicated viruses in the cell lysates.

【 授权许可】

Unknown